Home About us Contact
|
Home About us Contact | ||
|
|
||
Systemic Blood Pressure (systemic + blood_pressure)
Selected AbstractsEchocardiographic Estimation of Systemic Systolic Blood Pressure in Dogs with Mild Mitral RegurgitationJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2006DACVIM, Sandra P. Tou DVM Background:Systemic hypertension is likely underdiagnosed in veterinary medicine because systemic blood pressure is rarely measured. Systemic blood pressure can theoretically be estimated by echocardiography. According to the modified Bernoulli equation (PG = 4v2), mitral regurgitation (MR) velocity should approximate systolic left ventricular pressure (sLVP), and therefore systolic systemic blood pressure (sSBP) in the presence of a normal left atrial pressure (LAP) and the absence of aortic stenosis. The aim of this study was to evaluate the use of echocardiography to estimate sSBP by means of the Bernoulli equation. Hypothesis:Systemic blood pressure can be estimated by echocardiography. Animal: Seventeen dogs with mild MR. No dogs had aortic or subaortic stenosis, and all had MR with a clear continuous-wave Doppler signal and a left atrial to aorta ratio of , 1.6. Methods:Five simultaneous, blinded continuous-wave measurements of maximum MR velocity (Vmax) and indirect sSBP measurements (by Park's Doppler) were obtained for each dog. Pressure gradient was calculated from Vmax by means of the Bernoulli equation, averaged, and added to an assumed LAP of 8 mm Hg to calculate sLVP. Results:Calculated sLVP was significantly correlated with indirectly measured sSBP within a range of 121 to 218 mm Hg (P= .0002, r= .78). Mean ± SD bias was 0.1 ± 15.3 mm Hg with limits of agreement of-29.9 to 30.1 mm Hg. Conclusion: Despite the significant correlation, the wide limits of agreement between the methods hinder the clinical utility of echocardiographic estimation of blood pressure. [source] Evidence for altered ocular rigidity in glaucomaACTA OPHTHALMOLOGICA, Issue 2009L SCHMETTERER Purpose Based on theoretical models and animal studies altered biomechanical properties of the optic nerve head and the sclera have been implicated in the pathophysiology of glaucoma. Only few data have, however, demonstrated such biomechanical alterations in vivo. We tested the hypothesis that patients with primary open angle glaucoma (POAG) have an abnormal structural stiffness based on measurements of intraocular pressure amplitude and ocular fundus pulsation amplitude. Methods Seventy patients with POAG and 70 healthy control subjects matched for age, gender, intraocular pressure and systemic blood pressure were included in this study. The ocular pulse amplitude (PA) was assessed with pneumotonometry. The fundus pulsation amplitude (FPA) was measured using laser interferometry. Based on the Friedenwald equation a coefficient of structural stiffness (E1) was calculated relating PA to FPA. Results Systemic blood pressure, intraocular pressure, and ocular perfusion pressure was comparable between glaucoma patients and healthy control subjects. FPA as well as PA was lower in patients with glaucoma than in healthy controls. The calculated factor E1 was significantly higher in patients with POAG (0.0454 ± 0.0085 a.u.) than in healthy control subjects (0.0427 ± 0.0058 a.u., p = 0.03). Conclusion This study is indicative of increased structural stiffness of the sclera in patients with POAG. This is in agreement with a number of previous animal experiments and supports the idea that the biomechanical properties of ocular tissues play a role in the process of glaucomatous ONH damage. [source] Clinical and Hemodynamic Effects of Nesiritide (B-Type Natriuretic Peptide) in Patients With Decompensated Heart Failure Receiving , BlockersCONGESTIVE HEART FAILURE, Issue 2 2005William T. Abraham MD The use of , blockers in congestive heart failure presents a therapeutic challenge for patients with acute episodes of decompensation. Such patients may be less responsive to positive inotropic agents, whereas the beneficial effects of nesiritide, which are not dependent on the ,-adrenergic receptor signal-transduction pathway, may be preserved. This analysis of the Vasodilation in the Management of Acute CHF trial evaluated the safety and efficacy of nesiritide in decompensated congestive heart failure patients receiving , blockers. The Vasodilation in the Management of Acute CHF trial was a multicenter, randomized, controlled evaluation of nesiritide in 489 hospitalized patients with decompensated congestive heart failure. One hundred twenty-three patients were on chronic ,-blocker therapy at enrollment (31 randomized to placebo, 50 to nesiritide, and 42 to nitroglycerin). Primary end points included pulmonary capillary wedge pressure and dyspnea evaluation at 3 hours. Patients receiving nesiritide, but not IV nitroglycerin, had significantly reduced pulmonary capillary wedge pressure vs. placebo at 3 hours regardless of ,-blocker use. The use of , blockers did not alter the beneficial effects of nesiritide on systemic blood pressure, heart rate, or dyspnea evaluation. In nesiritide-treated subjects, safety profiles were similar regardless of ,-blocker use. Thus, the clinical and hemodynamic benefits and safety of nesiritide are preserved in decompensated congestive heart failure patients