Systemic and renal macro- and microcirculatory responses to arginine vasopressin in endotoxic rabbits

Arginine vasopressin is being used increasingly to treat vasodilatory hypotension, although little is known of its effects on regional perfusion. Arginine vasopressin hemodynamic effects in physiology are mainly mediated through the V1a receptor on blood vessels. To investigate this further, we studied the effect of arginine vasopressin on systemic and renal blood flow in anesthetized, ventilated rabbits given either intravenous saline or endotoxin, and the impact of blocking V1a receptors.

Prospective, randomized, controlled study.

Animal research laboratory.

Male White New Zealand rabbits.

Measurement was made of mean arterial blood pressure, aortic and renal blood flow velocities (pulsed Doppler), and renal cortical and medullary flow (laser Doppler).

In a first series of animals, incremental intravenous boluses of arginine vasopressin ranging from 1 to 1000 ng were administered 90 mins postendotoxin or saline. In control rabbits (n = 9), increasing doses of arginine vasopressin elevated mean arterial blood pressure but reduced both aortic and renal blood flow velocity and renal cortical flow (p <.05). In endotoxic animals (n = 6), arginine vasopressin produced a similar increase in mean arterial blood pressure although aortic flow was maintained while renal blood flow velocity increased, mostly in its diastolic component (p <.05). Pretreatment with the V1a receptor antagonist in a second series of animals blunted all the effects observed in both control (n = 5) and endotoxic (n = 6) animals, suggesting that arginine vasopressin acted mainly through V1a subtype in this early phase of sepsis.

Preservation of renal blood flow with arginine vasopressin during endotoxemia, in particular to the cortex, suggests it could be a promising agent for hemodynamic support during septic shock.