Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The radioprotective effect of vasopressin-induced intestinal ischemia was investigated in pigs. A bolus injection in the cranial mesenteric artery, of a vasopressin solution, 0.05 IU/kg body weight, was followed by irradiation of the small intestine with 6 MV roentgen rays. Three different fraction schedules were used. Weight changes in the animals and the histologic appearance of their intestines were recorded two weeks after irradiation and compared with the findings in untreated animals. Intra-arterial vasopressin was very effective in protecting the intestine. Vasopressin treatment given before 2 fractions with relatively high radiation doses in a 6-fraction regimen was so effective that it may form the basis of a treatment model applicable in man.
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PMID:The protective effect of intra-arterial vasopressin injections on the small bowel during fractionated abdominal irradiation. A study in pigs. 300 37

Leukotrienes have been implicated as mediators of ischemia and shock. Recent evidence has been obtained supporting the four major criteria of acceptance of leukotrienes as mediators of shock, namely (a) increased concentration in body fluids during shock states, (b) ability to exert significant pathophysiologic effects which aggravate ischemia and shock, (c) amelioration of the shock state by leukotriene synthesis inhibitors and leukotriene receptor antagonists, and (d) production of a shock-like state by exogenous administration of leukotrienes. In conclusion, both LTB4 and the peptide leukotrienes (e.g. LTC4, LTD4 and LTE4) also known as the slow reacting substance of anaphylaxis (SRS-A) can be considered as mediators of ischemia and shock. Although difficulties exist with measuring leukotrienes in circulating blood and in obtaining long lasting selective blockers of leukotriene synthesis, innovative experiments measuring leukotrienes in bile and other body fluids and in employing specific leukotriene receptor antagonists have helped in assessing the significance of the leukotrienes in shock states. Additional studies are necessary to evaluate these findings in perspective, and to compare and contrast the role of leukotrienes to that of other vascular mediators including prostaglandins and thromboxanes, as well as non-eicosanoids including serotonin, histamine, angiotensin II and vasopressin, all of which can play a mediator role in ischemia and shock states. Further clarification of these issues promises to open exciting new chapters in shock research.
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PMID:Leukotrienes as mediators of ischemia and shock. 300 83

Endoscopic reflectance spectrophotometry was used to compare the effect of vasopressin and propranolol on gastric mucosal hemodynamics in dogs with surgically induced esophageal varices and prehepatic portal hypertension. Reflectance spectrophotometry provides indices of mucosal hemoglobin concentration (IHB) and oxygen saturation (ISO2). Hyperemia (increased IHB, normal ISO2), ischemia without congestion (decreased IHB, decreased ISO2), and ischemia with congestion (increased IHB, decreased ISO2) are accompanied by characteristic patterns of IHB and ISO2. Under anesthesia, measurements were obtained on separate days from the gastric corpus mucosa of eight dogs before and 2 to 10 min after either 1 to 5 units of intravenous vasopressin or 1 mg of propranolol. Results revealed that vasopressin (in doses that significantly reduced variceal and portal venous pressure in this animal model) produced a reduction in both IHB and ISO2, indicating gastric mucosal ischemia secondary to splanchnic vasoconstriction. On the other hand, propranolol in a dose that significantly reduced pulse rate by 27 +/- 2% had no effect on IHB or ISO2, suggesting that this dose of propranolol has no direct vasoactive effect on the gastric (splanchnic) circulation.
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PMID:Endoscopic demonstration that vasopressin but not propranolol produces gastric mucosal ischemia in dogs with portal hypertension. 326 2

