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Hyperoxia
Kinds of Hyperoxia Selected AbstractsExposure of rats to hyperoxia enhances relaxation of isolated aortic rings and reduces infarct size of isolated heartsACTA PHYSIOLOGICA, Issue 4 2002P. Tähepõld ABSTRACT Exposure of rats to hyperoxia before organ harvesting protected their isolated hearts against global ischaemia,reperfusion injury in a previous study. The present study investigates whether hyperoxia influences vasomotor function and regional ischaemia of the heart. Isolated rings of the thoracic aorta were obtained from rats immediately or 24 h after in vivo exposure to 60 min of hyperoxia (>95% O2), and the in vitro dose,response to phenylephrine (PHE), prostaglandin F2, (PGF2,) and endothelin-1 (ET-1), acetylcholine (Ach) and sodium nitroprusside (SNP) was assessed. Hyperoxia in vivo increased the relaxation of aortic rings to Ach and SNP, while it delayed contraction to PHE. The effect was more evident when the vessels were harvested immediately rather than 24 h after hyperoxic exposure. In separate experiments rat hearts were isolated immediately after hyperoxia, buffer-perfused, and subjected to 30 min of regional ischaemia and reperfused for 120 min. Infarct size was determined by triphenyl tetrazolium chloride staining. Hyperoxia significantly reduced infarct size. In normoxic controls 23.0 ± 8.3% of the area at risk was infarcted, while in hyperoxic animals infarct size was 14.8 ± 5.6% of the area at risk (P = 0.012). Exposure of rats to hyperoxia modifies the vasomotor response of isolated aortic rings, and reduces the infarct size of isolated rat heart. These novel aspects of hyperoxic treatment require further studies to explore the potential of its clinical application. [source] Roles of Endothelial Cell Migration and Apoptosis in Vascular Remodeling during Development of the Central Nervous SystemMICROCIRCULATION, Issue 5 2000SUZANNE HUGHES ABSTRACT Objective: To examine the roles of apoptosis, macrophages, and endothelial cell migration in vascular remodeling during development of the central nervous system. Methods: The terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL) technique was combined with Griffonia simplicifolia isolectin B4 histochemistry to detect apoptotic endothelial cells in retinal whole-mount preparations derived from rats at various stages of postnatal development as well as from rat pups exposed to hyperoxia. Macrophages were detected by immunohistochemistry with the monoclonal antibody ED1, and proliferating endothelial cells were identified by incorporation of bromodeoxyuridine. Results: Only small numbers of TUNEL-positive endothelial cells were detected during normal development of the retinal vasculature, with the apoptotic cell density in the inner plexus peaking during the first postnatal week and decreasing markedly during the second week, at a time when vessel retraction was widespread. Neither apoptotic endothelial cells nor macrophages were apparent at sites of initiation of vessel retraction. TUNEL-positive endothelial cells were observed in vessels destined to remain. Hyperoxia induced excessive vessel withdrawal, resulting in the generation of isolated vascular segments containing apoptotic endothelial cells. A topographical analysis showed low numbers of proliferating endothelial cells at sites of angiogenesis whereas vascular proliferation was increased in the adjacent inner plexus. Conclusions: Endothelial cell apoptosis and macrophages do not initiate vessel retraction, but rather contribute to the removal of redundant cells throughout the vasculature. We suggest that vessel retraction is mediated by endothelial cell migration and that endothelial cells derived from retracting vascular segments are redeployed in the formation of new vessels. Only when retraction results in compromised circulation and redeployment is not possible, does endothelial cell apoptosis occur. [source] ORIGINAL RESEARCH: Phosphodiesterase Type 5 Regulation in the Penile Corpora CavernosaTHE JOURNAL OF SEXUAL MEDICINE, Issue S3 2009Ching-Shwun Lin PhD ABSTRACT Introduction., Penile detumescence depends on the hydrolysis of cyclic guanosine monophosphate (cGMP) by phosphodiesterase type 5 (PDE5). It is hoped that a review of publications relevant to the regulation of PDE5 in the penis will be helpful to both scientists and clinicians who are interested in the sciences of erectile function/dysfunction. Aims., The aim of this article is to comprehensively review the mechanisms by which PDE5 activity and expression in the penis are regulated. All published studies relevant to PDE5 regulation in the penis or penile cells will be reviewed. Methods., Entrez (PubMed) was used to search for publications relevant to the topics of this review. Keywords used in the searches included vascular, cavernous, penis, smooth muscle, signaling molecules, erection, priapism, and PDE5. Articles that are dedicated to the study of erectile function/dysfunction were prioritized for citation. Results., Regulation of PDE5 can occur at both protein and gene levels. At protein level, PDE5 is activated by phosphorylation and/or allosteric cGMP binding. Deactivation is carried out by protein phosphatase 1 and thus linked to the Rho-kinase signaling pathway. Cleavage of PDE5 into an inactive form has been shown as carried out by caspase-3. At the gene level, PDE5 expression is regulated at two alternative promoters, PDE5A and PDE5A2, both of which are positively regulated by cyclic adenosine monophosphate and cGMP. Downregulation of PDE5 has been observed in the penis of castrated animals; however, proof of androgen regulation of PDE5 gene requires examination of the smooth muscle content. Hyperoxia and hypoxia, respectively, regulate PDE5 expression positively and negatively. Hypoxic downregulation of PDE5 is a possible mechanism for the development of priapism. Conclusions., PDE5 can be regulated at protein and gene levels. In the penis, changes of PDE5 activity have been linked to its phosphorylation status, and downregulation of PDE5 expression has been associated with hypoxia. Lin CS. PDE5 regulation in the penile corpora nervosa. J Sex Med 2009;6(suppl 3):203,209. [source] Multiple Inert Gas Elimination Technique For Determining Ventilation/Perfusion Distributions In Rat During Normoxia, Hypoxia And HyperoxiaCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2001V Alfaro SUMMARY 1. The use of the multiple inert gas elimination technique (MIGET) in quantifying ventilation/perfusion distributions (V,A/Q,) in small animals, such as the rat, may cause results to be biased due to haemodilution produced by the large volume of liquid infused intravenously. 