receiving chronic , blockade. [source] Endothelin receptors blockade blunts hypoxia-induced increase in PAP in humansEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2010I. Pham Eur J Clin Invest 2010; 40 (3): 195,202 Abstract Background, Activation of the endothelin-1 (ET-1) pathway may be involved in hypoxia-induced pulmonary vasoconstriction, increase in pulmonary pressure and high altitude pulmonary oedema. Thus, we investigated the effect of the ETA/ETB receptor antagonist, bosentan, on pulmonary artery systolic pressure (PASP) in healthy subjects (n = 10). Design, We used a double-blind, placebo-controlled, randomized, cross-over design to study the effects of a single oral dose of bosentan (250 mg) on PASP after 90-min-exposure to normobaric hypoxia (FiO2 = 0·12). We measured PASP and cardiac output by echocardiography, systolic arterial blood pressure, arterial O2 saturation (SaO2), and blood gases at rest and during a sub-maximal exercise. Results, PASP in normoxia at rest was 23·5 ± 2·7 and during exercise 39·8 ± 11·6 mmHg (P < 0·0001). During the placebo period, hypoxia induced a significant decrease in SaO2, PaO2 and PCO2 and increase in pH. PASP at rest increased significantly: 32·1 ± 3·5 mmHg (P < 0·001 vs. normoxia). Bosentan significantly blunted the hypoxia-induced increase in PASP: bosentan: 27·0 ± 3·3 mmHg, P = 0·002 vs. placebo at rest, but not during exercise: bosentan 39·8 ± 11·6 vs. placebo 43·0 ± 8·5 mmHg, ns. Bosentan had no effect on the hypoxia-induced changes in blood gases, or on cardiac output and systolic arterial blood pressure, which were not modified by hypoxia. Conclusion, A single oral dose of bosentan blunted an acute hypoxia-induced increase in PASP in healthy subjects, without altering cardiac output or systemic blood pressure. [source] Management of blood pressure after acute ischemic stroke: An evidence-based guide for the hospitalistJOURNAL OF HOSPITAL MEDICINE, Issue 4 2007Ethan Cumbler MD Abstract Hospitalists are frequently called upon to manage blood pressure after acute ischemic stroke. A review of both post infarction cerebral perfusion physiology and the data from randomized trials of antihypertensive therapy is necessary to explain why consensus guidelines for blood pressure management after stroke differ from those of other hypertensive emergencies. The peri-infarct penumbra is the central concept in understanding post ischemic cerebral perfusion. This area of impaired cerebral blood flow is dependent on mean arterial blood pressure and acute reduction of blood pressure may expand the area of infarction. Review of clinical trials fails to show benefit from reduction of blood pressure after ischemic stroke and current guidelines suggest antihypertensive therapy be employed if the systemic blood pressure is greater than 180/105 mmHg after tPA is employed, or 220/120 mmHg when tPA is not used. Induced hypertension remains a promising but unproven therapy in the acute setting, but the evidence for long term control of blood pressure to less than 140/80 mmHG for secondary prevention of stroke is strong. Adherence to guidelines is poor but it is recognized that current evidence is limited by a lack of trials in which blood pressure is titrated to a pre-specified goal, as is common in clinical practice. Journal of Hospital Medicine 2007;2:261,267. © 2007 Society of Hospital Medicine. [source] Chronic fatigue syndrome: assessment of increased oxidative stress and altered muscle excitability in response to incremental exerciseJOURNAL OF INTERNAL MEDICINE, Issue 3 2005Y. JAMMES Abstract. Objectives., Because the muscle response to incremental exercise is not well documented in patients suffering from chronic fatigue syndrome (CFS), we combined electrophysiological (compound-evoked muscle action potential, M wave), and biochemical (lactic acid production, oxidative stress) measurements to assess any muscle dysfunction in response to a routine cycling exercise. Design., This case,control study compared 15 CFS patients to a gender-, age- and weight-matched control group (n = 11) of healthy subjects. Interventions., All subjects performed an incre-mental cycling exercise continued until exhaustion. Main outcome measures., We measured the oxygen uptake (Vo2), heart rate (HR), systemic blood pressure, percutaneous O2 saturation (SpO2), M-wave recording from vastus lateralis, and venous blood sampling allowing measurements of pH (pHv), PO2 (PvO2), lactic acid (LA), and three markers of the oxidative stress (thiobarbituric acid-reactive substances, TBARS, reduced glutathione, GSH, and ascorbic acid, RAA). Results., Compared with control, in CFS patients (i) the slope of Vo2 versus work load relationship did not differ from control subjects and there was a tendency for an accentuated PvO2 fall at the same exercise intensity, indicating an increased oxygen uptake by the exercising muscles; (ii) the HR and blood pressure responses to exercise did not vary; (iii) the anaerobic pathways were not accentuated; (iv) the exercise-induced oxidative stress was enhanced with early changes in TBARS and RAA and enhanced maximal RAA consumption; and (v) the M-wave duration markedly increased during the recovery period. Conclusions., The response of CFS patients to incremental exercise associates a lengthened and accentuated