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Selected AbstractsAttenuated endothelin-1 mRNA expression with endothelin-1 receptor blockade during hypoxaemia and reoxygenation in newborn pigletsACTA PAEDIATRICA, Issue 6 2000S Medbø We investigated the cause of decreased plasma endothelin-1 (ET-1) during hypoxaemia and reoxygenation in newborn piglets subjected to simultaneous blocking of the ET-1 receptors. Changes in plasma ET-1 and prepro-ET-1 mRNA expression in the main pulmonary artery and the left lower lobe in the lung were studied in 1-2-d-old piglets. Ten minutes prior to hypoxaemia, the hypoxaemia group (n = 10) was given saline, two groups (both n = 9) were given 1 and 5 mg/kg i.v. SB 217242 (an ET-1 receptor antagonist). Two groups served as normoxic controls, with and without SB 217242 5 mg/kg i.v. Hypoxaemia was induced by ventilating with 8% O2 until base excess was 20mmol/l or mean arterial blood pressure was < 20mmHg. Reoxygenation was performed for 2h with room air. During hypoxaemia, plasma ET-1 decreased in the hypoxaemia group, remained unchanged in the 1-mg group and increased in the 5-mg group. At the end of reoxygenation, plasma ET-1 was above baseline in the 1-mg and 5-mg groups. In the pulmonary artery, the hypoxaemia group showed 2- to 5-fold higher prepro-ET-1 mRNA expression compared to all the other groups (p < 0.05). There were trends for higher prepro-ET-1 mRNA expression in pulmonary tissue in the hypoxaemia group compared to the two receptor-blocking groups (p < 0.07). Conclusions: We conclude that hypoxaemia and reoxygenation increase prepro-ET-1 mRNA expression in the pulmonary artery in newborn piglets. These observations suggest that the half-life of ET-1 is decreased during hypoxaemia and reoxygenation in newborn piglets. [source] Amiodarone Attenuates Fluoride-induced Hyperkalemia in VitroACADEMIC EMERGENCY MEDICINE, Issue 2 2003Mark Su MD Abstract Poisoning by hydrofluoric acid or fluoride salts results in hypocalcemia, hypomagnesemia, and hyperkalemia with subsequent cardiac dysrhythmias. In previous studies, quinidine attenuated fluoride-induced hyperkalemia in vitro, and enhanced survival in animals. Like quinidine, amiodarone is a potassium channel blocker, although amiodarone is more familiar to clinicians due to its recent inclusion in advanced cardiac life support (ACLS) protocols. Objectives: This in-vitro study of human erythrocytes was designed to determine whether amiodarone could attenuate fluoride-induced hyperkalemia. Methods: Six healthy volunteers each donated 60 mL of blood on three occasions. Each specimen was divided into 12 tubes, incubated at 37°C, and oxygenated with room air. An aqueous sodium fluoride (F,) solution was added to tubes 1,9. Incremental amounts of quinidine were added to tubes 1,4 (Q1,Q4) to attain calculated concentrations of 0.73 ,g/mL, 1.45 ,g/mL, 2.9 ,g/mL, and 5.8 ,g/mL, respectively. Incremental amounts of amiodarone were added to tubes 5,8 (A1,A4) to attain calculated concentrations of 0.38 ,g/mL, 0.75 ,g/mL, 1.5 ,g/mL, and 3.0 ,g/mL, respectively. Tubes 9,12 were controls for each of F,, amiodarone, quinidine alone, and no additive, respectively. Extracellular potassium concentration ([K+]) was followed, and an objective endpoint was defined as the rise in potassium concentration at 6 hours. Results: Fluoride produced a significant change in [K+] by 6 hours in all samples. Quinidine produced a J-shaped curve in its ability to attenuate the rise in [K+], with only one concentration, Q3, demonstrating significance versus tube 9 (control). Amiodarone also demonstrated a J-shaped dose,response effect, with statistical significance at A1, A2, and A3 versus tube 9 (control). There was no significant difference among the effective concentrations (Q3, A1, A2, and A3) of both drugs. Conclusions: In this in-vitro model using human blood, amiodarone and quinidine both attenuated F, -induced hyperkalemia. Further study is indicated to determine whether amiodarone enhances survival in F, -poisoned animals. [source] Hypoxia modulates cholinergic but not opioid activation of G proteins in rat hippocampusHIPPOCAMPUS, Issue 10 2007V.S. Hambrecht Abstract Intermittent hypoxia, such as that associated with obstructive sleep apnea, can cause neuronal death and neurobehavioral dysfunction. The cellular and molecular mechanisms through which hypoxia alter hippocampal function are incompletely understood. This study used in vitro [35S]guanylyl-5,- O -(,-thio)-triphosphate ([35S]GTP,S) autoradiography to test the hypothesis that carbachol and DAMGO activate hippocampal G proteins. In addition, this study tested the hypothesis that in vivo exposure to different oxygen (O2) concentrations causes a differential activation of G proteins in the CA1, CA3, and dentate gyrus (DG) regions of the hippocampus. G protein activation was quantified as nCi/g tissue in CA1, CA3, and DG from rats housed for 14 days under one of three different oxygen conditions: normoxic (21% O2) room air, or hypoxia (10% O2) that was intermittent or sustained. Across all regions of the hippocampus, activation of G proteins by the cholinergic agonist carbachol and the mu opioid agonist [D-Ala2, N-Met-Phe4, Gly5] enkephalin (DAMGO) was ordered by the degree of hypoxia such that sustained hypoxia > intermittent hypoxia > room air. Carbachol increased G protein activation during sustained hypoxia (38%), intermittent hypoxia (29%), and room air (27%). DAMGO also activated G proteins during sustained hypoxia (52%), intermittent hypoxia (48%), and room air (43%). Region-specific comparisons of G protein activation revealed that the DG showed significantly less activation by carbachol following intermittent hypoxia and sustained hypoxia than the CA1. Considered together, the results suggest the potential for hypoxia to alter hippocampal function by blunting the cholinergic activation of G proteins within the DG. © 2007 Wiley-Liss, Inc. [source] Modeling and CFD prediction for diffusion and adsorption within room with various adsorption isothermsINDOOR AIR, Issue 2003S. Murakami Abstract This paper presents physical models that are used for analyzing numerically the transportation of volatile organic compounds (VOCs) from building materials in a room. The models are based on fundamental physicochemical principles of their diffusion and adsorption/desorption (hereafter simply sorption) both in building materials and in room air. The performance of the proposed physical models is examined numerically in a test room with a technique supported by computational fluid dynamics (CFD). Two building materials are used in this study. One is a VOC emitting material for which the emission rate is mainly controlled by the internal diffusion of the material. The other is an adsorptive material that has no VOC source. It affects the room air concentration of VOCs with its sorption process. The floor is covered with an emission material made of polypropylene styrene,butadiene rubber (SBR). An adsorbent material made of coal-based activated carbon is spread over the sidewalls. The results of numerical prediction show that the physical models and their numerical simulations explain well the mechanism of the transportation of VOCs in a room. [source] Does propofol and alfentanil-induced sedation cause periodic apnoea in chronic renal failure patients?INTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 1 2010S. M. Lee Summary Aims:, There is evidence suggesting that the respiratory response to sedation is different in patients with sleep apnoea, which is common in patients with chronic renal failure (CRF). This study examined the respiratory response of sedation with propofol and alfentanil, whose pharmacokinetics are not affected by the renal function, in CRF patients. Methods:, Chronic renal failure patients who underwent arteriovenous-fistular surgery (CRF group) and patients who underwent chemoport insertion (control group) were enrolled in this study. Sedation was induced by infusing propofol 1.5 ,/ml and alfentanil 0.2 ,/kg/min continuously in both groups. In the desaturation study, the respiratory rate and peripheral oxygen saturation in room air were checked. In the apnoea,hypopnoea study, the patient's sedation (Observer's Assessment of Alertness/Sedation) score, apnoea,hypopnoea index (AHI) was recorded using a portable ventilation effort recorder (microMesam) while applying 5 l/min of oxygen through a facial mask. Results:, The desaturation event was more common (21.5/h vs. 2/h, p = 0.001) in the CRF patients. Apnoea and hypopnoea (AHI: 13.0 vs. 1.6, p = 0.012, per cent of patients with an AHI > 5: 53.3% vs. 7.1%, p = 0.014) occurred more frequently in the CRF patients but the sedation score was not different. Conclusion:, Chronic renal failure patients have a higher risk of developing apnoea and hypopnoea during sedation, which highlights the need for careful monitoring and management in these patients. [source] ,1-Antitrypsin deficiency presenting with panniculitis and incidental discovery of chronic obstructive pulmonary diseaseINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 10 2007Gretchen Korver MD A 60-year-old man presented to the Emergency Department (ED) with large, painful, indurated plaques on the right thigh, left abdomen, left chest, and right chest, which began without any preceding trauma on the right thigh 3 weeks prior to presentation in the ED. He was initially treated with cefazolin 1 g three times daily as home infusions. When the lesions continued to progress, he was admitted to the hospital and placed on amoxicillin/clavulanate and vancomycin. He had a single episode of fever of 102°F, but his white blood cell count and differential remained normal. An initial biopsy showed a dermal inflammatory infiltrate composed primarily of neutrophils and eosinophils with rare flame figures in the dermis. There was minimal fat seen in this biopsy. A differential diagnosis of Wells or Sweet's syndrome was entertained, and he was placed on 60 mg/day prednisone with no resolution of his symptoms. The patient's past medical history included hypertension, hyperlipidemia, peripheral neuropathy, and hiatal hernia. His family history was significant for emphysema in both parents and coronary artery disease in his father. Both of his parents smoked cigarettes. His grandfather, who was a coal miner, also had emphysema. Whilst