2. We tested two methods of administering inert gases in rats using the MIGET: (i) standard continuous intravenous administration of inert gases (method A); and (ii) a new method based on the physicochemical properties of each inert gas (method B). This method included acute simultaneous inert gas administration using three pathways: inhalation, intravenous infusion and rectal infusion. Both MIGET methods were applied to obtain data while breathing three different inspiratory fractions of oxygen (FIO2): normoxia, hypoxia and hyperoxia. 3. Inert gas levels obtained from blood or expired air samples were sufficient for chromatographic measurement, at least during a 2 h period. The V,A/Q, distributions reported using both methods were acceptable for all the physiological conditions studied; therefore, the alternative method used here may be useful in further MIGET studies in rats because haemodilution resulting from continuous intravenous infusion of less-soluble gases can be avoided. 4. Normoxic rats showed lower mean values of the V,A/Q, ratio of ventilation distribution and higher mean values of the V,A/Q, ratio of perfusion distribution with the usual method of inert gas administration (method A). These non-significant differences were observed under almost all physiological conditions studied and they could be caused by haemodilution. Nevertheless, the effect of interindividual differences cannot be discarded. An additional effect of the low haematocrit on cardiovascular changes due to low FIO2, such as pulmonary vasoconstriction or increased cardiac output, may explain the lower dispersion of perfusion distributions found in group A during hypoxia. [source] High total antioxidant activity and uric acid in tracheobronchial aspirate fluid of preterm infants during oxidative stress: an adaptive response to hyperoxia?ACTA PAEDIATRICA, Issue 3 2000G Vento The effect of O2 exposure, expressed by mean daily fractional inspired oxygen concentration (FiO2), was evaluated during the first 6 d of life in the tracheobronchial aspirate fluid of 16 mechanically ventilated preterm infants in terms of both antioxidant response and oxidative damage, by measuring total antioxidant activity, uric acid concentrations and protein carbonyl content. Each day linear regression analysis was performed and a positive correlation was found between total antioxidant activity and FiO2 during the study period, especially on day 2 of life (r= 0.91, p < 0.0001), but uric acid correlated only in the first 3 d, especially on the 2nd day (r= 0.83, p < 0.0001). No correlation was found between carbonyl content and FiO2. The highest values of total antioxidant activity (416 and 790 ,mol l,1) were found in 2 babies ventilated with highest FiO2: 1 and 0.80, respectively. Total antioxidant activity was not detectable or was very low in the babies not requiring O2 therapy. The highest value of uric acid (270 ,mol l,1) was found in the baby ventilated with 100% oxygen. Uric acid concentrations obtained in these babies were much higher then those reported in the bronchoalveolar lavage fluid of adults. Preterm babies seem to have an antioxidant response in the tracheobronchial aspirate fluid following an oxidative stress and uric acid may be physiologically important as an antioxidant of the respiratory tract, especially during the first days of life. [source] Effects of normobaric hyperoxia on water content in different organs in ratsACTA PHYSIOLOGICA, Issue 1 2002L. E. B. Stuhr ABSTRACT Pulmonary oxygen toxicity is a dose-dependent effect on alveolar epithelial and endothelial cells resulting in pulmonary oedema. Any concomitant effects on systemic capillary endothelium would be expected to result in capillary leakage and an increase in the tissues' water content. Total tissue water (TTW) in different organs was therefore studied in freely moving rats exposed to 100% O2 at normobaric pressure for 24 or 48 h, and compared to air-breathing control rats. The TTW for the following tissues was measured: Trachea, left bronchus, left lung, left and right ventricle, left kidney, skin (left paw-hindlimb), skin (back of the rat), left brain, left eye and thigh muscle left side. There was a significant increase in TTW of the lung accompanied by pleural effusion after 48 h of oxygen exposure as expected in all exposed animals. There was a small increase in TTW of the paw only, and a small decrease or no change in other tissues after 24 and 48 h of exposure. We conclude that there is no evidence of systemic capillary dysfunction as measured by tissue water content after exposure to hyperoxia in a dosage causing pulmonary oedema. [source] Exposure of rats to hyperoxia enhances relaxation of isolated aortic rings and reduces infarct size of isolated heartsACTA PHYSIOLOGICA, Issue 4 2002P. Tähepõld ABSTRACT Exposure of rats to hyperoxia before organ harvesting protected their isolated hearts against global ischaemia,reperfusion injury in a previous study. The present study investigates whether hyperoxia influences vasomotor function and regional ischaemia of the heart. Isolated rings of the thoracic aorta were obtained from rats immediately or 24 h after in vivo exposure to 60 min of hyperoxia (>95% O2), and the in vitro dose,response to phenylephrine (PHE), prostaglandin F2, (PGF2,) and endothelin-1 (ET-1), acetylcholine (Ach) and sodium nitroprusside (SNP) was assessed. Hyperoxia in vivo increased the relaxation of aortic rings to Ach and SNP, while it delayed contraction to PHE. The effect was more evident when the vessels were harvested immediately rather than 24 h after hyperoxic exposure. In separate experiments rat hearts were isolated immediately after hyperoxia, buffer-perfused, and subjected to 30 min of regional ischaemia and reperfused for 120 min. Infarct size was determined by triphenyl tetrazolium chloride staining. Hyperoxia significantly reduced infarct size. In normoxic controls 23.0 ± 8.3% of the area at risk was infarcted, while in hyperoxic animals infarct size was 14.8 ± 5.6% of the area at risk (P = 0.012). Exposure of rats to hyperoxia modifies the vasomotor response of isolated aortic rings, and reduces the infarct size of isolated rat heart. These novel aspects of hyperoxic treatment require further studies to explore the potential of its clinical application. [source] The changes in neuromuscular excitability with normobaric hyperoxia in humansEXPERIMENTAL PHYSIOLOGY, Issue 1 2010Christelle Brerro-Saby Based on previous