This study assessed the contribution of angiotensin II, oxygen-free radicals, and vasopressin to the mortality of acute mesenteric ischemia in rats. Rats received saline replacement (16 ml/kg/hr) for 3 hr during and after 85 min of superior mesenteric artery (SMA) occlusion. Only 21% of rats that received saline alone (n = 14, control) survived 48 hr, significantly less than the 100% survival of sham-operated rats (no SMA occlusion, n = 5, P less than 0.01). Neither teprotide (an angiotensin converting-enzyme inhibitor), allopurinol (to reduce oxygen-free radical formation), nor a specific vasopressin antagonist [1-(beta-mercapto-beta,beta-cyclopentamethyleneproprionic acid), 2-(O-methyl) tyrosine arginine-vasopressin] improved 48-hr survival, which was 17% in each group (n = 6, each). Survival improved significantly to 86% (n = 7, P less than 0.001) when intravenous glucagon (1.6 micrograms/kg/min) was given for 2 hr after SMA reperfusion. Survival after dopamine infusion (12 micrograms/kg/min iv) was 67% at 48 hr, a nearly significant improvement (n = 9, P less than 0.06). These results suggest that angiotensin II, oxygen-free radicals, and vasopressin do not contribute significantly to the high mortality observed after acute intestinal ischemia in this rat model, but that glucagon, and to a lesser extent, dopamine, are potentially therapeutic.
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PMID:Pharmacologic treatment of occlusive mesenteric ischemia in rats. 337 18

Visual disturbance after marked and/or recurrent blood loss has been known for at least 25 centuries, since Hippocrates; however, so far its clinical features have been controversial and its pathogenesis enigmatic. The author studied seven patients, four of whom were seen soon after the visual loss and followed prospectively. A detailed review of the extensive literature and analysis of the cases provide relevant information on the subject. The blood loss is usually from the gastrointestinal (GI) tract, less often from other sites. There is typically a time lag between the bleeding and the onset of visual loss--usually up to 10 days, less often even 2 to 3 weeks. The ocular findings are typically those of anterior ischemic optic neuropathy (AION) and are usually bilateral. Considerable evidence has accumulated that blood loss, with or without arterial hypotension, causes increase in release of renin and endogenous vasoconstrictor agents (e.g., angiotensin, epinephrine, and vasopressin) because of activation of the sympathoadrenergic system and vasomotor center. Our experimental studies on renovascular malignant hypertension indicate that endogenous vasoconstrictor agents produce choroidal ischemia and AION. In view of all the evidence, it is postulated that in the production of AION after blood loss, release of endogenous vasoconstrictor agents is probably a very important factor, with arterial hypotension an additional factor; increased platelet aggregation may also play a role.
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PMID:Anterior ischemic optic neuropathy. VIII. Clinical features and pathogenesis of post-hemorrhagic amaurosis. 350 Apr 45

Mechanically and chemically sensitive receptors in the ventricle have been described histologically and electrophysiologically. Early experiments documented the hypotension and bradycardia that resulted from the intracoronary administration of one of the veratrum alkaloids (the Bezold-Jarisch reflex). Mechanical distension of the ventricles also results in a reflex decrease in heart rate and a reduction in peripheral resistance. Skeletal muscle and coronary vascular resistance appear to be most prominently affected by stimulation of ventricular receptors. Coronary ischemia has also been shown to evoke reflex effects which are attributable to stimulation of ventricular receptors. The resultant bradycardia can be especially ominous in acute myocardial infarction. Changes in myocardial inotropic state have been shown to alter ventricular receptor discharge in experimental animals. This stimulus may evoke reflex changes in peripheral hemodynamics. A variety of humoral substances can alter ventricular receptor discharge and evoke Bezold-Jarisch like responses. These include bradykinin and prostaglandins. PGI2, when given intracoronary in small doses or intravenously in larger doses will lower blood pressure while inhibiting the baroreflex induced tachycardia. It has also been shown in some experiments that PGI2 and arachidonic acid can evoke overt bradycardia and hypotension via a reflex mechanism. The role of prostaglandins in cardiovascular reflex control may be important in pathophysiologic states such as coronary ischemia and heart failure. Ventricular receptors can interact centrally with the arterial baroreceptors to attenuate the baroreflex control of both heart rate and peripheral resistance. Finally, the stimulation of ventricular receptors can alter a variety of humoral substances which are important regulators of cardiovascular and fluid volume homeostasis. These include vasopressin, renin and catecholamines. Those studies which have been done within the last 10 years or so, especially in unanesthetized animals, have demonstrated that the Bezold-Jarisch reflex is more important to cardiovascular control than previously thought. Future work will be necessary to determine the precise role ventricular receptors play in various pathological situations.
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PMID:Left ventricular receptors: physiological controllers or pathological curiosities? 354 77