on antibiotics and prednisone, the plaques on the patient's right thigh, right abdomen, and left chest expanded and ulcerated, draining an oily liquid (Figs 1 and 2). An incisional biopsy was obtained from his thigh. Histopathology showed a septal and lobular panniculitis with fat necrosis, neutrophils, and histiocytes (Fig. 3). Special stains for organisms were negative. Tissue sent for bacterial and fungal culture had no growth. Amylase and lipase levels were normal. Rheumatoid factor, antinuclear antibody (ANA), antineutrophil cytoplasmic antibody (ANCA), cryoglobulins, and antiphospholipid antibodies were all normal. The ,1-antitrypsin level was low at 25 mg/dL (ref. 75,135). The ,1-antitrypsin phenotype was PiZZ. Figure 1. Indurated plaques on right chest and thigh and left chest Figure 2. Ulcerated plaques on left chest Figure 3. Septal and lobular panniculitis with fat necrosis. Hematoxylin and eosin ×10 The patient had a normal glucose-6-phosphate dehydrogenase level and was placed on dapsone 200 mg/day. The inflammation resolved and, over the course of several months, the involved areas healed with scarring. The patient denied any pulmonary complaints but, during his hospitalization, was found incidentally to have an oxygen saturation of 88% on room air. He was sent for evaluation by a pulmonologist, and pulmonary function tests revealed a mixed restrictive and obstructive pattern with a forced expiratory volume in 1 to forced vital capacity (FEV1/FVC) ratio of 63% of predicted. He had never smoked. He was placed on supplemental oxygen but, as his pulmonary disease has been stable, he has not been treated with intravenous antitrypsin inhibitor. [source] Effects of an ethanol,gasoline mixture: results of a 4-week inhalation study in ratsJOURNAL OF APPLIED TOXICOLOGY, Issue 3 2005I. Chu Abstract The inhalation toxicity of an ethanol,gasoline mixture was investigated in rats. Groups of 15 male and 15 female rats were exposed by inhalation to 6130 ppm ethanol, 500 ppm gasoline or a mixture of 85% ethanol and 15% gasoline (by volume, 6130 ppm ethanol and 500 ppm gasoline), 6 h a day, 5 days per week for 4 weeks. Control rats of both genders received HEPA[sol ]charcoal-filtered room air. Ten males and ten females from each group were killed after 4 weeks of treatment and the remaining rats were exposed to filtered room air for an additional 4 weeks to determine the reversibility of toxic injuries. Female rats treated with the mixture showed growth suppression, which was reversed after 4 weeks of recovery. Increased kidney weight and elevated liver microsomal ethoxyresorufin- O -deethylase (EROD) activity, urinary ascorbic acid, hippuric acid and blood lymphocytes were observed and most of the effects were associated with gasoline exposure. Combined exposure to ethanol and gasoline appeared to exert an additive effect on growth suppression. Inflammation of the upper respiratory tract was observed only in the ethanol,gasoline mixture groups, and exposure to either ethanol and gasoline had no effect on the organ, suggesting that an irritating effect was produced when the two liquids were mixed. Morphology in the adrenal gland was characterized by vacuolation of the cortical area. Although histological changes were generally mild in male and female rats and were reversed after 4 weeks, the changes tended to be more severe in male rats. Brain biogenic amine levels were altered in ethanol- and gasoline-treated groups; their levels varied with respect to gender and brain region. Although no general interactions were observed in the brain neurotransmitters, gasoline appeared to suppress dopamine concentrations in the nucleus accumbens region co-exposed to ethanol. It was concluded that treatment with ethanol and gasoline, at the levels studied, produced mild, reversible biochemical hematological and histological effects, with some indications of interactions when they were co-administered. Copyright © 2005 John Wiley & Sons, Ltd. [source] Influence of hypobaric hypoxia on bispectral index and spectral entropy in volunteersACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 7 2009T. IKEDA Background: Hypoxia has been shown to change electroencephalogram parameters including frequency and amplitude, and may thus change bispectral index (BIS) and spectral entropy values. If hypoxia per se changes BIS and spectral entropy values, BIS and spectral entropy values may not correctly reflect the depth of anaesthesia during hypoxia. The aim of this study was to examine the changes in BIS and spectral entropy values during hypobaric hypoxia in volunteers. Methods: The study was conducted in a high-altitude chamber with 11 volunteers. After the subjects breathed 100% oxygen for 15 min at the ground level, the simulated altitude increased gradually to the 7620 m (25,000 ft) level while the subjects continued to breathe oxygen. Then, the subjects discontinued to breath oxygen and breathed room air at the 7620 m level for up to 5 min until they requested to stop hypoxic exposure. Oxygen saturation (SpO2), heart rate, 95% spectral edge frequency (SEF), BIS, response entropy (RE), and state entropy (SE) of spectral entropy were recorded