observations in hyperbaric hyperoxia, we hypothesized that normobaric hyperoxia, often used during general anaesthesia and resuscitation, might also induce a neuromuscular excitability. In heathy volunteers, we studied the consequences of a 50 min period of pure oxygen breathing on the neuromuscular conduction time (CT), the amplitude of the compound evoked muscle potential (M-wave), the latency and amplitude of the Hoffman reflex (H reflex) and the electromyographic tonic vibratory response (TVR) of the flexor digitorum superficialis muscle to explore the proprioceptive reflex loop. Hyperoxia-induced oxidative stress was measured by the changes in blood markers of lipid peroxidation (thiobarbituric acid reactive substances, TBARS) and antioxidant response (reduced ascorbic acid, RAA). During hyperoxia, the M-wave amplitude increased, both CT and H reflex latency were shortened, and the H reflex amplitude increased. By contrast, TVR significantly decreased. Concomitantly, an oxidative stress was assessed by increased TBARS and decreased RAA levels. This study shows the existence of dual effects of hyperoxia, which facilitates the muscle membrane excitability, nerve conduction and spinal reflexes, but reduces the gain of the proprioceptive reflex loop. The activation of the group IV muscle afferents by hyperoxia and the resulting oxidative stress might explain the TVR depression. [source] Breath-holding and its breakpointEXPERIMENTAL PHYSIOLOGY, Issue 1 2006M. J. Parkes This article reviews the basic properties of breath-holding in humans and the possible causes of the breath at breakpoint. The simplest objective measure of breath-holding is its duration, but even this is highly variable. Breath-holding is a voluntary act, but normal subjects appear unable to breath-hold to unconsciousness. A powerful involuntary mechanism normally overrides voluntary breath-holding and causes the breath that defines the breakpoint. The occurrence of the breakpoint breath does not appear to be caused solely by a mechanism involving lung or chest shrinkage, partial pressures of blood gases or the carotid arterial chemoreceptors. This is despite the well-known properties of breath-hold duration being prolonged by large lung inflations, hyperoxia and hypocapnia and being shortened by the converse manoeuvres and by increased metabolic rate. Breath-holding has, however, two much less well-known but important properties. First, the central respiratory rhythm appears to continue throughout breath-holding. Humans cannot therefore stop their central respiratory rhythm voluntarily. Instead, they merely suppress expression of their central respiratory rhythm and voluntarily ,hold' the chest at a chosen volume, possibly assisted by some tonic diaphragm activity. Second, breath-hold duration is prolonged by bilateral paralysis of the phrenic or vagus nerves. Possibly the contribution to the breakpoint from stimulation of diaphragm muscle chemoreceptors is greater than has previously been considered. At present there is no simple explanation for the breakpoint that encompasses all these properties. [source] Oxidative damage is a potential cause of cone cell death in retinitis pigmentosaJOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2005JiKui Shen Retinitis pigmentosa (RP) is a prevalent cause of blindness caused by a large number of different mutations in many different genes. The mutations result in rod photoreceptor cell death, but it is unknown why cones die. In this study, we tested the hypothesis that cones die from oxidative damage by performing immunohistochemical staining for biomarkers of oxidative damage in a transgenic pig model of RP. The presence of acrolein- and 4-hydroxynonenal-adducts on proteins is a specific indicator that lipid peroxidation has occurred, and there was strong immunofluorescent staining for both in cone inner segments (IS) of two 10-month-old transgenic pigs in which almost all rods had died, compared to faint staining in two 10-month-old control pig retinas. In 22- and 24-month-old transgenic pigs in which all rods and many cones had died, staining was strong in cone axons and some cell bodies as well as IS indicating progression in oxidative damage between 10 and 22 months. Biomarkers for oxidative damage to proteins and DNA also showed progressive oxidative damage to those macromolecules in cones during the course of RP. These data support the hypothesis that the death of rods results in decreased oxygen consumption and hyperoxia in the outer retina resulting in gradual cone cell death from oxidative damage. This hypothesis has important therapeutic implications and deserves rapid evaluation. © 2005 Wiley-Liss, Inc. [source] Increased expression of glial cell line-derived neurotrophic factor protects against oxidative damage-induced retinal degenerationJOURNAL OF NEUROCHEMISTRY, Issue 3 2007Aling Dong Abstract Oxidative damage contributes to retinal cell death in patients with age-related macular degeneration or retinitis pigmentosa. One approach to treatment is to identify and eliminate the sources of oxidative damage. Another approach is to identify treatments that protect cells from multiple sources of oxidative damage. In this study, we investigated the effect of increased expression of glial cell line-derived neurotrophic factor (GDNF) in three models of oxidative damage-induced retinal degeneration. Double transgenic mice with doxycycline-inducible expression of GDNF in the retina were exposed to paraquat, FeSO4, or hyperoxia, all sources of oxidative damage and retinal cell death. Compared to controls, mice with increased expression of GDNF in the retina showed significant preservation of retinal function measured by electroretinograms, reduced thinning of retinal cell layers, and fewer TUNEL-positive cells indicating less retinal cell death. Mice over-expressing GDNF also showed less staining for acrolein, nitrotyrosine, and 8-hydroxydeoxyguanosine, indicating less oxidative damage to lipids, proteins, and DNA. This suggests that GDNF did not act solely to allow cells to tolerate higher levels of oxidative damage before initiation of apoptosis, but also reduced damage from oxidative stress to critical macromolecules. These data suggest that gene transfer of Gdnf should be considered as a component of therapy for retinal degenerations in which oxidative damage plays a role. [source] Roles of Endothelial Cell Migration and Apoptosis in Vascular Remodeling during Development of the Central Nervous SystemMICROCIRCULATION, Issue 5 2000SUZANNE HUGHES ABSTRACT Objective: To examine the roles