Endogenous vasopressin does not mediate hypoxia-induced anapyrexia in rats

Abstract

The present study was designed to test the hypothesis that arginine vasopressin (AVP) mediates hypoxia-induced anapyrexia. The rectal temperature of awake, unrestrained rats was measured before and after hypoxic hypoxia, AVP-blocker injection, or a combination of the two. Control animals received saline injections of the same volume. Basal body temperature was 36.52 +/- 0.29 degreesC. We observed a significant (P < 0.05) reduction in body temperature of 1. 45 +/- 0.33 degreesC after hypoxia (7% inspired O2), whereas systemic and central injections of AVP V1- and AVP V2-receptor blockers caused no change in body temperature. When intravenous injection of AVP blockers was combined with hypoxia, we observed a reduction in body temperature of 1.49 +/- 0.41 degreesC (V1-receptor blocker) and of 1.30 +/- 0.13 degreesC (V2-receptor blocker), similar to that obtained by application of hypoxia only. Similar results were observed when the blockers were injected intracerebroventricularly. The data indicate that endogenous AVP does not mediate hypoxia-induced anapyrexia in rats.

Is lactate a mediator of hypoxia-induced anapyrexia?

“…Similar results have been observed for vasopressin, which, like lactate, increases in plasma and in cerebrospinal fluid during hypoxia [13,26] and also reduces T c when administered to mammals [21,27,31]. However, studies on Brattleboro rats (that lack vasopressin-producing neurons in the central nervous system) and vasopressin antagonists in Wistar rats have shown that rats develop anapyrexia regularly in response to hypoxia in the absence of vasopressin [9] or when its receptors are blocked [32].…”

Anti-inflammatory and antipyretic effects of Sonchus oleraceus in rats

“…Control T b was determined by four measurements at 30-min intervals. It should be pointed out that, for all protocols, 2 days before the experiment, the animals were habituated to temperature measurements that were performed quickly to avoid any stress-induced elevations in T b , such as those previously described (Steiner et al, 1999). The animals (n = 10 per group) were orally pre-treated with vehicle, SoHE (doses of 30, 100, and 300 mg/kg) or dexamethasone (1 mg/kg) 1 h before the intraperitoneal (i.p.)…”

Role of nitric oxide in thermoregulation during septic shock: involvement of vasopressin

“…Experiments were initiated 6 days after brain surgery. These procedures have been used previously [32].…”

“…Following these procedures, rats were immediately decapitated for collection of blood. The doses of LPS and L-NAME and the time interval between the drugs were chosen on the basis of previous studies [2,8,32] and because pilot experiments indicated that this protocol lead to the most consistent and repeatable results.…”

“…injection of either LPS 1.5 mg/kg, or the same volume of sterile saline (0.1 ml/100 g b.w.). The dose of AVP V1 receptor antagonist and the time interval between the drugs were chosen on the basis of a previous study on the effect of the AVP V1 receptor antagonist on body temperature [32] and because pilot experiments indicated that this protocol led to the most consistent and repeatable results. Control rats received i.v.…”