throughout the study period. Results: Of the 11 subjects, seven subjects who underwent hypoxic exposure for 4 min were analysed. SpO2 decreased to 69% at the 7620 m level without oxygen. However, SEF, BIS, RE, and SE before and during hypoxic exposure were almost identical. Conclusion: These data suggest that hypoxia of oxygen saturation around 70% does not have a strong effect on BIS and spectral entropy. [source] Effects of indomethacin on cerebral blood flow at rest and during hypercapnia: An arterial spin tagging study in humans,JOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 6 2002Keith S. St. Lawrence PhD Abstract Purpose To investigate using an arterial spin tagging (AST) approach the effect of indomethacin on the cerebral blood flow (CBF) response to hypercapnia. Materials and Methods Subjects inhaled a gas mixture containing 6% CO2 for two 5-minute periods, which were separated by a 10-minute interval, in which subjects inhaled room air. In six subjects, indomethacin (i.v., 0.2 mg/kg) was infused in the normocapnic interval between the two hypercapnic periods. Results Indomethacin reduced normocapnic gray matter CBF by 36 ± 5% and reduced the CBF increase during hypercapnia from 43 ± 9% to 16 ± 5% in gray matter (P < 0.001) and from 48 ± 11% to 35 ± 9% in white matter (P < 0.025). Conclusion The results demonstrate that an AST approach can measure the effects of indomethacin on global CBF increases during hypercapnia and suggest that an AST approach could be used to investigate pharmacological effects on focal CBF increases during functional activation. J. Magn. Reson. Imaging 2002;15:628,635. Published 2002 Wiley-Liss, Inc. [source] Effects of different exposures of hyperbaric oxygen on ligament healing in ratsJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 2 2002Yoshimasa Ishii Hyperbaric oxygen (HBO) is a method of augmenting, intermittently, oxygen availability to tissues. We examined the effect of three different HBO exposures on the healing of experimentally induced ligament lacerations in the right hind limb of 44 male Wistar rats. Animals were divided into four groups after ligament injury: (a) control group, animals breathed room air at 1 ATA (atmosphere absolute) in a hyperbaric chamber for 60 min; (b) HBO treatment at 1.5 ATA for 30 min once a day, (c) HBO treatment at 2 ATA for 30 min once a day, (d) 2 ATA for 60 min once a day. At 14 days post-ligament injury, we compared the ligaments of the four treatment groups for gross appearance, histology and expression of pro-,(I) mRNA by northern hybridization. Our results indicate that HBO was effective in promoting ligament healing compared to control (p < 0.01). Of these three exposures, HBO at 2 ATA for 60 min was the most effective, resulting in enhanced extra-cellular matrix deposition as measured by collagen synthesis. © 2002 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved. [source] Smoke Exposure and Ethanol Ingestion Modulate Intrapulmonary Polymorphonuclear Leukocyte Killing, but Not Recruitment or PhagocytosisALCOHOLISM, Issue 9 2006Elizabeth A. Vander Top Background: People who smoke and abuse alcohol are uniquely susceptible to pulmonary infections caused by Streptococcus pneumoniae, the pneumococcus. The primary cellular defense against pneumococci within the lungs is the polymorphonuclear leukocyte (PMN). Cigarette smoke and ethanol (EtOH) are known to alter certain PMN functions, but little is known about their concurrent effects. Methods: Male Sprague,Dawley rats were exposed twice daily for 8 weeks to cigarette smoke (smoke-exposed) or room air (sham-exposed). During the final week of exposure, the rats were pair-fed a liquid diet containing either 36 or 0% EtOH calories. Polymorphonuclear leukocytes were prerecruited into the rats' lungs by transtracheal injection of lipopolysaccharide. Five hours later, the rats were infected transtracheally with S. pneumoniae, and PMN recruitment, phagocytosis, and bactericidal activity were quantified within their lungs. Chemokine levels were also measured in bronchoalveolar lavage fluids, lung homogenates, and sera. Results: Neither PMN recruitment nor phagocytic uptake of pneumococci was altered by EtOH ingestion or smoke exposure. Killing of the organisms, however, was significantly decreased in sham-exposed, but not smoke-exposed, rats ingesting EtOH. Parallel results were determined for serum cytokine-induced neutrophil chemoattractant-1 (CINC-1), with EtOH ingestion significantly decreasing the levels in sham-exposed, but not smoke-exposed, rats. Pulmonary levels of macrophage inflammatory protein-2 (MIP-2) and CINC-1 were highly elevated by the combination of EtOH and smoke. Conclusions: One week of EtOH ingestion by rats impaired the ability of their PMNs to kill S. pneumoniae within their lungs. This was not due to decreased recruitment of the PMNs to the lungs or to diminished phagocytosis of intrapulmonary pneumococci. The addition of twice-daily cigarette smoke exposure to this short-term EtOH ingestion model restored PMN bactericidal ability to levels observed in the absence of either treatment. These EtOH-induced and smoke-induced alterations in PMN killing may be related to