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 Carvedilol Acute Myocardial Infarction Study (CAMIS) investigates cardiac remodeling in patients (n = 250) randomized to carvedilol vs atenolol and treated for 12 months after acute myocardial infarction. In a sub-study, we compared sympathetic, hemorrheological and vascular effects in small but particularly well-matched groups of participants who had been on reasonably equipotent but unchanged doses of carvedilol (n = 10) or atenolol (n = 10) for at least 4 weeks. Blood pressures (p < 0.05), plasma adrenaline (p = 0.034), plasma vasopressin (p = 0.022) and whole blood viscosity at shear rate 0.5 cp (p = 0.050), 1.1 cp (p = 0.023), 5.8 cp (p = 0.049) and 201 cp (p = 0.060) taken in the laboratory at baseline before 2 h of using the hyperinsulinemic, isoglycemic glucose clamp were lower on carvedilol. Plasma noradrenaline was lower on carvedilol at baseline and throughout the clamp (p < 0.0005). Forearm vascular resistance as measured by plethysmography during the clamp tended to be lower on carvedilol (p = 0.074). No significant difference was found between the groups in glucose disposal rate measured by clamp, maximal forearm blood flow and minimal forearm vascular resistance after 10 min of ischemia, or in ambulatory blood pressure and heart rate taken a few days later. Thus, potential benefits of carvedilol vs atenolol were seen in these post-infarction patients in a laboratory setting. These findings suggest that the inhibitory effects on the sympathetic nervous system and related blood viscosity are stronger with carvedilol than with atenolol.
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PMID:Lower plasma noradrenaline and blood viscosity on carvedilol vs atenolol in men with recent myocardial infarction. 1252 82

The objective of this research was to compare the effects of an alpha- and beta-adrenergic agonist, epinephrine, a selective alpha(2)-adrenergic agonist, alpha-methylnorepinephrine (alpha-MNE), and a non-adrenergic vasopressin on post-resuscitation myocardial function and duration of survival. Epinephrine continues to be the primary adrenergic agent for advanced cardiac life support. However, its major inotropic actions and especially its beta-adrenergic and, to a lesser extent, its alpha(1)-actions increase the severity of global ischemia during cardiac arrest and adversely affect post-resuscitation myocardial function and survival. We had previously observed significantly better outcomes with a selective alpha(2)-adrenergic agonist when compared with epinephrine. Non-adrenergic vasopressin also has promise of more favorable actions. The present study was, therefore, undertaken to compare a selective alpha(2)-adrenergic vasopressor drug with vasopressin, epinephrine, and saline placebo. Ventricular fibrillation (VF) was induced in 20 Sprague-Dawley rats. Mechanical ventilation and precordial compression were initiated after 8 min of untreated VF. About 2 min later, alpha-MNE in a dose of 100 microgram/kg, vasopressin in a dose of 0.4 U/kg, epinephrine in a dose of 30 microgram/kg, or saline control was administered. Defibrillation was attempted after 6 min of CPR. Left ventricular pressure, dP/dt(40), -dP/dt, and cardiac index were measured for an interval of 240 min after resuscitation. Except for saline controls, comparable increases in coronary perfusion pressure (CPP) were observed after each drug intervention. All animals were successfully resuscitated. Post-resuscitation myocardial function and survival were significantly better in animals treated with alpha-MNE. Both post-resuscitation myocardial function and survival were most improved after administration of the selective alpha(2)-adrenergic agonist, intermediate after vasopressin and least after epinephrine and saline placebo.
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PMID:A comparison of alpha-methylnorepinephrine, vasopressin and epinephrine for cardiac resuscitation. 1266 5

Traditionally, embolization has been reserved for treatment of upper gastrointestinal bleeding whereas lower gastrointestinal (LGI) bleeding has been controlled with vasopressin infusion. This is based on findings in older literature in which infarction frequently complicated LGI embolization. With modern embolization techniques, clinically significant bowel ischemia has become an uncommon complication. Although the efficacies of vasopressin and embolization are fairly comparable, embolotherapy has advantages in terms of quicker completion of therapy and decreased likelihood of systemic complications. Although vasopressin is still probably preferable for diffuse lesions and cases in which superselective catheterization is not technically possible, embolization should be considered a primary option for treating LGI bleeding.
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PMID:Treatment of lower gastrointestinal bleeding: vasopressin infusion versus embolization. 1276 6