oxidative stress together with marked alterations of the muscle membrane excitability. These two objective signs of muscle dysfunction are sufficient to explain muscle pain and postexertional malaise reported by our patients. [source] Echocardiographic Estimation of Systemic Systolic Blood Pressure in Dogs with Mild Mitral RegurgitationJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2006DACVIM, Sandra P. Tou DVM Background:Systemic hypertension is likely underdiagnosed in veterinary medicine because systemic blood pressure is rarely measured. Systemic blood pressure can theoretically be estimated by echocardiography. According to the modified Bernoulli equation (PG = 4v2), mitral regurgitation (MR) velocity should approximate systolic left ventricular pressure (sLVP), and therefore systolic systemic blood pressure (sSBP) in the presence of a normal left atrial pressure (LAP) and the absence of aortic stenosis. The aim of this study was to evaluate the use of echocardiography to estimate sSBP by means of the Bernoulli equation. Hypothesis:Systemic blood pressure can be estimated by echocardiography. Animal: Seventeen dogs with mild MR. No dogs had aortic or subaortic stenosis, and all had MR with a clear continuous-wave Doppler signal and a left atrial to aorta ratio of , 1.6. Methods:Five simultaneous, blinded continuous-wave measurements of maximum MR velocity (Vmax) and indirect sSBP measurements (by Park's Doppler) were obtained for each dog. Pressure gradient was calculated from Vmax by means of the Bernoulli equation, averaged, and added to an assumed LAP of 8 mm Hg to calculate sLVP. Results:Calculated sLVP was significantly correlated with indirectly measured sSBP within a range of 121 to 218 mm Hg (P= .0002, r= .78). Mean ± SD bias was 0.1 ± 15.3 mm Hg with limits of agreement of-29.9 to 30.1 mm Hg. Conclusion: Despite the significant correlation, the wide limits of agreement between the methods hinder the clinical utility of echocardiographic estimation of blood pressure. [source] Checkpoints and pitfalls in the experimental neuropathology of circulatory disturbanceNEUROPATHOLOGY, Issue 1 2003Toshihiko Kuroiwa In neural tissue injury many pathological processes are common to different neurological disorders, including cerebral ischemia. Because ischemia has a fundamentally simple impact on neural tissue, good laboratory modeling can help improve the general understanding of the neuropathological processes involved. Summarized here are some basic principles that should be followed to ensure that cerebral ischemia studies are reproducible and informative: (i) selection of an appropriate model of cerebral ischemia in an appropriate species (although rodents are widely used for genomic studies, the use of larger animals, with brain structures macroscopically similar to those of humans, is appropriate for many studies, e.g. of white matter lesions or the pathophysiology of cerebral edema); (ii) correct maintenance of physiological parameters, including body temperature, systemic blood pressure, and blood gas tensions, under appropriate general anesthesia; (iii) selection of an appropriate method of cerebral blood flow (CBF) monitoring (decisions include whether or not the experiment requires real-time monitoring, in vivo measurement, and CBF mapping); (iv) appropriate timing of drug application in therapeutic studies (many drugs that are effective when given immediately after a short period of ischemi are ineffective in clinical trials, probably because of longer periods of ischemia and delayed drug delivery in clinical settings); and (v) multiparametric evaluation of therapeutic effect (with the recent increase in diagnosis of cases of mild stroke, measurement of mortality and infarct size have proven to be insufficient for the evaluation of therapeutic effect). Use of mild ischemia models and batteries of neurological tests for individual neurological functions, such as motor, somatosensory, and visual function, are becoming important in experimental ischemia research. In histological evaluation, assessment of the extent of both selective neuronal loss and the infarct will become mandatory. Regional analysis of each brain structure and coordination of the results with the apparent neurological dysfunction is a promising approach. [source] Targeted deletion of the ,-adducin gene (Add3) in mice reveals differences in ,-adducin interactions in erythroid and nonerythroid cells,AMERICAN JOURNAL OF HEMATOLOGY, Issue 6 2009Kenneth E. Sahr In red blood cells (RBCs) adducin heterotetramers localize to the spectrin-actin junction of the peripheral membrane skeleton. We previously reported that deletion of ,-adducin results in osmotically fragile, microcytic RBCs and a phenotype of hereditary spherocytosis (HS). Notably, ,-adducin was significantly reduced, while ,-adducin, normally present in limited amounts, was increased ,5-fold, suggesting that ,-adducin requires a heterologous binding partner for stability and function, and that ,-adducin can partially substitute for the absence of ,-adducin. To test these assumptions we generated ,-adducin null mice. ,-adducin null RBCs appear normal on Wright's stained peripheral blood smears and by scanning electron microscopy. All membrane skeleton proteins examined are present in normal amounts, and