alterations in both pulmonary and systemic inflammatory chemokine levels. [source] Smoke Exposure Exacerbates an Ethanol-Induced Defect in Mucociliary Clearance of Streptococcus pneumoniaeALCOHOLISM, Issue 5 2005Elizabeth A. Vander Top Background: Alcoholics and smokers are particularly susceptible to pulmonary infections caused by Streptococcus pneumoniae, the pneumococcus. Infection begins when pneumococci colonizing the nasopharynx are aspirated into the lower respiratory tract. The major host defense against this movement is the mucociliary clearance apparatus. Both cigarette smoke and ethanol (EtOH) exposure alter ciliary beating and protein kinase activity in the respiratory mucosa in vitro, but their effects on bacterial clearance in the intact animal have not been determined. Methods: Male Sprague Dawley rats were exposed twice daily for 12 weeks to either the smoke generated from 30 cigarettes (smoke,exposed) or room air (sham,exposed). For the last five weeks of smoke exposure, the rats were fed Lieber-DeCarli liquid diets containing 0%, 16%, 26%, or 36% EtOH calories. The rats then were infected intranasally with S. pneumoniae, and movement of the organisms into the lower respiratory tract was quantified by plate counts of the tracheas and lungs 4 hr later. Ciliary beat frequency (CBF) analysis was performed on tracheal ring explants from each animal before and after stimulation with the ,-agonist isoproterenol, and tracheal epithelial cell protein kinase C (PKC) activity was measured. Results: Ingestion of any of the EtOH-containing diets resulted in a dose-dependent increase in movement of S. pneumoniae into the rats' lungs. This EtOH-induced defect was augmented further by concurrent smoke exposure, although smoke exposure alone had little effect on S. pneumoniae movement. Smoke, but not EtOH exposure, activated tracheal epithelial cell PKC. Increased movement of organisms into lungs correlated with a decrease in CBF and loss of the ciliary response to isoproterenol. Conclusion: EtOH ingestion in our model facilitated movement of S. pneumoniae into rats' lungs, a phenomenon exacerbated by concurrent smoke exposure. Furthermore, the organism's movement into the lungs correlated with a blunting of the rats' ciliary response to an established stimulus. Defects in mucociliary clearance thus may be one cause of the increased risk of pneumococcal infections in people who abuse alcohol, particularly if they also smoke. [source] Pulmonary gas exchange abnormalities in liver transplant candidatesLIVER TRANSPLANTATION, Issue 9 2002Rosmawati Mohamed Abnormal diffusing capacity is the commonest pulmonary dysfunction in liver transplant candidates, but severe hypoxemia secondary to hepatopulmonary syndrome and significant pulmonary hypertension are pulmonary vascular manifestations of cirrhosis that may affect the perioperative course. We prospectively assessed the extent of pulmonary dysfunction in patients referred for liver transplantation. A total of 57 consecutive patients with chronic liver disease were evaluated. All patients had a chest radiograph, standing arterial blood gas on room air, pulmonary function testing, and Doppler echocardiogram. Those patients with arterial hypoxaemia (PaO2 < 10 kPa) also underwent 99mTc-macroaggregated albumin lung scan, and nine patients had agitated normal saline injection during echocardiography to define further the existence of pulmonary vascular dilatation. Reduced diffusing capacity for carbon monoxide less than 75% of the predicted value was found in 29 of 57 (51%) patients. Although elevated alveolar-arterial oxygen tension difference was detected in 35% (20/57) of the patients, only four (7%) patients had hypoxemia. We were unable to find evidence of intrapulmonary vascular dilatation either on the lung scan or saline-enhanced echocardiography in any of these patients. Reduction in diffusing capacity for carbon monoxide was noted in 75% (18/24) of patients who were transplanted for primary biliary cirrhosis and was accompanied by widened alveolar-arterial oxygen tension in 10 out of 18 (56%) of patients. This study shows that in liver transplant candidates, diffusion impairment and widened alveolar-arterial oxygen tension difference were frequently detected, especially in patients with primary biliary cirrhosis. [source] Baseline physiological state and the fMRI-BOLD signal response to apnea in anesthetized ratsNMR IN BIOMEDICINE, Issue 5 2003Sridhar S. Kannurpatti Abstract To decipher the biophysical mechanism behind the fMRI-BOLD response to apnea and its dependence on the baseline cerebral blood flow and oxygenation, fMRI and laser Doppler flow (LDF) studies were carried out in anesthetized rats. Baseline cerebral blood flow (CBF) and PaO2 were modulated by ventilating with different gas mixtures namely, room air (21% O2), 100% O2, carbogen (95% O2+5% CO2), 2% CO2 in air or 5% CO2 in air, respectively. A decrease in BOLD signal intensity was observed after the onset of apnea with either room air, 2% CO2 or 5% CO2 ventilation. PaO2 and cerebral tissue PO2 decreased during apnea under these conditions. However, the apnea-induced BOLD signal intensity was unaffected with carbogen