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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this experiments is to study the role of arginine vasopressin (AVP) in acute ischemic brain edema of mongolian gerbils. The results showed that the contents of AVP in ischemic cortex, hypothalamus and striatum increased remarkably in 15-120 minutes after ischemia, while the contents of AVP had no change in pons-medulla which was not affected from ischemia, and there was relationship between the contents of AVP in cortex and the ischemic cortical edema. Intracerebroventricular injection (ICV) of AVP exacerbated the ischemic cortical edema and it showed dose-response correlation. While ICV of AVP antiserum significantly decreased ischemic cortical edema. These suggested that AVP was involved in the pathophysiologic process of acute ischemic brain edema. The increasing of AVP contents in ischemic brain regions could exacerbate the formation of ischemic brain edema.
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PMID:[An experimental study of arginine vasopressin on acute ischemic brain edema in gerbils (1)]. 147 42

To investigate the ability of arginine vasopressin (AVP) to compete with metabolic vasodilatory factors in the coronary circulation, we examined the coronary vascular and myocardial effects of AVP in isolated working rat hearts during normoxic and hypoxic perfusion. In normoxic hearts, AVP treatment (777 +/- 67 pg/ml) reduced coronary flow by 38.4 +/- 2.6%. Myocardial function was also significantly decreased by AVP whereas efficiency significantly increased. In contrast, the same dose of AVP administered to hypoxic hearts resulted in substantially smaller effects on coronary flow (-11.5 +/- 2.8%), myocardial function, and efficiency. In hearts treated first with AVP and then with hypoxia, the greater degree of coronary vasodilation compared with that observed in hearts treated with hypoxia alone also indicated an antagonizing effect of hypoxia on AVP-mediated coronary constriction. It was also noted that the hypoxia treatment alone resulted in reductions of O2 supply and consumption identical to those produced by AVP treatment during normoxia. However, hypoxia was associated with a significantly greater effect on myocardial function and, in contrast to the effect of AVP, a marked reduction in efficiency. The rate of lactate release was greater during hypoxia alone (2.07 +/- 0.08 mumol/min) than with AVP treatment during normoxia (0.76 +/- 0.05 mumol/min). These results indicate that the effect of AVP on the coronary vessels, as well as its effect on the myocardium, is significantly attenuated during hypoxia. In addition, AVP-constricted vessels appear to retain considerable vasodilatory reserve despite evidence of ischemic conditions. Thus, although the effects of AVP resemble ischemia, the increased efficiency and the relatively small effect of AVP on contractile function, as well as the preserved vasodilatory reserve, suggest otherwise. A physiological explanation for these observations is proposed wherein the constricting effects of AVP modulate the effects of autoregulatory factors such that blood flow requirements are minimized while allowing preservation of adequate blood flow for vital tissue function.
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PMID:Attenuation of vasopressin-mediated coronary constriction and myocardial depression in the hypoxic heart. 230 3

The present work was performed on uninephrectomized rabbits recovering from ischemic acute renal failure (ARF) in an attempt to elucidate whether or not intraglomerular events are a determinant factor in the development of resistance to ARF. 14 days after a 2-hour clamping of the renal artery (the recovery phase), the animals did not show resistance to an additional ischemia. On the other hand, glomeruli derived from normal kidneys displayed a contractile response to angiotensin II, arginine vasopressin or norepinephrine in Eagle's minimum essential medium, whereas glomeruli from rabbits recovering from ischemic ARF were refractory to the vasoconstrictor agents. The findings suggest that glomerular refractoriness to contractile stimuli does not provide resistance to an additional renal ischemia in the ischemic model of ARF.
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PMID:Glomerular refractoriness to contractile stimuli in rabbits recovering from ischemic acute renal failure. 336 77

Glomerular responses to angiotensin II (AII), arginine vasopressin (AVP), and norepinephrine (NE) were estimated in rabbits recovering from uranium-mediated nephropathy or ischemic acute renal failure (ARF) to examine roles of intraglomerular events in resistance to ARF. Uranyl acetate (UA, 0.8 mg/kg) produced ARF in some animals but did not in others. Rabbits recovering from UA-induced ARF were highly resistant to a rechallenge with a larger dose of the agent (2 mg/kg). Their glomeruli did not respond to AII, AVP and NE in vitro. In animals having not experienced ARF following the initial insult, however, resistance to the rechallenge was lower than in animals recovering from ARF, and the glomerular response to contractile stimuli was well sustained. A two hour clamping of the renal artery induced ARF in uninephrectomized rabbits. These animals were not resistant to an additional ischemia in the recovery phase, despite inhibited glomerular contractile responses to AII. These data indicate a nonspecific inhibition of glomerular responses to contractile stimuli in the recovery phase of ARF. It is unlikely, however, that resistance to ARF can be attributed to the loss of the glomerular contractile response.
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PMID:Loss of glomerular responses to vasoconstrictor agents in rabbits recovering from ARF. 354 13