all hematological parameters measured are normal. Despite a loss of ,70% of ,-adducin in ,-adducin null platelets, no bleeding defect is observed and platelet structure appears normal. Moreover, systemic blood pressure and pulse are normal in ,-adducin null mice. ,- and ,-adducin null mice were intercrossed to generate double null mice. Loss of ,-adducin does not exacerbate the ,-adducin null HS phenotype although the amount ,-adducin is reduced to barely detectable levels. The stability of ,-adducin in the absence of a heterologous binding partner varies considerably in various tissues. The amount of ,-adducin is modestly reduced (,15%) in the kidney, while in the spleen and brain is reduced by ,50% with the loss of a heterologous ,- or ,-adducin binding partner. These results suggest that the structural properties of adducin differ significantly between erythroid and various nonerythroid cell types. Am. J. Hematol., 2009. © 2009 Wiley-Liss, Inc. [source] The emerging role of ACE2 in physiology and disease,THE JOURNAL OF PATHOLOGY, Issue 1 2007I Hamming Abstract The renin,angiotensin,aldosterone system (RAAS) is a key regulator of systemic blood pressure and renal function and a key player in renal and cardiovascular disease. However, its (patho)physiological roles and its architecture are more complex than initially anticipated. Novel RAAS components that may add to our understanding have been discovered in recent years. In particular, the human homologue of ACE (ACE2) has added a higher level of complexity to the RAAS. In a short period of time, ACE2 has been cloned, purified, knocked-out, knocked-in; inhibitors have been developed; its 3D structure determined; and new functions have been identified. ACE2 is now implicated in cardiovascular and renal (patho)physiology, diabetes, pregnancy, lung disease and, remarkably, ACE2 serves as a receptor for SARS and NL63 coronaviruses. This review covers available information on the genetic, structural and functional properties of ACE2. Its role in a variety of (patho)physiological conditions and therapeutic options of modulation are discussed. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source] Effects of Natriuretic Peptides on Intracavernous Pressure and Blood Pressure in Conscious RatsTHE JOURNAL OF SEXUAL MEDICINE, Issue 10 2008Naoki Aizawa PhD ABSTRACT Introduction., Natriuretic peptides activate particulate guanylyl cyclases and have been shown to induce penile erection in rats, rabbits, and humans. Aim., We investigated the effects of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) on intracavernous pressure (ICP) and systemic blood pressure (BP) in conscious, free-moving rats. Methods., ICP and BP were measured in male Sprague,Dawley rats after catheters were inserted into the crus corpus cavernosum and carotid artery, respectively. Natriuretic peptides were given by intravenous bolus (3, 10, and 30 nmol/kg) or continuous (0.1 and 1 nmol/kg/minute) administration. Main Outcome Measures., The number of animals with increases in ICP were determined. Amplitudes and durations of ICP responses and changes in BP were also evaluated. Results., More animals had multiple transient increases of ICP in response to ANP and BNP than to CNP. The increases in ICP were transient and appeared to be an "all or none" response. ANP and BNP decreased BP more than CNP, especially with bolus administration. Conclusions., These findings show that in rats, erectile responses can be initiated by ANP, BNP, and less effectively, by CNP. ANP and BNP have a high affinity for the natriuretic peptide receptor-A, suggesting that this receptor is involved in the responses. Aizawa N, Ishizuka O, Ogawa T, Mizusawa H, Igawa Y, Nishizawa O, and Andersson K-E. Effects of natriuretic peptides on intracavernous pressure and blood pressure in conscious rats. J Sex Med 2008;5:2312,2317. [source] Biological properties of a specific G,q/11 inhibitor, YM-254890, on platelet functions and thrombus formation under high-shear stressBRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2006Toshio Uemura 1The effects of YM-254890, a specific G,q/11 inhibitor, on platelet functions, thrombus formation under high-shear rate condition and femoral artery thrombosis in cynomolgus monkeys were investigated. 2YM-254890 concentration dependently inhibited ADP-induced intracellular Ca2+ elevation, with an IC50 value of 0.92±0.28 ,M. 3P-selectin expression induced by ADP or thrombin receptor agonist peptide (TRAP) was strongly inhibited by YM-254890, with IC50 values of 0.51±0.02 and 0.16±0.08 ,M, respectively. 4YM-254890 had no effect on the binding of fibrinogen to purified GPIIb/IIIa, but strongly inhibited binding to TRAP-stimulated washed platelets. 5YM-254890 completely inhibited platelet shape change induced by ADP, but not that induced by collagen, TRAP, arachidonic acid, U46619 or A23187. 6YM-254890 attenuated ADP-, collagen-, TRAP-, arachidonic acid- and U46619-induced platelet aggregation with IC50 values of <1 ,M, whereas it had no effect on phorbol 12-myristate 13-acetate-, ristocetin-, thapsigargin- or A23187-induced platelet aggregation. 7High-shear stress-induced platelet aggregation and platelet-rich thrombus formation on a collagen surface under high-shear flow conditions were concentration dependently inhibited by YM-254890. 