ventilation and increased with 100% O2 ventilation, during which PaO2 remained constant and cerebral tissue PO2 increased. When baseline CBF was high during hypercapnia, a faster decrease occurred in the apnea-induced BOLD signal. Apnea induced the largest increase in CBF of 85±25% when ventilated with 2% CO2 while a 44±8% increase was observed with room air. During the other ventilatory conditions, minimal or no significant change in CBF was observed during apnea. These results show a significant correlation between the BOLD signal change and tissue PO2 in response to apnea under different physiological conditions. Apnea-induced increase in CBF affects the magnitude of the BOLD signal response when PaO2 remains constant or changes minimally. Copyright © 2001 John Wiley & Sons, Ltd. [source] Effects of meconium aspiration in isolated perfused rat lungsPEDIATRIC PULMONOLOGY, Issue 4 2005Wlodzimierz M. Wisniewski MD Abstract Our objective was to study meconium-induced lung injury in isolated perfused rat lungs exposed to anoxia. Our working hypothesis was that meconium-induced lung injury is independent of preexisting hypoxia, and that hypoxia will increase severity of lung injury observed after meconium aspiration. We comparde five different groups of animals (n,=,5) for pulmonary arterial pressure (PAP), weight lung changes, and TNF, expression. Group I had lungs instilled with 4 ml of normal saline. Group II had lungs exposed to 5 min of anoxia. Group III had lungs instilled with 4 ml of 30% filtered human meconium. Group IV had lungs exposed to 5 min of anoxia and then instilled with 4 ml of 30% filtered human meconium. Group V had lungs instilled with 4 ml of 30% unfiltered human meconium. Our subjects were adult Sprague-Dawley rats. The isolated rat lung model was prepared according to Levey and Gast (J Appl Physiol 1966;21:313,316). Lungs were ventilated with room air. Anoxia was caused by the use of N2. The pulmonary artery was cannulated, and pulmonary arterial pressure and lung weight were measured. Lung weight and pulmonary arterial pressure were monitored for 120 min, and TNF, levels were measured in effluent at 15, 30, 60, and 120 min. Experiments were done at the Michael Reese Hospital (Chicago, IL). At the end of the experiment, PAP reached its highest values in group V (10.0,±,1.7 mmHg). Final PAPs in groups I,IV were: 4.85,±,0.3, 4.99,±,0.4, 5.93,±,0.3, and 7.25,±,0.51 mmHg, respectively). Lung wet weight increased significantly only in groups IV and V vs. group I; at 120 min, they were: 0.96,±,0.3 g, P,<,0.01, and 1.5 g,±,0.2 g, P,<,0.01, respectively. TNF, levels did not change significantly over time in group I. TNF, is a marker as well as proprietor of pulmonary inflammatory response. TNF, reached its highest levels in groups IV and V: 595 and 753 pg/ml at 120 min, respectively. In conclusion, a short episode of anoxia prior to meconium aspiration may increase lung sensitivity to meconium-induced lung injury. This effect may be moderated by the TNF, present in the pulmonary circulation. Pediatr Pulmonol. 2005; 39:368,373. © 2005 Wiley-Liss, Inc. [source] Altered expression of antimicrobial molecules in cigarette smoke-exposed emphysematous mice lungsRESPIROLOGY, Issue 7 2008Yoko SHIBATA Background and objective: The natural history of COPD, a disease usually caused by cigarette smoking, is associated with frequent respiratory infections. Consistent with human COPD, bacterial clearance in the lungs has been reported to be impaired in mice exposed to cigarette smoke. In the airways, several antimicrobial molecules such as surfactant proteins (SP), beta-defensins (BD), secretory leucocyte protease inhibitor (SLPI) and lysozyme play important roles in the defence against invading pathogens. This study evaluated the expression of antimicrobial molecules in mice lungs with cigarette smoke-induced emphysematous changes. Methods: Six B6C3F1 mice were exposed to cigarette smoke (2 cigarettes/day/mouse for 6 months) or room air. Gene expression within the lungs of mice in both groups was assessed by RT-PCR. Results: The expression of SP-A, BD2, BD3 and SLPI was significantly elevated in the lungs of cigarette smoke-exposed mice compared with air-exposed mice. BD1 expression decreased in the smoke-exposed mice and lysozyme expression was unchanged. Conclusions: Chronic cigarette smoke exposure did not suppress the expression of antimicrobial molecules in the lung. Altered expression of antimicrobial molecules in this mouse model does not explain the impaired host defence against respiratory microbes seen in patients with COPD. [source] Hypoxic preconditioning protects rat hearts against ischaemia,reperfusion injury: role of erythropoietin on progenitor cell mobilizationTHE JOURNAL OF PHYSIOLOGY, Issue 23 2008Jih-Shyong Lin Preconditioning, such as by brief hypoxic exposure, has been shown to protect hearts against severe ischaemia. Here we hypothesized that hypoxic preconditioning (HPC) protects injured hearts by mobilizing the circulating progenitor cells. Ischaemia,reperfusion (IR) injury was induced by left coronary ligation and release in rats kept in room air or preconditioned with 10% oxygen for 6 weeks. To study