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

To clarify the role of the sugar polyols, sorbitol and myo-inositol, in cerebral cell volume regulation, we studied the effect of sorbinil, an inhibitor of aldose and aldehyde reductase, on the size of the cerebral water compartments in rats with hypernatremia, hyponatremia and normonatremia. Experimental animals were pretreated with sorbinil, while comparison rats received the drug vehicle. Rats were made hypernatremic for 96 h by water deprivation and injections of hypertonic saline, while hyponatremia was provoked over 48 h by daily administration of 5% dextrose in water and vasopressin. Sorbinil treatment was continued throughout the hyper- and hyponatremic periods. The severity of hypernatremia and hyponatremia was similar in sorbinil-treated and corresponding vehicle-treated rats. Brain electrolyte content and the size of the cerebral intracellular water compartment were comparable in sorbinil-treated rats vs. controls under hypernatremic and hyponatremic conditions. Sorbinil reduced the cerebral sorbitol content by approximately 50%, irrespective of the serum Na+ concentration. In contrast, sorbinil had no effect on brain myo-inositol content which rose by 114% during chronic hypernatremia (P less than 0.0001). Cerebral levels of myo-inositol did not decline in hyponatremic rats. We conclude that (1) sorbitol is not an essential cerebral osmolyte; and (2) myo-inositol is involved in the maintenance of brain cell volume during severe hypernatremia but not under hyponatremic conditions.
 ...
PMID:The role of polyols in cerebral cell volume regulation in hypernatremic and hyponatremic states. 190 5

While these preliminary results in humans seem promising, no large trials have been conducted to compare vasopressin and epinephrine in CPR. At this time, standard guidelines using epinephrine are still preferred.
 ...
PMID:Vasopressin use in cardiopulmonary resuscitation. 941 93

In laboratory investigations, vasopressin given during CPR resulted in improved vital organ blood flow when compared with epinephrine. Given the profound and long lasting vasopressor effects of vasopressin, we tested the hypothesis that vasopressin given during CPR would result in renal and splanchnic hypoperfusion in the post-resuscitation period when compared with epinephrine. After 4 min of ventricular fibrillation, 16 pigs were randomly assigned to receive either 0.045 mg x kg(-1) epinephrine or 0.4 U X kg(-1) vasopressin before defibrillation. Splanchnic and renal blood flow were measured 30, 90, and 240 min after restoration of spontaneous circulation (ROSC) in the epinephrine and vasopressin groups and in a control group of eight pigs using radiolabeled microspheres. Hepatic blood flow was measured before arrest and 30, 90, and 240 min after ROSC by means of indocyanine green infusion. Thirty minutes after ROSC, renal and adrenal blood flow were significantly lower in the vasopressin group (300 [273-334] and 256 [170-284] ml X min(-1) x 100 g(-1)) (median and 25th and 75th percentile) as compared with the epinephrine group (370 [346-429] and 360 [326-420] ml x min(-1) x 100 g(-1); P < 0.05). Pancreatic, intestinal, and hepatic blood flow were not significantly different in animals after receiving epinephrine or vasopressin. In comparison to epinephrine, vasopressin given during cardiac arrest impairs renal and adrenal perfusion temporarily but does not lead to intestinal or hepatic hypoperfusion in the post-resuscitation phase.
 ...
PMID:Splanchnic and renal blood flow after cardiopulmonary resuscitation with epinephrine and vasopressin in pigs. 978 5

In August 2000, the American Heart Association and the European Resuscitation Council published the conclusions of the International Guidelines 2000 Conference on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care which contains both the new recommendations and an in-depth review. The discussions and drafting began at a conference in March 1999, followed by a second conference in September 1999, both attended by approx. 250 participants and another conference in February 2000 which was attended by approx. 500 participants. Review of the current state of science, discussion and final consensus continued subsequently via email, conference calls, fax, and personal conversation. During the entire process, scientists and resuscitation councils from all over the world participated, with participants from the United States comprising approx. 60%, and scientists from outside of the United States comprising approx. 40%. In order to ensure that the CPR recomendations are not dominated by any given nation or resuscitation council, most topics were reviewed and interpretated by two scientists from the United States and two scientists from outside of the United States. Accordingly, changes in these new CPR recommendations are the result of an evidence-based review by worldwide experts. The most important changes in the recommendations according to the authors are discontinuation of the pulse-check for lay people, 500 ml instead of 800-1200 ml tidal volume during bag-valve-mask ventilation (FiO2 > 0.4) of a patient with an unprotected airway, verifying correct endotracheal intubation with capnography and an esophageal detector, employing mechanical devices such as interposed abdominal compression CPR, vest CPR, active-compression-decompression CPR, and the inspiratory threshold valve (ITV) CPR as alternatives or adjuncts to standard manual chest compressions, defibrillation with < 200 Joule biphasic instead of with 200-360 Joule monophasic impulses, vasopressin (40 units) and epinephrine (1 mg) as comparable drugs to treat patients with ventricular fibrillation, amiodarone (300 mg) for shock-refractory ventricular fibrillation and intravenous lysis for patients who have suffered a stroke.
 ...
PMID:[The new international guidelines for cardipulmonary resuscitation: an analysis and comments on the most important changes]. 1176 Apr 84

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.
 ...
PMID:A comparison of alpha-methylnorepinephrine, vasopressin and epinephrine for cardiac resuscitation. 1266 5

Mice that lack the aquaporin-1 gene (AQP1) lack a functional countercurrent multiplier mechanism, fail to concentrate the inner medullary (IM) interstitium, and present with a urinary concentrating defect. In this study, we use DNA microarrays to identify the gene expression profile of the IM of AQP1 null mice and corresponding changes in gene expression resulting from a loss of a hypertonic medullary interstitium. An ANOVA analysis model, CARMA, was used to isolate the knockout effect while taking into account experimental variability associated with microarray studies. In this study 5,701 genes of the possible approximately 12,000 genes on the array were included in the ANOVA; 531 genes were identified as demonstrating a >1.5-fold up- or downregulation between the wild-type and knockout groups. We randomly selected 35 genes for confirmation by real-time PCR, and 29 of the 35 genes were confirmed using this method. The overall pattern of gene expression in the AQP1 null mice was one of downregulation compared with gene expression in the renal medullas of the wild-type mice. Heat shock proteins 105 and 94, aldose reductase, adenylate kinase 2, aldolase B, aldehyde reductase 6, and p8 were decreased in the AQP1 null mice. Carboxylesterase 3, matrilin 2, lipocalin 2, and transforming growth factor-alpha were increased in IM of AQP1 null mice. In addition, we observed a loss of vasopressin type 2 receptor mRNA expression in renal medullas of the AQP1 null mice. Thus the loss of the hyperosmotic renal interstitium, due to a loss of the concentrating mechanism, drastically altered not only the phenotype of these animals but also their renal medullary gene expression profile.
 ...
PMID:Renal medullary gene expression in aquaporin-1 null mice. 1550 45