8The antithrombotic effect of YM-254890 was evaluated in a model of cyclic flow reductions in the femoral artery of cynomolgus monkeys. The intravenous bolus injection of YM-254890 dose dependently inhibited recurrent thrombosis without affecting systemic blood pressure or prolonging template bleeding time. 9YM-254890 is a useful tool for investigating G,q/11 -coupled receptor signaling and the physiological roles of G,q/11. British Journal of Pharmacology (2006) 148, 61,69. doi:10.1038/sj.bjp.0706711 [source] Possible involvement of endothelium-derived hyperpolarizing factor (EDHF) in the depressor responses to platelet activating factor (PAF) in ratsBRITISH JOURNAL OF PHARMACOLOGY, Issue 6 2000Yoshio Tanaka In anaesthetized rats, platelet activating factor (PAF; 1 ,g kg,1) decreased mean arterial blood pressure by around 60 mmHg (n=18). This depressor response was completely blocked by the PAF antagonist, CV-6209 (1 mg kg,1), indicating the role of PAF-specific receptor in the response. NG -nitro- L -arginine methyl ester (L -NAME; 50 mg kg,1), an NO synthase inhibitor, profoundly elevated systemic blood pressure (n=19), indicating an important role of NO in the basal blood pressure regulation. The depressor response to PAF (1 ,g kg,1) normalized against that to sodium nitroprusside (SNP) (10 ,g kg,1) was not substantially different between rats treated without and with L -NAME (n=4). In contrast, the depressor effect of acetylcholine (0.03,1.0 ,g kg,1) normalized against that of SNP (10 ,g kg,1) was significantly attenuated by L -NAME (n=5). Charybdotoxin (0.4 mg kg,1) plus apamin (0.2 mg kg,1) significantly attenuated the depressor response to PAF (1 ,g kg,1) (n=5) without affecting the blood pressure change due to SNP (1 mg kg,1) (n=3). Charybdotoxin (0.4 mg kg,1) (n=4) or apamin (0.2 mg kg,1) (n=4) alone did not affect the PAF-induced depressor response. These findings suggest that EDHF may make a significant contribution to the depressor response to PAF in rats. Although NO plays the determinant role in the basal blood pressure regulation, its contribution to PAF-produced depressor response seems to be less as compared with that to the depressor response to acetylcholine. British Journal of Pharmacology (2000) 131, 1113,1120; doi:10.1038/sj.bjp.0703681 [source] Bedside biochemical monitoring of the penumbra zone surrounding an evacuated acute subdural haematomaACTA NEUROLOGICA SCANDINAVICA, Issue 3 2003N. Ståhl We describe a penumbra zone with increased biochemical vulnerability in cerebral cortex underlying an evacuated acute subdural haematoma. Two microdialysis catheters were placed in this zone and one catheter was placed in the opposite, less injured hemisphere. The microdialysis perfusates were analysed bedside for glucose, pyruvate, lactate, glutamate, and glycerol. In the penumbra zone, but not in the opposite hemisphere, energy metabolism was seriously disturbed with signs of cell membrane degradation. During an adverse event (decrease in haemoglobin level, systemic blood pressure and cerebral perfusion pressure) the perturbation of energy metabolism increased in this zone. Energy metabolism recovered and the signs of cell membrane degradation disappeared after normalization of the physiological parameters. We use the term biochemical penumbra zone to describe an area with signs of energy failure and cell membrane degradation, which has a capacity to regain a normal metabolic pattern but also an increased vulnerability to secondary insults. [source] 2224: Oxygenation of the human retinaACTA OPHTHALMOLOGICA, Issue 2010E STEFANSSON Purpose Partial pressure of oxygen in the optic nerve and retina is regulated by the intraocular pressure and systemic blood pressure, the resistance in the blood vessels and oxygen consumption of the tissue. The PO2 is autoregulated and moderate changes in intraocular pressure, blood pressure or tissue oxygen consumption do not affect the retinal and optic nerve oxygen tension. Methods If the intraocular pressure is increased above 40 mmHg or the ocular perfusion pressure decreased below 50 mmHg the autoregulation is overwhelmed and the optic nerve becomes hypoxic. The levels of perfusion pressure that lead to optic nerve hypoxia in the laboratory correspond remarkably well to the levels that increase the risk of glaucomatous optic nerve atrophy in human glaucoma patients. Medical intervention can affect optic nerve PO2. Lowering the intraocular pressure tends to increase the optic nerve PO2, even though this effect may be masked by the autoregulation when the optic nerve PO2 and perfusion pressure is in the normal range. Results Carbonic anhydrase inhibitors increase retinal PO2 through a mechanism of vasodilatation and lowering of the intraocular pressure. Carbonic anhydrase inhibition reduces the removal of CO2 from the tissue and the CO2 accumulation induces vasodilatation resulting in increased blood flow and improved oxygen supply. This effect is inhibited by indomethacin but not other cyclo-oxygenase inhibitors. Conclusion Carbonic anhydrase inhibitors increase retinal blood flow and increase oxygen delivery. Glaucoma drugs and glaucoma surgery lower intraocular pressure, increase ocular perfusion pressure and blood flow. Demand of oxygen by retinal cells may be reduced through apoptosis