the role of erythropoietin (EPO), another HPC + IR group was given an EPO receptor (EPOR) antibody via a subcutaneous mini-osmotic pump 3 weeks before IR induction. HPC alone gradually increased haematocrit, cardiac and plasma EPO, and cardiac vascular endothelial growth factor (VEGF) only in the first two weeks. HPC improved heart contractility, reduced ischaemic injury, and maintained EPO and EPOR levels in the infarct tissues of IR hearts, but had no significant effect on VEGF. Interestingly, the number of CD34+CXCR4+ cells in the peripheral blood and their expression in HPC-treated hearts was higher than in control. Preconditioning up-regulated cardiac expression of stromal derived factor-1 (SDF-1) and prevented its IR-induced reduction. The EPOR antibody abolished HPC-mediated functional recovery, and reduced SDF-1, CXCR4 and CD34 expression in IR hearts, as well as the number of CD34+CXCR4+ cells in blood. The specificity of neutralizing antibody was confirmed in an H9c2 culture system. In conclusion, exposure of rats to moderate hypoxia leads to an increase in progenitor cells in the heart and circulation. This effect is dependent on EPO, which induces cell homing by increased SDF-1/CXCR4 and reduces the heart susceptibly to IR injury. [source] Nasal Nitric Oxide in Children: A Novel Measurement Technique and Normal Values,,THE LARYNGOSCOPE, Issue 10 2002Hamid Daya FRCS (ORL) Abstract Objectives To develop and standardize a technique for measuring nasal nitric oxide (NO) output in children and to determine normal values in this population. Study Design Prospective study evaluating a new technique for measuring nasal nitric oxide in a cohort of normal patients and a cohort of patients with nasal disease. Methods Nasal NO was measured using an aspiration technique, aspirating room air through the nasal cavities by means of a Teflon nozzle placed in one nasal vestibule while maintaining velopharyngeal closure using a party "blow-out" toy Results Nasal NO measurements were performed in 45 children (mean age, 11.0 y; age range, 3.2,17.6 y) There were 20 girls and 25 boys. All children were able to perform the maneuvers necessary for measurement of nasal NO output. Among the subgroup of normal healthy children (30), there was considerable variation in NO output between subjects, with a mean NO output of 481 nL/min and an SD of 283 nL/min. Conclusions Nasal NO can be readily measured in children using the presented technique. There is considerable variability in the values for nasal NO output in normal children. [source] Improved Survival After Liver Transplantation in Patients with Hepatopulmonary SyndromeAMERICAN JOURNAL OF TRANSPLANTATION, Issue 2 2010S. Gupta Hepatopulmonary syndrome (HPS) is present in 10,32% of chronic liver disease patients, carries a poor prognosis and is treatable by liver transplantation (LT). Previous reports have shown high LT mortality in HPS and severe HPS (arterial oxygen (PaO2) ,50 mmHg). We reviewed outcomes in HPS patients who received LT between 2002 and 2008 at two transplant centers supported by a dedicated HPS clinic. We assessed mortality, complications and gas exchange in 21 HPS patients (mean age 51 years, MELD score 14), including 11/21 (52%) with severe HPS and 5/21 (24%) with living donor LT (median follow-up 20.2 months after LT). Overall mortality was 1/21 (5%); mortality in severe HPS was 1/11 (9%). Peritransplant hypoxemic respiratory failure occurred in 5/21 (24%), biliary complications in 8/21 (38%) and bleeding or vascular complications in 6/21 (29%). Oxygenation improved in all 19 patients in whom PaO2 or SaO2 were recorded. PaO2 increased from 52.2 ± 13.2 to 90.3 ± 11.5 mmHg (room air) (p < 0.0001) (12 patients); a higher baseline macroaggregated albumin shunt fraction predicted a lower rate of postoperative improvement (p = 0.045) (7 patients). Liver transplant survival in HPS and severe HPS was higher than previously demonstrated. Severity of HPS should not be the basis for transplant refusal. [source] Hypoxia induces cardiac malformations via A1 adenosine receptor activation in chicken embryos,BIRTH DEFECTS RESEARCH, Issue 3 2008Satish K. Ghatpande Abstract BACKGROUND: The current understanding of the effects of hypoxia on early embryogenesis is limited. Potential mediators of hypoxic effects include adenosine, which increases dramatically during hypoxic conditions and activates A1 adenosine receptors (A1ARs). METHODS: To examine the influences of hypoxia and adenosine signaling on cardiac development, chicken embryos were studied. Real time RT-PCR assay was used to examine the A1AR gene expression during embryogenesis and after siRNA- mediated knock down. Cell proliferation was determined by counting cell nuclei and PhosphoHistone H3 positive cells. Apoptosis was determined by TUNEL assay. RESULTS: A1ARs were found to be expressed in chicken embryos during early embryogenesis. Treatment of Hamburger and Hamilton stage 4 embryos with the A1AR agonist N6 -cyclopentyladenosine caused cardiac bifida and looping defects in 55% of embryos. Hamburger and Hamilton stage 4 embryos exposed to 10% oxygen for 6, 12, 18, and 24 h followed by recovery in room air until stage 11, exhibited