of apoptosis, macrophages, and endothelial cell migration in vascular remodeling during development of the central nervous system. Methods: The terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL) technique was combined with Griffonia simplicifolia isolectin B4 histochemistry to detect apoptotic endothelial cells in retinal whole-mount preparations derived from rats at various stages of postnatal development as well as from rat pups exposed to hyperoxia. Macrophages were detected by immunohistochemistry with the monoclonal antibody ED1, and proliferating endothelial cells were identified by incorporation of bromodeoxyuridine. Results: Only small numbers of TUNEL-positive endothelial cells were detected during normal development of the retinal vasculature, with the apoptotic cell density in the inner plexus peaking during the first postnatal week and decreasing markedly during the second week, at a time when vessel retraction was widespread. Neither apoptotic endothelial cells nor macrophages were apparent at sites of initiation of vessel retraction. TUNEL-positive endothelial cells were observed in vessels destined to remain. Hyperoxia induced excessive vessel withdrawal, resulting in the generation of isolated vascular segments containing apoptotic endothelial cells. A topographical analysis showed low numbers of proliferating endothelial cells at sites of angiogenesis whereas vascular proliferation was increased in the adjacent inner plexus. Conclusions: Endothelial cell apoptosis and macrophages do not initiate vessel retraction, but rather contribute to the removal of redundant cells throughout the vasculature. We suggest that vessel retraction is mediated by endothelial cell migration and that endothelial cells derived from retracting vascular segments are redeployed in the formation of new vessels. Only when retraction results in compromised circulation and redeployment is not possible, does endothelial cell apoptosis occur. [source] Anesthesia for free vascularized tissue transferMICROSURGERY, Issue 2 2009Natalia Hagau M.D., Ph.D. Anesthesia may be an important factor in maximizing the success of microsurgery by controlling the hemodynamics and the regional blood flow. The intraanesthetic basic goal is to maintain an optimal blood flow for the vascularized free flap by: increasing the circulatory blood flow, maintaining a normal body temperature to avoid peripheral vasoconstriction, reducing vasoconstriction resulted from pain, anxiety, hyperventilation, or some drugs, treating hypotension caused by extensive sympathetic block and low cardiac output. A hyperdynamic circulation can be obtained by hypervolemic or normovolemic hemodilution and by decrease of systemic vascular resistance. The importance of proper volume replacement has been widely accepted, but the optimal strategy is still open to debate. General anesthesia combined with various types of regional anesthesia is largely preferred for microvascular surgery. Maintenance of homeostasis through avoidance of hyperoxia, hypocapnia, and hypovolemia (all factors that can decrease cardiac output and induce local vasoconstriction) is a well-established perioperative goal. As the ischemia,reperfusion injury could occur, inhalatory anesthetics as sevoflurane (that attenuate the consequences of this process) seem to be the anesthetics of choice. © 2008 Wiley-Liss, Inc. Microsurgery, 2009. [source] Cell-specific expression of manganese superoxide dismutase protein in the lungs of patients with respiratory distress syndrome, chronic lung disease, or persistent pulmonary hypertension,PEDIATRIC PULMONOLOGY, Issue 3 2001Tiina M. Asikainen MD Abstract The developmental profile of manganese superoxide dismutase (MnSOD) and its regulation in hyperoxia vary between species. We hypothesized that MnSOD increases in human lung in response to oxygen treatment, although this response could be restricted to certain cell types and depend on gestational age. Therefore, the cell-specific expression of pulmonary immunoreactive MnSOD protein was investigated during development, and in patients with respiratory distress syndrome (RDS), chronic lung disease (CLD), or persistent pulmonary hypertension (PPHN). Throughout ontogenesis, all cell types expressed MnSOD, but the most intense positivity was found in bronchiolar epithelium and (pre-) type-II pneumocytes. MnSOD protein did not increase during development. The MnSOD staining pattern in arterial endothelium was more intense in RDS patients than in age-matched controls, but this may be related to induction of MnSOD by increased blood flow rather than by oxygen. MnSOD expression in other cell types of RDS, CLD, or PPHN patients did not differ from that in age-matched controls. We conclude that, in terms of mitochondrial enzymatic superoxide scavenging capacity, preterm infants are not more vulnerable than term infants to oxygen-induced lung injury at physiological oxygen concentrations. However, the inability to induce MnSOD in response to oxygen treatment may result in a poor outcome. Pediatr Pulmonol. 2001; 32:193,200. © 2001 Wiley-Liss, Inc. [source] Original Article: Detection of p16 promoter methylation in premature rats with chronic lung disease induced by hyperoxiaPEDIATRICS INTERNATIONAL, Issue 4 2010Xiaohong Yue Abstract Background:, The aim of the present study was to investigate p16 promoter methylation in premature rats with chronic lung disease (CLD) induced by hyperoxia. Methods:, Eighty Wistar rats were randomized into the hyperoxia group (fraction of inspired oxygen [FiO2]= 900 mL/L) or the control group (FiO2= 210 mL/L), 40 for each group. Semi-nested methylation-specific polymerase chain reaction (sn-MSP) was applied to detect p16 promoter hypermethylation in lung tissues. Additionally, p16 mRNA and protein expression was detected on reverse transcription,polymerase chain reaction (RT-PCR), western blot and the strept actividin,biotin complex method. Results:, Extended exposure to hyperoxia led to increased methylation, and the methylation level reached a peak in the period of maximum pulmonary fibrosis in the hyperoxia group, while the methylation did not occur in the control group. The methylation rates on semi-nested PCR (sn-PCR) and nested-MSP were, respectively, 52.5% and 42.5% in the hyperoxia group. There was no statistically significant difference between the two methods. The p16 mRNA and protein expression was significantly higher in those with p16 promoter hypermethylation than those without. Conclusion:, Exposure to hyperoxia may induce p16 promoter hypermethylation in lung tissues