Constitutive nitric oxide modulates the injurious actions of vasopressin on rat intestinal microcirculation in acute endotoxaemia.

Department of Pharmacology, Wellcome Research Laboratories, Beckenham, Kent, UK.
European Journal of Pharmacology (Impact Factor: 2.59). 09/1994; 260(2-3):265-8. DOI: 10.1016/0014-2999(94)90349-2
Source: PubMed

ABSTRACT The administration of the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 5 mg/kg s.c.) concurrently with Escherichia coli endotoxin (3 mg/kg i.v.) increased vascular permeability and caused mucosal damage in the rat intestine 1 h later. The vasopressin V1 receptor antagonist, [Mca1,Tyr(Me)2, Arg8]vasopressin (0.01-0.2 microgram/kg s.c., 15 min before endotoxin) dose-dependently reduced this damage. These results suggest a beneficial role of NO, counteracting the injurious vascular actions of endogenous vasopressin, in maintaining intestinal mucosal integrity in acute endotoxaemic states.

  • Source
    12/2007: pages 229-254;
  • [Show abstract] [Hide abstract]
    ABSTRACT: The role of endogenous vasopressin was studied in the development of mucosal erosions induced by haemorrhagic shock in the duodenum of the rat. Ischaemia-reperfusion provoked duodenal haemorrhagic lesions and elevated circulating and intramucosal vasopressin level. This mucosal injury was significantly attenuated by a vasopressin pressor receptor antagonist. Moreover, in the vasopressin-deficient Brattleboro homozygous rat, mucosal injury induced by haemorrhagic shock was also reduced. By contrast, when the vasopressin agonist, lysin-vasopressin, was administered, significant aggravation of ischaemia-reperfusion-induced duodenal mucosal injury was seen. These findings indicate the aggressive role of endogenous vasopressin, via its pressor receptors, in the generation of duodenal mucosal stress erosions in haemorrhagic shock.
    Inflammopharmacology 01/1996; 4(4):379-385.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Objective – To discuss 3 potential mechanisms for loss of peripheral vasomotor tone during vasodilatory shock; review vasopressin physiology; review the available animal experimental and human clinical studies of vasopressin in vasodilatory shock and cardiopulmonary arrest; and make recommendations based on review of the data for the use of vasopressin in vasodilatory shock and cardiopulmonary arrest.Data Sources – Human clinical studies, veterinary experimental studies, forum proceedings, book chapters, and American Heart Association guidelines.Human and Veterinary Data Synthesis – Septic shock is the most common form of vasodilatory shock. The exogenous administration of vasopressin in animal models of fluid-resuscitated septic and hemorrhagic shock significantly increases mean arterial pressure and improves survival. The effect of vasopressin on return to spontaneous circulation, initial cardiac rhythm, and survival compared with epinephrine is mixed. Improved survival in human patients with ventricular fibrillation, pulseless ventricular tachycardia, and nonspecific cardiopulmonary arrest has been observed in 4 small studies of vasopressin versus epinephrine. Three large studies, though, did not find a significant difference between vasopressin and epinephrine in patients with cardiopulmonary arrest regardless of initial cardiac rhythm. No veterinary clinical trials have been performed using vasopressin in cardiopulmonary arrest.Conclusion – Vasopressin (0.01–0.04 U/min, IV) should be considered in small animal veterinary patients with vasodilatory shock that is unresponsive to fluid resuscitation and catecholamine (dobutamine, dopamine, and norepinephrine) administration. Vasopressin (0.2–0.8 U/kg, IV once) administration during cardiopulmonary resuscitation in small animal veterinary patients with pulseless electrical activity or ventricular asystole may be beneficial for myocardial and cerebral blood flow.
    Journal of Veterinary Emergency and Critical Care. 03/2009; 19(2):145 - 157.