and tissue atrophy, as well as active destruction of tissue by laser photocoagulation. [source] Autoregulation in the choroidACTA OPHTHALMOLOGICA, Issue 2009S ORGUL Purpose To compare subfoveal choroidal blood flow (ChBF) in sitting and supine position in normal volunteers. Methods ChBF was measured with laser Doppler flowmetry in 22 healthy volunteers (mean age ± SD: 24 ± 5 years). Six independent measurements of choroidal blood flow were obtained in one randomly selected eye of each subject. Subsequently, the subjects assumed a supine position for 30 minutes and a new series of 6 measurements was obtained. Parallel hereto, systemic blood pressure and intraocular pressure were measured. Ocular perfusion pressure (OPP) was calculated based on formulas derived from ophthalmodynamometric studies. The influence of changing OPP on the change in ChBF was assessed in a linear regression analysis. Results The coefficient of variation for ChBF was 10.28% and 9.58% in the sitting and the supine position respectively. ChBF decreased by 6.6% (p=0.0017) in the supine position. The estimate for ophthalmic blood pressure in the supine position was adjusted to obtain a result of no change in OPP for no change in ChBF, yielding an average decrease for the estimate of OPP of 6.7% (p=0.0002). Change in OPP correlated significantly with change in ChBF (R2: 0.20; p=0.036) with a slope for the regression line of 1.04. Conclusion The comparable degree of change in ChBF and OPP and the linear relationship between the two parameters suggest a passive response of the choroidal circulation to the posture change. In contrast, the OPP estimates suggest a marked buffering of the change in perfusion pressure by the carotid system, compatible with a close control of the gradient in perfusion pressure between the heart and its branches within the carotid system. [source] Disease mechanisms leading to impaired blood flow in glaucomaACTA OPHTHALMOLOGICA, Issue 2009D GHERGHEL Purpose SIS lecture Methods Literature search Results Although primary open-angle glaucoma (POAG), is associated more closely with elevated intraocular pressure (IOP), other risk factors already implicated in the aetiology of this disease and especially in the aetiology of normal-tension glaucoma are: abnormal ocular circulation, ocular and systemic vascular dysregulation, as well as systemic blood pressure (BP) alterations. Oxidative stress, which occurs as a result of an imbalance between generation of reactive oxygen species (ROS) and antioxidant defence mechanisms and is implicated in the pathogenesis of disorders ranging from atherosclerosis to neurodegenerative disorders, diabetes and aging, may also contribute to the general vascular disturbances observed in glaucoma. Moreover, increasing evidence shoes that oxidative stress plays a role in promoting endothelial dysfunction, which is a key factor in progression of vascular diseases. Indeed, glaucomatous optic nerve damage has been related to endothelial damage/dysfunction. This presentation explores the role of various ocular and systemic circulatory factors in the pathogenesis of glaucomatous neuropathy. [source] Impact of medication on ocular blood flowACTA OPHTHALMOLOGICA, Issue 2009L SCHMETTERER Purpose Reduced ocular blood flow appears to play a role in the pathophysiology of glaucoma. Hence, there is considerable interest in drugs that are capable of improving ocular perfusion. Methods A large numer of clinical trials have been performed investigating the ocular hemodynamic effects of topical and systemic medications. Such trials used a variety of different methods to assess ocular blood flow parameters. Results When adminsitered systemically most vasodilators decrease systemic blood pressure thereby reducing ocular perfusion pressure (OPP). Only few classes of drugs have been reported to increase ocular blood flow with no or minimal effect on OPP. Among these carbonic anhydrase inhibitors and endothelin receptor anatgonists show the most prononced ocular vasodilator effects. The ocular hemodynamoic effects of topical medications is generally considered small. Conclusion When drugs are given systemically the effects on OPP have to be considered. In addition, the potentially positive effects on ocular perfusion need to be carefully weighed against the side effects. With topically administered drugs the ocular hemodynamic effects will be generally small, because the drugs reach the posterior pole of the eye in small concentrations only. [source] Evidence for altered ocular rigidity in glaucomaACTA OPHTHALMOLOGICA, Issue 2009L SCHMETTERER Purpose Based on theoretical models and animal studies altered biomechanical properties of the optic nerve head and the sclera have been implicated in the pathophysiology of glaucoma. Only few data have, however, demonstrated such biomechanical alterations in vivo. We tested the hypothesis that patients with primary open angle glaucoma (POAG) have an abnormal structural stiffness based on measurements of intraocular pressure amplitude and ocular fundus pulsation amplitude. Methods Seventy patients with POAG and 70 healthy control subjects matched for age, gender, intraocular pressure and systemic blood pressure were included in this study. The ocular pulse amplitude (PA) was assessed with pneumotonometry. The fundus