in premature rats, and methylation risk increases as exposure extends. p16 promoter methylation induced by hyperoxia may be one of the mechanisms for low p16 mRNA and protein expression. [source] Activation of the retrotrapezoid nucleus by posterior hypothalamic stimulationTHE JOURNAL OF PHYSIOLOGY, Issue 21 2009Michal G. Fortuna The retrotrapezoid nucleus (RTN) contains chemically defined neurons (ccRTN neurons) that provide a pH-regulated excitatory drive to the central respiratory pattern generator. Here we test whether ccRTN neurons respond to stimulation of the perifornical hypothalamus (PeF), a region that regulates breathing during sleep, stress and exercise. PeF stimulation with gabazine increased blood pressure, phrenic nerve discharge (PND) and the firing rate of ccRTN neurons in isoflurane-anaesthetized rats. Gabazine produced an approximately parallel upward shift of the steady-state relationship between ccRTN neuron firing rate and end-tidal CO2, and a similar shift of the relationship between PND and end-tidal CO2. The central respiratory modulation of ccRTN neurons persisted after gabazine without a change in pattern. Morphine administration typically abolished PND and reduced the discharge rate of most ccRTN neurons (by 25% on average). After morphine administration, PeF stimulation activated the ccRTN neurons normally but PND activation and the central respiratory modulation of the ccRTN neurons were severely attenuated. In the same rat preparation, most (58%) ccRTN neurons expressed c-Fos after exposure to hypercapnic hyperoxia (6,7% end-tidal CO2; 3.5 h; no hypothalamic stimulation) and 62% expressed c-Fos under hypocapnia (,3% end-tidal CO2) after PeF stimulation. Under baseline conditions (,3% end-tidal CO2, hyperoxia, no PeF stimulation) few (11%) ccRTN neurons expressed c-Fos. In summary, most ccRTN neurons are excited by posterior hypothalamic stimulation while retaining their normal response to CNS acidification. ccRTN neurons probably contribute both to the chemical drive of breathing and to the feed-forward control of breathing associated with emotions and or locomotion. [source] The cardiovascular effects of normobaric hyperoxia in patients with heart rate fixed by permanent pacemakerANAESTHESIA, Issue 2 2010K. J. Anderson Summary To investigate whether the established reductions in heart rate and cardiac output with hyperoxia in humans are primary effects or secondary to increases in systemic vascular resistance, we paced the hearts of nine patients with permanent pacemakers at a fixed rate when breathing either medical air (inspired O2 fraction 0.21) or oxygen (inspired O2 fraction 0.80) in a randomised, double-blind fashion. A thoracic bio-impedance machine was used to measure heart rate, stroke volume and blood pressure and calculate cardiac index and systemic vascular resistance index. Oxygen caused no change in cardiac index (p = 0.18), stroke index (p = 0.44) or blood pressure (p = 0.52) but caused a small (5.5%) increase in systemic vascular resistance index (p = 0.03). This suggests that hyperoxia has no direct myocardial depressant effects, but that the changes in cardiac output reported in previous studies are secondary to changes in systemic vascular resistance. [source] T2*-weighted magnetic resonance imaging with hyperoxia in acute ischemic strokeANNALS OF NEUROLOGY, Issue 1 2010Krishna A. Dani MBChB Objective We describe the first clinical application of transient hyperoxia ("oxygen challenge") during T2*-weighted magnetic resonance imaging (MRI), to detect differences in vascular deoxyhemoglobin between tissue compartments following stroke. Methods Subjects with acute ischemic stroke were scanned with T2*-weighted MRI and oxygen challenge. For regions defined as infarct core (diffusion-weighted imaging lesion) and presumed penumbra (perfusion-diffusion mismatch [threshold = Tmax ,4 seconds], or regions exhibiting diffusion lesion expansion at day 3), T2*-weighted signal intensity,time curves corresponding to the duration of oxygen challenge were generated. From these, the area under the curve, gradient of incline of the signal increase, time to maximum signal, and percentage signal change after oxygen challenge were measured. Results We identified 25 subjects with stroke lesions >1ml. Eighteen subjects with good quality T2*-weighted signal intensity,time curves in the contralateral hemisphere were analyzed. Curves from the diffusion lesion had a smaller area under the curve, percentage signal change, and gradient of incline, and longer time to maximum signal (p < 0.05, n = 17) compared to normal tissue, which consistently showed signal increase during oxygen challenge. Curves in the presumed penumbral regions (n = 8) showed varied morphology, but at hyperacute time points (<8 hours) showed a tendency to greater percentage signal change. Interpretation Differences in T2*-weighted signal intensity,time curves during oxygen challenge in brain regions with different pathophysiological states after stroke are likely to reflect differences in deoxyhemoglobin concentration, and therefore differences in metabolic activity. Despite its underlying complexities, this technique offers a possible novel mode of metabolic imaging in acute stroke. ANN NEUROL 2010;68:37,47 [source] CURRENT CONTROVERSIES IN THE MANAGEMENT OF PATIENTS WITH SEVERE TRAUMATIC BRAIN INJURYANZ JOURNAL OF SURGERY, Issue 3 2006Alexios A. Adamides Background: Traumatic brain injury is a major cause of mortality and morbidity, particularly among young men. The efficacy and safety of most of the interventions used in the management of patients with traumatic brain injury remain unproven. Examples include the ,cerebral perfusion pressure-targeted' and ,volume-targeted' management strategies for optimizing cerebrovascular haemodynamics and specific interventions, such as hyperventilation, osmotherapy, cerebrospinal fluid drainage, barbiturates, decompressive craniectomy, therapeutic hypothermia, normobaric hyperoxia and hyperbaric oxygen therapy. Methods: A review of the literature was performed to examine the evidence base behind each intervention. Results: There is no class I evidence to support the routine use of any of the therapies examined. Conclusion: Well-designed, large, randomized controlled trials are needed to determine therapies that are safe and effective from those that are ineffective or harmful. [source] Acid,base balance in sea bass (Dicentrarchus labrax L.) in relation to water oxygen concentrationAQUACULTURE RESEARCH, Issue 12 2003S Cecchini Abstract The influence of water oxygen concentration