Abstract |
To investigate the effect of arginine vasopressin (AVP) in the peripheral circulation on burn shock in the rat, AVP and its nonselective V1/ V2 receptor antagonist d(CH2)5Tyr (Et)VAVP were administered intravenously in burn shocked rats. Cardiovascular parameters were recorded including left ventricular systolic pressure (LVSP), +/- dP/dt max, total area of the cardiac force loop (Lo), mean arterial blood pressure (MAP), heart rate (HR) and electrocardiogram (ECG). Our results showed that AVP failed to increase MAP in burned rats whereas it elicited a greater fall in LVSP, +/- dP/dt max and Lo and MAP than seen in control burned rats and hastened the onset of the decompensatory phase of burn shock resulting in the early death of burn shocked animals. The receptor antagonist d(CH2)5Tyr(Et)VAVP elevated LVSP, +/- dp/dt max and Lo for the eight hour observation period, and allowed MAP to recover from the initial profound fall following burn injury. Furthermore, it prolonged the survival time of the burned rats. AVP treated rats also displayed earlier abnormal changes such as elevation of S-T segment, inversion of T wave and ventricular fibrillation in ECG. The onset of these changes was much delayed in antagonist treated rats.
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Authors | K Sun, A Gong, C H Wang, B C Lin, H N Zhu |
Journal | Neuropeptides
(Neuropeptides)
Vol. 17
Issue 1
Pg. 17-22
(Sep 1990)
ISSN: 0143-4179 [Print] Netherlands |
PMID | 2148815
(Publication Type: Journal Article)
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Chemical References |
- Angiotensin Receptor Antagonists
- Receptors, Vasopressin
- Arginine Vasopressin
- 1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)-2-(O-ethyl-Tyr)-4-Val-arginine vasopressin
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Topics |
- Angiotensin Receptor Antagonists
- Animals
- Arginine Vasopressin
(analogs & derivatives, pharmacology)
- Burns
(complications)
- Electrocardiography
(drug effects)
- Heart Rate
(drug effects)
- Histocytochemistry
- Injections, Intravenous
- Male
- Myocardial Contraction
(drug effects)
- Rats
- Rats, Inbred Strains
- Receptors, Vasopressin
- Shock, Traumatic
(etiology, physiopathology)
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