pulsation amplitude (FPA) was measured using laser interferometry. Based on the Friedenwald equation a coefficient of structural stiffness (E1) was calculated relating PA to FPA. Results Systemic blood pressure, intraocular pressure, and ocular perfusion pressure was comparable between glaucoma patients and healthy control subjects. FPA as well as PA was lower in patients with glaucoma than in healthy controls. The calculated factor E1 was significantly higher in patients with POAG (0.0454 ± 0.0085 a.u.) than in healthy control subjects (0.0427 ± 0.0058 a.u., p = 0.03). Conclusion This study is indicative of increased structural stiffness of the sclera in patients with POAG. This is in agreement with a number of previous animal experiments and supports the idea that the biomechanical properties of ocular tissues play a role in the process of glaucomatous ONH damage. [source] Factors affecting ocular rigidity in normal human eyesACTA OPHTHALMOLOGICA, Issue 2009AI DASTIRIDOU Purpose To measure the ocular rigidity coefficient and evaluate its relation with axial length (AL), age and mean systemic blood pressure (SBP). Methods Sixty three patients (63 eyes) undergoing cataract surgery, with different refractive errors and no ocular or systemic pathology were enrolled in this study. An invasive, computer controlled device comprising a microdosimetric pump and a pressure sensor, is connected to the anterior chamber under topical anaesthesia with drops. The system is used to raise the intraocular pressure (IOP) from 15 to 40mmHg, by infusing the eye with a saline solution. After each 4 ul infusion step, the IOP is continuously recorded for 2 seconds. From an initial level of 40mmHg an IOP decay curve of 1 minute is obtained. SBP and pulse rate are measured during the procedure. The rigidity coefficient is calculated by an exponential fit to the pressure volume data after correction for outflow. The study was approved by the Institutional Board and performed under the patient's informed consent. Results Mean AL was 24.8 (range 21.2-32.5). Mean age and SBP was 59 (12) years and 93.7 (10.5) mmHg respectively. The mean ocular rigidity coefficient was 0.021 (0.005) ul-1. Increasing axial length is associated with a decrease in the rigidity coefficient (r=-0.61, p<0.01). A positive correlation between the rigidity coefficient and age of the patients is found (r=0.31, p=0.01), whereas similar findings were not observed for SBP (p>0.05). Conclusion This manonetric approach of measuring ocular rigidity provides a normative database of this parameter in living human eyes. Axial length and age influence ocular rigidity. These results may have implications on tonography and ocular pulse studies. [source] Relationship between ocular pulse amplitude and systemic blood pressure measurementsACTA OPHTHALMOLOGICA, Issue 3 2009Matthias C. Grieshaber Abstract. Purpose:, This study aimed to determine whether ocular pulse amplitude (OPA) measured with dynamic contour tonometry (DCT) is related to systemic blood pressure (BP) parameters. Methods:, Blood pressure was measured continuously and simultaneously with OPA in one randomly selected eye in 29 healthy subjects. Systemic parameters of interest were: systolic and diastolic BPs and their difference (BP amplitude), and left ventricle ejection time (LVET; defined as the time between the diastolic trough and the incisural notch in the BP curve). In addition, the axial length (AL) of the eye was measured. Associations between OPA, AL and systemic cardiovascular parameters were analysed in a multivariate regression model. Results:, Measurements of OPA ranged from 1.0 mmHg to 4.9 mmHg (mean 2.3 ± 0.9 mmHg, median 1.9 mmHg). In a univariate analysis with one predictor at a time, means of intraocular pressure (IOP) (p = 0.008), AL (p = 0.046) and LVET (p = 0.037) were significantly correlated with OPA, whereas systolic and diastolic BPs and their amplitude were not. A multiple linear regression analysis showed that mean IOP (p < 0.005), AL (p = 0.01) and LVET (p = 0.002) all independently contributed to OPA. Conclusions:, The OPA readings measured with DCT in healthy subjects were not related to BP levels and amplitude. It seems that the OPA strongly depends on the time,course of the cardiac contraction. Regulating mechanisms in the carotid system as well as scleral rigidity may be responsible for dampening the direct effect of BP variations. [source] The short-term effect of latanoprost on intraocular pressure and pulsatile ocular blood flowACTA OPHTHALMOLOGICA, Issue 1 2002Gerasimos T. Georgopoulos ABSTRACT. Purpose:, There is evidence that ocular blood flow plays a critical role in the clinical course of glaucoma. Any reduction in ocular blood flow due to topical antiglaucoma treatment should therefore be avoided. This study aimed to evaluate the short-term effect of local latanoprost application on ocular hemodynamics. Methods:, Intraocular pressure (IOP), ocular pulse amplitude (OPA), ocular pulse volume (OPV), systemic blood pressure, heart rate and the pulsatile component of ocular blood flow (POBF) were recorded using a pneumotonometer linked to the Langham Ocular Blood Flow System in 24 patients in a prospective, open-label study before and after 1 week of topical latanoprost application in both eyes. Twenty of the subjects