on the acid,base balance of sea bass was evaluated. Fish weighing 200,250 g were cultured under different dissolved oxygen concentrations of 64%, 97%, 150% and 250% saturation (92.7, 140.5, 217.5 and 362.7 mmHg respectively) under mild hypoxia, normoxia, mild hyperoxia and high hyperoxia conditions. The results showed that high hyperoxia and mild hypoxia conditions modified some blood parameters significantly when compared with fish held under the normoxia condition, while no differences were shown with respect to the acid,base balance of fish cultured under normoxia and mild hyperoxia conditions. This testifies that the mild hyperoxia condition does not produce physiological disturbances in the acid,base status of sea bass and it could be considered a favourable condition in sea bass land-based farming, mainly in comparison with the mild hypoxia condition, responsible for other physiological problems. [source] Effects of in vitro exposure to ozone and/or hyperoxia on superoxide dismutase, catalase, glutathione and lipid peroxidation in red blood cells and plasma of rainbow trout, Oncorhynchus mykiss (Walbaum)AQUACULTURE RESEARCH, Issue 3 2002O Ritola Abstract In aquaculture, ozone is used as a disinfectant. In its production, extensive amounts of oxygen are formed resulting in hyperoxic conditions in culture units. Both ozone and hyperoxia have the potential to be toxic via pro-oxidant mechanisms and to activate antioxidant defence systems in cultured species. To eliminate systemic effects, blood of rainbow trout, Oncorhynchus mykiss (Walbaum), was exposed in vitro for 5 min to ozone/hyperoxia or hyperoxia, and changes in antioxidant defences and lipid peroxidation were measured after exposure. Ozone exposure caused severe damage in red blood cells (rbc) detected as increased lipid peroxidation and oxidized glutathione (GSSG) levels in both plasma and rbc. Oxygen exposure alone increased intracellular lipid peroxidation and GSSG levels 10 min after exposure and was not evident in the plasma at any time. Ozone, but not oxygen exposure, decreased reduced glutathione (GSH) levels in plasma, and the changes were negatively correlated with increased lipid peroxidation in rbc, indicating that extracellular GSH has a dynamic role in the protection of rbc from direct oxidation by ozone. Both ozone and hyperoxic conditions increased superoxide dismutase (SOD) activity in rbc 3 and 6 h after exposure. In contrast, catalase activity was only increased 10 min after oxygen exposure, suggesting other catalase activation mechanisms rather than enzyme induction. The recovery of lipid peroxidation and GSSG levels in rbc after hyperoxia, but not ozone exposure, indicated a capacity to defend against hyperoxia-produced oxidative damage, but an overwhelming of antioxidant defences by ozone in rainbow trout rbc in vitro. [source] Protective effects of triamcinolone acetonide upon the upregulation and phosphorylation of GAP 43 in an animal model of retinopathy of prematurityACTA OPHTHALMOLOGICA, Issue 6 2010In Y. Chung Acta Ophthalmol. 2010: 88: e217,e221 Abstract. Purpose:, The aim of the current study was to investigate the effects of triamcinolone acetonide (TA) upon the expression and phosphorylation of growth-associated protein 43 (GAP 43) in the retinas of oxygen-induced retinopathy (OIR) rats. Methods:, Oxygen-induced retinopathy was induced by exposing Sprague-Dawley rats to hyperoxia (80% oxygen) from postnatal (P) days 2,14 and then returning the rats to normoxic conditions. Triamcinolone acetonide or a conditioned saline (control) was injected intravitreally into the right or left eye, respectively, of OIR rats at P15. We then assessed the molecular and histological changes in the expression of GAP 43 and phospho-GAP 43 in OIR and control rat retinas, and also after treatment with TA by RT-PCR, Western blotting and immunohistochemistry. Results:, Growth-associated protein 43 mRNA levels were found to be increased by 1.6-fold (p = 0.001, n = 5) in the retinas of P18 OIR rats compared with the control rats. The protein levels of GAP 43 and phospho-GAP43 were found to be elevated in the retina of P18 OIR rats (2.40- and 2.39-fold greater than each control, p<0.001, n = 5, respectively). Immunoreactivities of GAP 43 and phospho-GAP 43 were stronger in the inner plexiform layer in OIR rat retinas compared with the control. However, treatment with TA attenuated GAP 43 and phospho-GAP 43 upregulation in the OIR retinas. Conclusion:, Our results indicate that GAP 43 and phospho-GAP 43 participate in retinal (potentially pathologic) changes following oxygen-induced damage. Triamcinolone acetonide protects the retinal damage in relatively hypoxic retinas of OIR rats. Therefore, TA treatment does not induce the expression and phosphorylation of GAP 43 in OIR rat retinas. [source] 3122: Regulation of retinal tissue oxygenationACTA OPHTHALMOLOGICA, Issue 2010CJ POURNARAS Purpose To evaluate the changes in the retinal oxygen partial pressure (PO2) following physiological stimuli. Methods Evaluation of either the preretinal and intraretina partial pressure of oxygen (PO2) distribution, using oxygen sensitive microelectrodes, in various animal models. Measurements were obtained during changes of the perfusion pressure, systemic hyperoxia, hypoxia, hypercapnia, carbogen breathing and following carbonic anydrase inhibitors use. Results The oxygen tension (PO2) in the inner half of the retina remains largely unaffected by moderate changes in perfusion pressure. The increase of the systemic PaO2 through breathing of 100% O2 (hyperoxia) induces endothelin (ET) mediated marked vasoconstriction of the inner retinal arterioles in both anesthetized animals and normal human subjects. The regulatory vasoconstriction maintains the PO2 in retinal tissue constant. A decrease in PaO2 (hypoxia) induces a vasodilation of the retinal arterioles through endothelium-derived NO release. As a result, trans-retinal PO2 profiles made during steps of systemic hypoxia have shown that the values measured in the inner retina up to half of its thickness, remain rather stable. By contrast, the PO2 values, measured close to the choroid and in the outer retina, decrease in a linear manner with the decrease of the PaO2. An increase in the PaCO2 (hypercapnia) of arteriolar blood, produces an increase in retinal blood flow and retinal tissue PO2. Intravenous injection of acetazolamide (carbonic anhydrase inhibitor) produces an increase in preretinal PO2 due to dilation of the retinal vessels Conclusion Thanks to the autoregulatory capability of the retinal