Hemodynamic effects of naloxone in early canine hypovolemic shock.
The contribution of endorphins (endogenous opiates) to the pathophysiology of shock was evaluated by the administration of naloxone (NAL) at different time intervals after inducing hypovolemia. Forty-four dogs were bled into a reservoir to a mean arterial pressure (MAP) of 40-45 mmHg and maintained at this pressure for 30, 45, or 60 minutes. The animals were then given either intravenous 0.9% NaCl (S) or NAL. Animals treated after 30 minutes of hypovolemia at a fixed MAP had similar hemodynamic responses to both NAL or S. After 45 minutes, the NAL-treated animals showed significant improvement in MAP, cardiac output (CO), and survival (P less than 0.05) when compared with S-treated animals. Animals treated with NAL after 60 minutes showed little significant hemodynamic difference from animals treated with S but all S-treated animals died during the 60-minute treatment period. Plasma endorphinlike activity (PELA) rose with hypovolemia and then returned toward control levels in all NAL treated animals before reinfusion of shed blood while it remained elevated in S-treated animals until after reinfusion.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D004285:Dogs; D004723:Endorphins / Q000097:blood; D006439:Hemodynamics / Q000187:drug effects*; D009270:Naloxone / Q000494:pharmacology*; D011957:Receptors, Opioid / Q000187:drug effects; D012769:Shock / Q000188:drug therapy / Q000503:physiopathology*; D013318:Stroke Volume / Q000187:drug effects; D013997:Time Factors; D014655:Vascular Resistance / Q000187:drug effects
D004723:Endorphins; D011957:Receptors, Opioid; D009270:Naloxone