had primary open-angle glaucoma and four had ocular hypertension. Results:, After 1 week of latanoprost treatment, IOP decreased significantly 6.2 ± 2.9 mmHg in OD (P < 0.001) and 6.2 ± 3.2 mmHg in OS (P < 0.001). Pulsatile OBF increased significantly by 201.2 ± 167.4 µL/min in OD (P < 0.001) and 203.8 ± 187.3 µL/min in OS (P < 0.001). Ocular pulse amplitude and OPV showed statistically significant increases (P < 0.05 and P < 0.001 respectively). Blood pressure and heart rate did not change significantly. Conclusion:, Our results indicate that 1 week after latanoprost application, POBF, OPA and OPV were significantly increased in the eyes treated. More information on the perfusion of the optic nerve head is needed before the relevance of these findings to optic nerve head blood flow can be interpreted correctly. [source] Assessment of the spontaneous pulsations of the central retinal vein in daily ophthalmic practiceCLINICAL & EXPERIMENTAL OPHTHALMOLOGY, Issue 9 2007Ulrich Legler MD Abstract The purpose of this study is to assess the frequency of eyes with a spontaneous pulsation of the central retinal vein in the setting of a busy daily ophthalmic practice. The clinical observational case-series study included 690 eyes (345 subjects). The optic disc was ophthalmoscopically assessed using a non-contact ophthalmoscopic lens at the slit lamp. Out of the study population, 526 eyes (76.2%) of 265 (76.8%) subjects showed a detected spontaneous pulsation of the central retinal vein (prevalence rate: 76.2 ± 1.6% [mean ± standard error] per eye, and 76.8 ± 2.3% per subject). In univariate analysis, the presence of a detected spontaneous central retinal vein pulsations was statistically associated with systolic systemic blood pressure (P = 0.04) and with the ocular perfusion pressure (P = 0.03). The results suggest that as examined in the setting of a busy daily ophthalmic practice, the central retinal vein was found to show a spontaneous pulsation in about 80% of the subjects. [source] Acute decrease of coronary flow after indomethacin delivery in newborn lambsACTA PAEDIATRICA, Issue 10 2007Solweig Harling Abstract Aim: To document the effects of indomethacin (IND) on coronary flow. Methods: We studied nine premature lambs during the first day of life. The gestational age varied between 132 and 134 days (term 145 days) and weight 3.1,4.7 kg. Coronary flow velocities were recorded with an intracoronary Doppler guide wire in the proximal left anterior descending coronary artery (LAD). Average peak flow velocity was measured before, during and after an intravenous IND injection of 0.2 mg per kilogram of body weight. Results: IND increased systemic blood pressure (p < 0.05) and rate pressure product (RPP; p < 0.05) indicating that IND increased cardiac workload. IND decreased coronary average peak flow velocity in all lambs (p < 0.05). The maximal fall in coronary velocity appeared after 3 min (range 1,7 min) and was regained 10 min (range 4,53 min) after the drug delivery. The maximal reduction of coronary average peak flow velocity was 52% (median 26). The recovery time was directly related to the maximal reduction of the coronary average peak flow velocity (R = 0.91, R2 0.84, p < 0.002). Conclusion: Coronary flow velocity decreased markedly in premature born lambs given a bolus dose of IND. [source] Cardiac diastolic dysfunction in renal-transplant recipients is associated with increased circulating AdrenomedullinCLINICAL TRANSPLANTATION, Issue 3 2006Bernard Geny Abstract:, Background:, Renal transplantation is an excellent therapeutic alternative for end-stage renal diseases. Nevertheless, the cardiac function is often impaired in renal-transplant patients (RTR) and importantly determines their prognosis. Adrenomedullin (ADM), a peptide involved in cardiovascular homeostasis, is believed to protect both cardiac and renal functions , by increasing local blood flows, attenuating the progression of vascular damage and remodelling and by reducing glomerular injury , and might be involved in renal-transplantation physiopathology. This work was performed to investigate whether an increase in circulating ADM might be related to RTR cardiac function. Methods:, Twenty-nine subjects, 19 RTR and 10 healthy subjects, participated in the study. After 15 min rest in supine position, heart rate and systemic blood pressure were measured together with cyclosporine through levels, creatinine and ADM. Systolic and diastolic cardiac functions were assessed, using Doppler echocardiography. Results:, Subjects were similar concerning age, weight, heart rate and blood pressure. Creatinine and ADM (53.8±6.9 vs. 27.2±4.1 pmol/L, p = 0.02) were significantly increased in RTR (73±10 months after transplantation). Cardiac systolic function was normal, but a reduced mitral E:A ratio was observed in RTR (0.90±0.06 vs. 1.38±0.10, p<0.001), reflecting their impaired left ventricular relaxation. Such a ratio was negatively correlated with ADM (r = ,0.55, p = 0.002). Conclusions:, RTR present with an increased ADM is likely related to cardiac diastolic dysfunction. In view of its protective effect on the cardiovascular system, these data support further studies to better define the role and the therapeutic potential of ADM after renal transplantation. [source] | ||||||||||||||||||||||