circulation, the oxygen tension (PO2) in the inner half of the retina, remains largely unaffected during physiological stimuli. [source] Retinal arterioles have impaired reactivity to hyperoxia in type 1 diabetesACTA OPHTHALMOLOGICA, Issue 4 2010Birgitte L. Justesen Abstract. Purpose:, Diabetes has adverse effects on the retinal microvasculature. The purpose of this study was to compare the effects of inhalation of hypoxic, hyperoxic and normoxic,hypercapnic gas mixtures on retinal vessel diameter in people with and without diabetes. Methods:, Sixty-one participants (aged 24,50 years) 29 with (male : female ratio 2.6 : 1) and 32 without (male : female ratio 0.7 : 1) diabetes, inhaled hypoxic, hyperoxic and normoxic,hypercapnic gas mixtures for 3,5 mins. The diameters of arterioles and venules were measured using digital retinal images taken before and after gas inhalation. Results:, There was no significant difference in the diameters of arterioles and venules prior to gas inhalation in people with and without diabetes. Inhalation of the hyperoxic gas mixture caused a statistically significant decrease in arteriolar and venular diameters without altering mean arterial pressure significantly. Arteriolar vasoconstriction in response to the hyperoxic gas mixture was significantly reduced in people with diabetes (3.95% versus 7.75%; p = 0.04), but venular vasoconstriction did not differ significantly. A hypoxic gas mixture caused increased arteriolar and venular diameter and a normoxic,hypercapnic gas mixture had no significant effect on vessel diameter. Responses to hypoxic and normoxic,hypercapnic gas did not differ significantly between diabetes and non-diabetes subjects. Conclusions:, Type 1 diabetes impairs retinal arteriolar responses to hyperoxia. Abnormalities in retinal arteriolar reactivity in response to oxygen may play a role in the development of diabetic retinopathy and this technique may represent a simple means of identifying early abnormalities in the reactivity of retinal arterioles in diabetes. [source] Retinal photocoagulation and oxygenationACTA OPHTHALMOLOGICA, Issue 2009CJ POURNARAS Purpose The clinical role of photocoagulation for the treatment of hypoxia related complications of retinal ischemic microangiopathies is well established. Methods Measurements of the partial pressure of oxygen (PO2) distribution within the the retina in various animal species using oxygen sensitive microelectrodes and evaluation of the retinal vessels reactivity by laser doppler velocimetry gave additional insights concerning photocoagulation mechanisms. Results The PO2 within the vitreo-retinal interface is heterogeneous. Preretinal and trans-retinal PO2 profiles indicate that the preretinal PO2 far away from vessels remain constant in all retinal areas. Intervascular intraretinal PO2 gradually decreases from both the vitreo-retinal interface and the choroid towards the mid-retina. Close to the pigment epithelium, it is significantly higher than at the vitreoretinal interface due to the much higher O2 supply provided by choroidal compaires to retinal circulation. Laser photocoagulation reduces the outer retina O2 consumption and allows O2 diffusion into the inner retina from the choroid raising the PO2 in the inner healthy retinal layers and in the preretinal intervascular normal areas. In this way laser treatment relieves retinal hypoxia in experimental branch vein occlusion (BRVO). In patients with diabetic retinopathy (DR), the retinal PO2 is higher in areas previously treated with laser. Following photocoagulation, the resulting reversal of hypoxia, the retinal vasculature constriction and the improvement of the regulatory response to hyperoxia all affect favorably both the retinal neovascularisation and macular edema. Conclusion Photocoagulation induces an increase of the inner retinal oxygenation reversing the retinal hypoxia and improving the regulatory response of the retinal vessels [source] New insights into the development of retinopathy of prematurity , importance of early weight gainACTA PAEDIATRICA, Issue 4 2010A Hellström Abstract Evidence is accumulating that one of the strongest predictors of retinopathy of prematurity (ROP), in addition to low gestational age, is poor weight gain during the first weeks of life. In infants born preterm, the retina is not fully vascularised. The more premature the child, the larger is the avascular area. In response to hypoxia, vascular endothelial growth factor (VEGF) is secreted. For appropriate VEGF-induced vessel growth, sufficient levels of insulin-like growth factor I (IGF-I) in serum are necessary. IGF-I is a peptide, related to nutrition supply, which is essential for both pre- and post-natal general growth as well as for growth of the retinal vasculature. In prematurely born infants, serum levels are closely related to gestational age and are lower in more prematurely born infants. At preterm birth the placental supply of nutrients is lost, growth factors are suddenly reduced and general as well as vascular growth slows down or ceases. In addition, the relative hyperoxia of the extra-uterine milieu, together with supplemental oxygen, causes a regression of already developed retinal vessels. Postnatal growth retardation is a major problem in very preterm infants. Both poor early weight gain and low serum levels of IGF-I during the first weeks/months of life have been found to be correlated with severity of ROP. Conclusion: This review will focus on the mechanisms leading to ROP by exploring factors responsible for poor early weight gain and abnormal vascularisation of the eye of the preterm infant. [source] Glutamine attenuates hyperoxia-induced acute lung injury in miceCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1 2010Wann-Cherng Perng Summary 1.,Glutamine is an amino acid that is used to treat various diseases. Glutamine has been reported to have protective effects in human pulmonary epithelia-like cells exposed to hyperoxia. However, the effects of glutamine in hyperoxia-induced lung injury have not been investigated in vivo. 2.,Mice treated with saline or glutamine [(750 mg/kg) intravenously] were randomly exposed to hyperoxia for 48 or 72 h. Control mice treated with saline or glutamine were exposed to room air. Cytokine levels in bronchoalveolar lavage fluid (BALF), heat shock protein (HSP) 70, the wet/dry (W/D) weight ratio, malondialdehyde (MDA) levels, myeloperoxidase (MPO) activity and pathoglogical findings in lung tissue were evaluated to determine the effects of glutamine on acute lung injury. In addition, survival was monitored. 