To examine the coronary effects of arginine-vasopressin and its interaction with nitric oxide and prostanoids during partial ischemia and reperfusion, left circumflex coronary artery flow was electromagnetically measured and partial occlusion of this artery was induced for 60 min, followed by reperfusion in anesthetized goats (seven non-treated, six treated with N(W)-nitro-L-arginine methyl esther (L-NAME) and five with meclofenamate). During partial coronary occlusion, coronary vascular conductance decreased by 20-31% (P<0.01), and the coronary vasodilatation in response to acetylcholine (3-100 ng) and sodium nitroprusside (1-10 microg) was much reduced in every case; the vasoconstriction in response to arginine-vasopressin (0.03-0.3 microg) was attenuated in non-treated animals; this attenuation was reversed by L-NAME and was accentuated by meclofenamate. At 30 min of reperfusion, coronary vascular conductance remained decreased by 11-25% (P<0.05 or P<0.01), and the vasodilatation in response to acetylcholine and sodium nitroprusside as well as the vasoconstriction with arginine-vasopressin was as in the control and comparable in the three groups of animals. These results suggest: (1) that, during ischemia, the coronary vasodilator reserve is greatly reduced and the vasoconstriction with arginine-vasopressin is attenuated, with preservation of the modulatory role of nitric oxide and probable involvement of vasoconstrictor prostanoids in this vasoconstriction; and (2) that, during reperfusion, the coronary vasodilator reserve and the coronary reactivity to acetylcholine and arginine-vasopressin recover, but the modulatory role of nitric oxide in this reactivity may be attenuated.
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PMID:Coronary effects of vasopressin during partial ischemia and reperfusion in anesthetized goats. Role of nitric oxide and prostanoids. 1287 38

The present study was designed to investigate the protective effects of calcitonin gene-related peptide (CGRP) in a porcine model of cardiopulmonary resuscitation (CPR). Twelve pigs were anesthetized, paralyzed, mechanically ventilated with oxygen, and were monitored for electrocardiograph (ECG), arterial pressure, right atrial pressure, airway pressure. Ventricular fibrillation (VF) was induced in all animals by the application of 30 V of alternating current (60 Hz) across the heart, and remained untreated for 3 min, followed by conventional CPR with pneumatic piston device (Thumper) for 15 min. At 18 min of VF a single dose of vasopressin was given, and followed by defibrillation attempts. Two groups were studied. Group 1: Six pigs were used as saline control. Group 2: 0.3 nmol/kg CGRP was given 15 min prior to induction of VF. All animals in the CGRP pretreated group achieved a return of spontaneous circulation (ROSC) and survived more than 2 h (100%), whereas none of the saline control animals achieved ROSC. Blood gases were not significantly different between the groups. However, CGRP group had significantly higher arterial blood pressure and coronary perfusion pressure than control group during CPR. Pretreatment with CGRP affords a cardioprotective effect in this model of whole body ischemia.
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PMID:Calcitonin gene-related peptide protects against whole body ischemia in a porcine model of cardiopulmonary resuscitation. 1458 Jul 45

Sudden cardiac death is mainly caused by arrhythmic events, triggered by ischemia. About half of the affected persons had no previous diagnosis of coronary heart disease, thus rendering them practically unreachable for specific preventive measures. This fact makes it necessary to optimize reanimation conditions. The establishment of international reanimation standards (ILCOR) has stimulated an intensified scientific evaluation of therapeutic options. While the use of vasopressin, adrenaline and reanimation by bystanders is being evaluated at the moment, amiodarone has not fulfilled the expectation of reducing mortality. Secondary prevention of sudden cardiac death after cardiac events is based on betablockers, ACE inhibitors and antilipemic therapy. Guidelines on prevention of sudden cardiac death also recommend aldosterone blockade and n-3-fatty acids. Persons at highest risk gain most from the use of ICDs, yet it has not been shown that their use immediately after myocardial infarction reduces mortality.
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PMID:[Sudden cardiac death (SCD) and guidelines for SCD]. 1502 98

Transarterial therapies used for the treatment of acute nonvariceal gastrointestinal (GI) hemorrhage have traditionally included vasopressin infusion and embolization. However, for patients with diffuse or multifocal hemorrhage and severe refractory thrombocytopenia, these options are suboptimal because platelet counts and coagulation parameters may not be adequate to allow for the formation of a stable clot. Herein two such patients treated with direct intraarterial (IA) infusion of platelets into the vascular territory supplying the hemorrhage are described. In both patients, after IA platelet infusion, blood product requirements were immediately reduced, bleeding from the GI tract resolved by clinical and laboratory criteria, and no significant bowel ischemia was seen.
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PMID:Intraarterial platelet infusion for patients with intractable gastrointestinal hemorrhage and severe refractory thrombocytopenia. 1506 44