The development of tolerance to morphine analgesia in amnesic model mice and the role of arginine vasopressin (AVP) in the underlying mechanism was examined. Hypoxia, brain ischemia, scopolamine and electroconvulsive shock (ECS) manipulation caused amnesia in the step-through type passive avoidance learning test performed at 24 h after the training trial. The amnesic state lasted for at least 3 days and recovered to naive control level on the 20th day after each manipulation. In all amnesic groups, radioimmunoassayable AVP content in hypothalamus was decreased, in particular, the reduction was significant in hypoxia and ischemic induced amnesic animals, then recovered to the control level by 20 days after each treatment. Daily morphine, 10 mg/kg, s.c. easily resulted in the development of tolerance to the analgesic effect in control animals; however, such treatment failed to develop tolerance in amnesic model animals, leaving the analgesic effect unchanged to the control levels. Daily pretreatment with i.c.v. AVP, dose-dependently reinstated the development of tolerance in amnesic model mice. When morphine injection was started from 20 days after the amnesia inducing treatment, tolerance developed as in a similar pattern as in control animals. Thus, amnesic model mice are deficient in brain AVP levels, and consequently, a certain level of AVP in the hypothalamus is required for maintaining the normal function such as the development of tolerance to morphine and the recovery from amnesia.
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PMID:Lack of the development of morphine tolerance in experimental amnesia: role of arginine vasopressin. 850 24

The normal functional state of the vasculature and the events leading to the development of significant arterial disease involve the interaction of important vasoactive substances, which play important modulating or initiating roles in the development of hypertension and arteriosclerosis. Three endothelins have now been identified, of which ET-1 is the best characterized. ET-1 is produced by epithelial, mesangial, neuronal and glial, and liver cells, and is the most potent vasoconstrictor yet found. Each endothelin is derived from a different gene on separate chromosomes, and each binds to at least 2 types of receptor. The plasma half-life of ET-1 is about 7 min, and this provides a rapid mechanism for adjusting vascular resistance or blood pressure. The actions of endothelin are mediated through several pathways of postreceptor signaling, including activation of the mitogen-activated protein kinase cascade, which give rise to its growth-stimulating properties. Secretion of ET-1 from cultured endothelial cells is stimulated by a wide range of substances, and is inhibited by some prostaglandins. Endothelin in turn stimulates secretion of nitric oxide, arginine vasopressin and atrial natriuretic peptide, and participates in the hormonal control of salt and water balance. Hypoxia and ischemia augment ET-1 secretion, as does insulin, and this could play a role in the accelerated vascular disease of diabetes. ET-1 also causes bronchoconstriction and has been implicated in the development of acute asthma, primary pulmonary hypertension and pulmonary fibrosis. Its role in hypertension is still debatable, though most of the manifestations of congestive heart failure can theoretically be explained by the actions of ET-1. Endothelin also has extensive renovascular and parenchymal effects in the kidney. It is hoped that a fuller understanding of the role of endothelins in normal or pathologic vasculature will lead to effective therapy based on antagonism or augmentation of specific functions.
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PMID:Endothelins as cardiovascular peptides. 873 84

Mongolian gerbils were used as delayed neuronal damage (DND) animal models. At the end of 15 minute cerebral ischemia and at various reperfusion time ranging from 1 to 96 hours, the content of water and arginine vasopressin (AVP) in the CA1 sector of hippocampus were measured by the specific gravity method and radioimmunoassay. Furthermore, we also examined the effect of intracerebroventricular (ICV) injection of AVP, AVP antiserum on calcium, Na+, K(+)-ATPase activity in the CA1 sector after ischemia and 96 hour reperfusion. The results showed that AVP contents of CA1 sector of hippocampus during 6 to 96 hour recirculation, and the water content of CA1 sector during 24 to 96 hour were significantly and continuously increased. After ICV injection of AVP, the water content and calcium in CA1 sector of hippocampus at cerebral ischemia and 96 hour recirculation further increased, and the Na+, K(+)-ATPase activity in CA1 sector was remarkably decreased as compared with that of control. While ICV injection of AVP antiserum, the water content and calcium in CA1 sector were significantly decreased as compared with that of control. These suggested that AVP was involved in the pathophysiologic process of DND in hippocampus following cerebral ischemia and reperfusion. Its mechanism might be through the change of intracellular action mediated by specific AVP receptor to lead to Ca ions over-load of neuron and inhibit the Na+, K(+)-ATPase activity, thereby to exacerbate the DND in hippocampus.
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PMID:Effect of vasopressin on delayed neuronal damage in hippocampus following cerebral ischemia and reperfusion in gerbils. 938 16

