Sympathetic and hemodynamic adjustments to hemorrhage: A possible role for endogenous opioid peptides

Abstract

The traditional view of the decrease in blood pressure during blood loss is that it is a passive phenomenon. Blood pressure falls due to the inability of the compensatory mechanisms to keep pace with blood loss. However, recent evidence indicates that this transition from normotension to hypotension may involve an active decrease in compensation by the sympathetic nervous system. In the conscious, chronically prepared rabbit, blood pressure is maintained early in hemorrhage primarily by sympathetically mediated compensatory increases in vascular resistance and heart rate. When blood loss exceeds approximately 20% of total blood volume, hypotension develops abruptly due to a decrease in vascular resistance. This vasodilation is accompanied by decreased plasma norepinephrine (NE) levels and decreased sympathetic nerve activity. Therefore, the transition from normotension to hypotension during hemorrhage involves an active change, a decrease in vascular resistance, associated with a decrease in sympathetic nerve activity. Opioid receptor blockade with naloxone reverses acute hemorrhagic hypotension by increasing vascular resistance. The increase in resistance is accompanied by increased plasma NE and increased sympathetic nerve activity. Thus, the transition to hypotension during acute hemorrhage may be an active event brought on by a decrease in sympathetic outflow. Naloxone's reversal of the hypotension is consistent with the central involvement of endogenous opioid peptides in this phenomenon and thus in the pathogenesis of hypotension during blood loss.