Cardiovascular responses to hemorrhage and naloxone in conscious barodenervated rabbits.

The hemodynamic and plasma catecholamine response to hypotensive hemorrhage and subsequent opioid receptor blockade with naloxone were evaluated before and after complete sinoaortic denervation (SAD). This study was done to test the general hypothesis that opioid-mediated failure of the baroreflex accounts for the hypotension of hemorrhage. The specific hypothesis we tested was that SAD would abolish the pressor effect of opioid receptor blockade with naloxone. The studies were done in conscious chronically prepared rabbits. Hemorrhage of 12 ml/kg did not change mean arterial blood pressure in intact animals due to a compensatory increase in heart rate and vascular resistance. When blood loss exceeded 12 ml/kg, pressure decreased abruptly due to a decrease in vascular resistance. Plasma norepinephrine (NE) and epinephrine (E) were higher after hemorrhage than before. Plasma E levels increased almost 70 times. After SAD, mean blood pressure began to decrease at the beginning of hemorrhage, the heart rate increase was abolished, and vascular resistance decreased throughout the blood loss. Plasma NE was no different after hemorrhage than before. Plasma E increased, but the increase was only fivefold. Naloxone increased mean arterial blood pressure, vascular resistance, cardiac index, and plasma NE before and after SAD. The increases in blood pressure and plasma norepinephrine were significantly greater after SAD. Therefore the pressor effect of naloxone in this model is not due to increased baroreflex sensitivity. Rather, intact baroreflexes buffer naloxone's effects.