Standard therapy for variceal bleeding includes endoscopic sclerotherapy and esophageal balloon tamponade. In addition, pharmacologic therapies, including arginine vasopressin (AVP), are frequently used in hemodynamically unstable patients or where sclerotherapy has been unsuccessful. A case is described herein of a 30-year-old woman with a history of ethanol abuse, hematemeisis, and biopsy-proven hepatic cirrhosis in which the addition of AVP to an antivariceal regimen of octreotide was associated with a paradoxical episode of hypotension, bradycardia, and hypoxia. Indeed, within 15 minutes after initiation of an AVP infusion, the patient exhibited hypotension with a systolic blood pressure of 80 mmHg, a relative bradycardia to 76 beats per minute, and a desaturation of blood oxygen to 84%. The AVP infusion was discontinued 2 hours later and blood pressure, heart rate, and oxygen saturation rapidly returned to baseline. This temporal correlation between the onset and termination of the physiologic effects and the initiation and discontinuation of the AVP infusion suggests a causal relationship. The paradoxical physiologic effects might reflect cardiac ischemia secondary to vasospasm and/or central suppression of the autonomic nervous system induced by AVP.
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PMID:Paradoxical hypotension and bradycardia after intravenous arginine vasopressin. 954 67

Ischemia-induced brain edema formation is mediated by increased transport of Na and Cl across an intact blood-brain barrier (BBB). Our previous studies have provided evidence that a luminally located BBB Na-K-Cl cotransporter is stimulated during cerebral ischemia to increase transport of Na and Cl into the brain. The main focus of the present study was to evaluate the effects of arginine vasopressin (AVP), previously shown to be increased in the brain during ischemia and to promote edema formation, on activity of the BBB cotransporter. Cerebral microvascular endothelial cell (CMEC) monolayers were cultured in astroglial cell conditioned medium, and Na-K-Cl cotransporter activity was assessed as bumetanide-sensitive (86)Rb influx. In both human and bovine CMECs, as well as in freshly isolated microvessels, AVP stimulated cotransport activity. This stimulatory effect was mimicked by V(1) but not V(2) vasopressin agonists and was blocked by V(1) but not V(2) vasopressin antagonists. Consistent with a V(1) vasopressin receptor mechanism of action, AVP caused an increase in CMEC intracellular [Ca] that was blocked by a V(1) antagonist. Exposing the cells to [Ca]-free media and/or reducing intracellular [Ca] by BAPTA also blocked AVP stimulation of CMEC cotransporter activity, as did the phospholipase C inhibitor U-73122. Finally, we found that while stimulation of CMEC cotransporter activity by AVP occurred within minutes, it was also sustained for hours in the continued presence of AVP. These findings support the hypothesis that AVP, through a V(1) receptor- and [Ca]-dependent mechanism, stimulates the BBB Na-K-Cl cotransporter to participate in ischemia-induced edema formation.
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PMID:Arginine vasopressin stimulation of cerebral microvascular endothelial cell Na-K-Cl cotransporter activity is V1 receptor and [Ca] dependent. 1580 57

In addition to controlling systemic blood pressure, angiotensin II (Ang II) has several roles in the brain, including the regulation of cerebrovascular flow and the reaction to stress. In order to clarify the central effects of Ang II and its type 1 (AT1) receptors, we reviewed the literature reporting recent research on the effects of pretreatment with the AT1-receptor blocker, candesartan, on experimental ischemia, cerebrovascular remodeling, and inflammation in spontaneously hypertensive rats (SHRs), and the responses to stress induced by isolation and by cold-restraint. Angiotensin II regulates the brain circulation through stimulation of AT1-receptors located in the cerebrovascular endothelium and central pathways. SHRs express greater numbers of endothelial AT1-receptors and a central sympathetic overdrive, resulting in pathological cerebrovascular growth, inflammation, decreased cerebrovascular compliance, and enhanced vulnerability to brain ischemia. Sustained central AT1-receptor antagonism reverses these effects. Sustained reduction of AT1-receptor stimulation before stress prevents the hormonal and sympathoadrenal stress responses during isolation and prevents the gastric ulceration stress response to cold-restraint, indicating that increased AT1-receptor stimulation is essential to enhance the central sympathetic response and the formation and release of corticotropin-releasing factor (CRF) and arginine vasopressin that occur during stress. AT1-receptor blocking agents reverse the cortical alterations in CRF1 and benzodiazepine receptors characteristic of isolation stress, effects probably related to their anti-anxiety effect in rodents. Sustained reduction of Ang II tone by AT1-receptor antagonism could be considered as a preventive and therapeutic approach for brain ischemia and stress-related and mood disorders. Additional preclinical studies and controlled clinical trials are necessary to confirm the efficacy of this novel therapeutic approach.
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PMID:Angiotensin II: multitasking in the brain. 1660 66


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