cardia bifida and looping defects in 34, 45, 60, and 86% of embryos respectively. Hypoxia-induced abnormalities were reduced when A1AR signaling was inhibited by the A1AR antagonist 1,3 dipropyl-8-cyclopentylxanthine or by siRNA-targeting A1ARs. Hypoxia treatment did not increase apoptosis, but decreased embryonic cell proliferation. CONCLUSIONS: These data indicate that hypoxia adversely influences cardiac malformations during development, in part by A1AR signaling. Birth Defects Research (Part A), 2008. © 2008 Wiley-Liss, Inc. [source] Randomized clinical trial to evaluate the effects of perioperative supplemental oxygen administration on the colorectal anastomosisBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 6 2006S. A. García-Botello Background: Perioperative supplemental oxygen therapy may have beneficial effects on wound healing following colorectal surgery. The aim of this study was to evaluate the effects of such therapy on colorectal anastomotic pH and partial pressure of carbon dioxide (PCO2) gap. Methods: Forty-five patients undergoing anterior resection for rectal or sigmoid cancer were randomized to receive 30 or 80 per cent perioperative oxygen. Administration was commenced after induction of anaesthesia and maintained for 6 h after surgery. Intragastric and anastomotic tonometric catheters were placed in each patient and intramucosal pH (pHi) was measured immediately after operation, and 6 and 24 h later. Gastric and anastomotic pHi and PCO2 gap in each group were compared. Results: There was a significantly lower anastomotic pHi and wider PCO2 gap for gastric readings in the 30 per cent O2 group, both 30 min (pHi, P = 0·006; PCO2 gap, P = 0·006) and 6 h (pHi, P = 0·024; PCO2 gap, P = 0·036) after surgery. There were no differences 24 h after surgery while breathing room air (pHi, P = 0·131; PCO2 gap P = 0·139). No difference was found between gastric and anastomotic readings at any time point in the 80 per cent O2 group. Conclusion: Perioperative administration of 80 per cent O2 both during surgery and for 6 hours afterwards is associated with an improvement in relative anastomotic hypoperfusion as assessed by the measurement of pHi and PCO2 gap. Copyright © 2006 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] Effect of breathing a mixture of 92% O2 + 8% CO2 on flicker induced vasodilatationACTA OPHTHALMOLOGICA, Issue 2009M LASTA Purpose It has been shown that increased neural activity evoked by stimulation with diffuse luminance flicker increases retinal and optic nerve head blood flow. Beside others, an increased oxygen demand has been attributed to evoke the flicker response. This study seeks to investigate whether the flicker light induced increase in retinal vessel diameters is different in subjects breathing 92% O2 + 8% CO2 compared to breathing room air. Methods 24 healthy volunteers were included in the study. Diameters of retinal vessels were recorded continuously with a Retinal Vessel Analyzer. During this measurement flicker stimulation was applied at a frequency of 8 Hz. Subjects were breathing a combination of 92% O2 + 8% CO2 and room air in a randomized, two way cross over design. Flicker responses were assessed during the two breathing periods. Blood gas values were determined from capillary blood samples. Results Under room air conditions flicker stimulation significantly increased retinal venous diameters (p<0.05). Breathing of 92% O2 + 8% CO2 increased pO2 from 88±18 mmHg to 277±71 mmHg (p<0.05) and pCO2 from 37±3 mmHg to 46±6 mmHg (p<0.05). Breathing a combination of 92% O2 + 8% CO2 significantly increased flicker induced vasodilatation in retinal veins compared to room air (p<0.05). Conclusion Breathing of a combination of 92% O2 + 8% CO2 increases the response of retinal venous diameters to stimulation with flicker light. The reason for this effect has, however, yet to be clarified. [source] Helmet-delivered continuous positive airway pressure with heliox in respiratory syncytial virus bronchiolitisACTA PAEDIATRICA, Issue 2 2010J Mayordomo-Colunga Abstract Aim:, The objective of this study was to check the feasibility and efficacy of helmet-delivered heliox-continuous positive airway pressure (CPAP) in infants with bronchiolitis. Methods:, Children <3 months of age diagnosed with respiratory syncytial virus bronchiolitis and recurrent apnoeas or a venous PCO2 >55 mmHg or a transcutaneous oxygen saturation <92% in room air were eligible for inclusion in the study. CPAP was delivered by a noninvasive ventilator connected to a heliox port. The interface was a helmet. Results:, Eight consecutive infants fulfilled the inclusion criteria. Apnoeas were present in six children before respiratory support was started; they disappeared in five of them. Two infants had to be changed to pressure support noninvasive ventilation, and one of them required intubation. No side effects were recorded. Conclusion:, We propose a relatively new device to deliver heliox-CPAP in small infants with bronchiolitis. Although this is just a descriptive study with a short sample, this system seems to be feasible and effective. [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] | ||||||||||||||||||||||