Af. Vanleeuwen et al., CORRECTION OF HYPOVOLEMIC HYPOTENSION BY CENTRALLY ADMINISTERED NALOXONE IN CONSCIOUS RABBITS, American journal of physiology. Heart and circulatory physiology, 43(4), 1998, pp. 1371-1377
Our goal was to test directly whether the vasoconstrictor action of na
loxone during hypovolemic hypotension is centrally mediated. In eight
chronically instrumented rabbits, progressive central hypovolemia and
fall in cardiac output (GO) were produced by gradually inflating a cuf
f on the thoracic vena cava. Central hypovolemia was then sustained fo
r 8 min by holding CO constant. In the main experiment (n = 4), each r
abbit was studied eight times over 4 experimental days. Saline or nalo
xone treatment commenced 10 min before progressive hypovolemia (early
treatment) or 2 min after the onset of sustained hypovolemia (late tre
atment), given by intravenous infusion or into the fourth ventricle (V
-4) With saline treatment, there was spontaneous recovery of systemic
vasoconstriction and arterial pressure during sustained hypovolemia. L
ate treatment with naloxone (4 mg/kg iv; 4-37 mu g/kg V-4) accelerated
and exaggerated these changes. Thus, under conditions of constant CO
and central blood volume, the vasodilatation of the decompensatory pha
se of acute hypovolemia is not sustained, and intravenous naloxone's v
asoconstrictor action is via a brain stem mechanism.