Although uncommon, medication-induced colonotoxicity is important to recognize because medication cessation generally leads to prompt clinical improvement, while medication continuation results in disease exacerbation. This review categorizes the association between medications and colonotoxicity as "well-established" or "probable," according to the following criteria: total number of reported cases, number of different research groups reporting an association, experimental and pharmacologic evidence of an association, and validity of an association in each reported case. Cocaine, ergotamine, estrogen, sodium polystyrene, alosetron, amphetamines, pseudoephedrine, and vasopressin are associated with colonic ischemia. The mechanisms include vasospasm, thrombogenesis, and shunting of blood from mesenteric vessels. Narcotics, phenothiazines, vincristine, atropine, nifedipine, and tricyclic antidepressants are associated with colonic pseudo-obstruction. The mechanisms include antagonizing prokinetic neurotransmitters, stimulating antikinetic neurotransmitters, promoting dysmotility, relaxing smooth muscle, and injuring enteric neurons. Numerous antibiotics are associated with pseudomembranous colitis; ampicillin is associated with hemorrhagic colitis; chemotherapy is associated with neutropenic colitis; and deferoxamine is associated with Yersinia enterocolitis. Mechanisms of these toxicities include altering normal bowel flora, weakening immunologic defenses, promoting microorganism virulence, and mucosal injury. Gold compounds, nonsteroidal antiinflammatory drugs, alpha-methyldopa, salicylates, and sulfasalazine are associated with an inflammatory or cytotoxic colitis. The mechanisms include direct mucosal cytotoxicity, antimetabolite effects, or drug allergy. Nonsteroidal antiinflammatory drugs, cyclo 3 fort, flutamide, lansoprazole, and ticlopidine are associated with lymphocytic colitis. The mechanisms include immunologic activation or attenuated immunologic defenses. Chronic cathartic use leads to colonic hypomotility and abdominal distention. Intrarectally administered corrosive compounds can produce a toxic colitis.
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PMID:Colonic toxicity of administered drugs and chemicals. 1518 Jul 42

To examine the coronary effects of arginine-vasopressin during reperfusion after a short ischemia, left circumflex coronary artery flow was electromagnetically measured, and 15 min total occlusion of this artery followed by reperfusion was induced in anesthetized goats (five nontreated, five treated with the inhibitor of nitric oxide synthesis Nomega-nitro-L-arginine methyl ester (L-NAME) and five treated with the inhibitor of cyclooxygenase meclofenamate). The vasoactive drugs and L-NAME were intracoronarily injected, and meclofenamate by i.v. route. At 60 min of reperfusion, coronary vascular conductance was not changed significantly in nontreated and was decreased by 35% (P<0.01) in L-NAME-treated and by 30% (P<0.01) in meclofenamate-treated animals. During reperfusion, the coronary vasodilatation with acetylcholine (3-100 ng) and sodium nitroprusside (1-10 microg) was not altered in nontreated animals, and the vasodilatation with acetylcholine but not with sodium nitroprusside was partially decreased in L-NAME--but not in meclofenamate-treated animals. The vasoconstriction in response to arginine-vasopressin (0.03-0.3 microg) was increased during reperfusion in nontreated, was not changed in L-NAME-treated and was decreased in meclofenamate-treated animals. Therefore, it is suggested that during reperfusion after a short ischemia: (1) the coronary vasodilator reserve is preserved; (2) the coronary vasodilatation with acetylcholine is also preserved, but in this vasodilatation, the role of nitric oxide may be attenuated and prostanoids may be not involved; and (3) the coronary vasoconstriction with arginine-vasopressin is increased, probably due to both attenuation of the modulatory role of nitric oxide and the release of vasoconstrictor prostanoids.
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PMID:Vasopressin effects on the coronary circulation after a short ischemia in anesthetized goats: role of nitric oxide and prostanoids. 1524 67

Septic shock that requires therapy with adrenergic agents is associated with high rates of mortality. Inappropriately normal or low serum concentrations of vasopressin contribute to the development of hypotension during sepsis. We critically evaluated the role of administering exogenous vasopressin to patients with septic shock. A computerized search of MEDLINE from January 1966--December 2003 and a manual search of relevant journals for abstracts were conducted. Eleven retrospective, six prospective cohort, and four prospective randomized studies were identified. Most studies evaluated short-term infusions of vasopressin at 0.08 U/minute or less as add-on therapy in patients requiring adrenergic agents. The results show that starting vasopressin in patients with septic shock increases systemic vascular resistance and arterial blood pressure, thus reducing the dosage requirements of adrenergic agents. These effects are rapid and sustained. Substantial enhancement of urine production, likely due to increased glomerular filtration rate, was shown in several studies. A few studies demonstrated clinically significant reduced cardiac output or cardiac index after vasopressin was begun, necessitating cautious use in patients with cardiac dysfunction. Vasopressin was associated with ischemia of the mesenteric mucosa, skin, and myocardium; elevated hepatic transaminase and bilirubin concentrations; hyponatremia; and thrombocytopenia. Limiting the dosage to 0.03 U/minut or less may minimize the development of these adverse effects. Vasopressin 0.03 U/minute or less should be considered if response to one or two adrenergic agents is inadequate or as a method to reduce the dosage of adrenergic agents. At present, vasopressin therapy should not be started as first-line therapy. Additional studies are needed to determine the optimum dosage, duration, and place in therapy of vasopressin relative to adrenergic agents. A multicenter, comparative study of vasopressin 0.03 U/minute as add-on therapy is under way and should provide mortality data.
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PMID:The role of vasopressin in vasodilatory septic shock. 1533 53


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