3.,Lung expression of HSP70 was significantly enhanced in both the control (room air) and 48 and 72 h hyperoxic glutamine-treated mice. The W/D ratio, BALF concentrations of tumour necrosis factor-, and interleukin-6, MDA levels, MPO activity, neutrophil infiltration and interstitial oedema in lung tissue were significantly lower at 48 and 72 h of hyperoxia in glutamine-treated mice compared with saline-treated mice. 4.,In a separate series of experiments evaluating survival, after 96 h continuous exposure to hyperoxia, all saline-treated mice died. In contrast, all glutamine-treated mice died after 108 h exposure to hyperoxia. 5.,The data suggest that glutamine administered to mice during hyperoxia has a protective effect against hyperoxia-induced acute lung injury and improves survival. [source] Multiple Inert Gas Elimination Technique For Determining Ventilation/Perfusion Distributions In Rat During Normoxia, Hypoxia And HyperoxiaCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2001V Alfaro SUMMARY 1. The use of the multiple inert gas elimination technique (MIGET) in quantifying ventilation/perfusion distributions (V,A/Q,) in small animals, such as the rat, may cause results to be biased due to haemodilution produced by the large volume of liquid infused intravenously. 2. We tested two methods of administering inert gases in rats using the MIGET: (i) standard continuous intravenous administration of inert gases (method A); and (ii) a new method based on the physicochemical properties of each inert gas (method B). This method included acute simultaneous inert gas administration using three pathways: inhalation, intravenous infusion and rectal infusion. Both MIGET methods were applied to obtain data while breathing three different inspiratory fractions of oxygen (FIO2): normoxia, hypoxia and hyperoxia. 3. Inert gas levels obtained from blood or expired air samples were sufficient for chromatographic measurement, at least during a 2 h period. The V,A/Q, distributions reported using both methods were acceptable for all the physiological conditions studied; therefore, the alternative method used here may be useful in further MIGET studies in rats because haemodilution resulting from continuous intravenous infusion of less-soluble gases can be avoided. 4. Normoxic rats showed lower mean values of the V,A/Q, ratio of ventilation distribution and higher mean values of the V,A/Q, ratio of perfusion distribution with the usual method of inert gas administration (method A). These non-significant differences were observed under almost all physiological conditions studied and they could be caused by haemodilution. Nevertheless, the effect of interindividual differences cannot be discarded. An additional effect of the low haematocrit on cardiovascular changes due to low FIO2, such as pulmonary vasoconstriction or increased cardiac output, may explain the lower dispersion of perfusion distributions found in group A during hypoxia. [source] Hyperoxia-induced arterial compliance decrease in healthy manCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 1 2005Pascal Rossi Summary Introduction:, Oxygen therapy is commonly used in emergency department and intensive care units without careful evaluation of its effects, especially on the haemodynamics and artery characteristics. Materials and methods:, A prospective laboratory study evaluated brachial circulatory effects of normobaric hyperoxia using ultrasonography-Doppler. The study was set in a hospital research laboratory. The subjects were thirteen healthy volunteers. Investigations were performed under normal air ventilation and after 20 min of hyperoxic mixture ventilation using a high concentration mask. Two dimensional images and brachial blood flow velocities were recorded using ultrasonography and pulsed Doppler to study changes in cross sectional area, blood flow, resistance index, and cross-sectional compliance coefficient. Results:, During hyperoxic exposure, mean PaO2 was 372 ± 21 mmHg. A significant decrease of heart rate was observed. Arterial pressures (systolic and diastolic arterial pressures) were not modified. A decrease of cross sectional areas at end diastole and end systole was observed. Pulsed Doppler study showed a decrease of brachial artery blood flow and an increase of the resistance index. Furthermore, a decrease of the cross-sectional compliance coefficient was observed during hyperoxic exposure in all subjects. Conclusion:, This study using two-dimensional ultrasonography and pulsed Doppler could demonstrate an increase in brachial arterial tone and a decrease in brachial blood flow under normobaric hyperoxia. [source] Reactive Oxygen Species, Aging, and Antioxidative NutraceuticalsCOMPREHENSIVE REVIEWS IN FOOD SCIENCE AND FOOD SAFETY, Issue 1 2004J. Lee ABSTRACT The important roles of reactive oxygen species in diseases related to aging and the necessity and benefits of antioxidative nutraceuticals in the prevention of diseases and promotion of healthy aging have been extensively reported in recent years. Oxygen is an essential component of living organisms. The generation of reactive oxygen species such as superoxide anion, hydrogen peroxide, hydroxyl radicals, and singlet oxygen is inevitable in aerobic metabolism of the body. Reactive oxygen species cause lipid oxidation, protein oxidation, DNA strand break and base modification, and modulation of gene expression. In the past several years, unprecedented progress has been made in the recognition and understanding of roles of reactive oxygen species in many diseases. These include atherosclerosis, vasospasms, cancers, trauma, stroke, asthma, hyperoxia, arthritis, heart attack, age pigments, dermatitis, cataractogenesis, retinal damage, hepatitis, liver injury, and periodontis, which are age-related. The body protects itself from the potential damages of reactive oxygen species. Its first line of defense is superoxide dismutases, glutathione peroxidases, and catalase. Scientists have indicated that antioxidant nutraceuticals supplied from daily diets quench the reactive oxygen species or are required as cofactors for antioxidant enzymes. Nutraceuticals play significant roles in the prevention of a number of age-related diseases and are essential for healthy aging. Epidemiological studies also reported the relevance of antioxidative nutraceuticals to health issues and the prevention of age-related diseases. Health-conscious consumers have made antioxidative nutraceuticals the leading trend in the food industry worldwide in recent years. 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