Ion transport properties and some components of lipid structure in myocardial sarcolemma were studied under conditions of short-term acute ischemia simulated in rabbits by means of intravenous administration of vasopressin at a dose of 0.2 U/kg. The acute coronary insufficiency was accompanied by distinct alterations in the parameters specific for calcium metabolism and transport: activity of Na+, K+-ATPase and the rate of Na+Ca2+ turnover were decreased, while 45Ca-binding ability and content of Ca2+ were increased in the myocardial sarcolemma. Alterations in lipid structure, phospholipid composition of membranes and accumulation of free fatty acids appear to be responsible for the phenomenon observed. The increased rate of calcium ions transport found may occur due to alterations in the sarcolemma structure.
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PMID:[Ion-transport system and various components of sarcolemma structure during acute myocardial ischemia]. 357 53

We evaluated the effects of common vasoactive agents on collateral blood flow to an ischemic segment of small intestine and on the hemodynamic determinants of that flow. Two adjacent canine jejunal segments were isolated together, and the artery to each was cannulated for autoperfusion from a femoral and a carotid artery, respectively. Arterial pressure, arterial blood flow into, and venous outflow from each segment was measured separately. Venous pressure was zero. Vascular resistances were calculated. After clamping the arterial circuit to one segment, designated "ischemic," its steady-state venous outflow was taken as the collateral blood flow from the nonischemic into the ischemic segment. Without drugs, collateral blood flow was equal to 29 +/- 4 ml/min X 100 gm or, 56% +/- 8% of normal, well above the level needed to sustain oxygen consumption and thereby prevent ischemic injury. Local intra-arterial infusion of the vasodilators isoproterenol and papaverine not only failed to increase collateral flow but actually caused a small but (with isoproterenol) significant reduction, caused by vasodilation in the nonischemic bed, and a resulting drop in arterial pressure distal to the occlusion in the ischemic segment (i.e., a steal phenomenon). The vasoconstrictors levarterenol and vasopressin also reduced collateral flow but by direct and preferential vasoconstriction of the dilated ischemic bed. These findings suggest that collateral blood flow may be optimal without drugs and is decreased only by vasoactive agents, including vasodilators. This contradicts the rationale for vasodilator therapy for the direct augmentation of collateral blood flow in acute occlusive intestinal ischemia.
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PMID:Collateral blood flow in segmental intestinal ischemia: effects of vasoactive agents. 373 47

The authors report a case of pituitary apoplexy associated with oculomotor defects and focal cerebral signs; the visual pathways were intact. Computed tomography documented a mass of heterogeneous density within an enlarged sella turcica and a right parietal infarct. Angiograms revealed bilateral carotid spasm and occlusion of the right angular artery. Treatment was conservative. Control angiograms showed spontaneous resolution of the vasospasm and recanalization of the cortical artery. The patient made a complete neurological recovery; he needed only treatment with vasopressin due to transient diabetes insipidus. The risk of vasospasm and brain ischemia should be kept in mind when treating pituitary apoplexy. The early occurrence of vasospasm in our case suggests the participation of powerful vasoactive agents liberated from the tumor.
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PMID:Pituitary apoplexy, bilateral carotid vasospasm, and cerebral infarction in a 15-year-old boy. 380 76

Nafazatrom is an antithrombic drug that has been shown to have beneficial effects in traumatic shock and organ ischemia. This study evaluated the effect of nafazatrom on cardiovascular, sympathetic, and endocrine consequences to moderate or severe hemorrhagic shock in the conscious rat. Nafazatrom (2 mg/kg, i.v.) had no effect on the blood pressure, heart rate, and circulatory norepinephrine, vasopressin, and leukotriene C4 responses to bleeding. Nafazatrom significantly reduced plasma TXB2 and 6-keto-PGF1 alpha and blocked the increment in these cyclooxygenase metabolites in response to hemorrhage. It is concluded that nafazatrom does not increase survival after moderate hypovolemic hypotension and decreases survival to severe hemorrhage. Nafazatrom does not modify the cardiovascular, sympathetic, and neuroendocrine responses to hypovolemic hypotension.
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PMID:Effects of nafazatrom on cardiovascular, sympathetic, and endocrine responses to hemorrhagic shock in conscious rats. 384 Oct 32


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