beta-Endorphin in canine hemorrhagic shock.

Endogenous opiate peptides have been implicated in the cardiovascular depression of hemorrhagic shock. Beta-endorphin immunoreactivity was measured during hemorrhagic shock and the effects of beta-endorphin suppression during shock on cardiac hemodynamics and myocardial blood flow were studied. Fourteen dogs (group 1) were pretreated with 30 milligrams per kilogram of methylprednisolone (MP) prior to shock. Ten dogs (group 2) received saline solution and were the control group. All dogs were bled to a mean arterial blood pressure of 35 millimeters of mercury for two hours, then resuscitated with blood and lactated Ringer's solution. Beta-endorphin concentrations increased 600 per cent during shock in the control group. Dogs pretreated with MP had lower beta-endorphin concentrations (p less than 0.05) during shock than did dogs in the control group. The rate of left ventricular pressure rise (dp/dt) was significantly improved during shock (p less than 0.04) and after resuscitation (p less than 0.006) in dogs with suppressed beta-endorphin immunoreactivity. Blood flow from the coronary artery was higher during shock and after resuscitation (p less than 0.001) in the dogs in group 1. Our data indicate significant correlation between improved ventricular performance and decreased beta-endorphin levels in shock and after resuscitation.