Blockade of opiate receptors with naloxone improves survival and cardiac performance in canine endotoxic shock
Reynolds, D.G.; Gurll, N.J.; Vargish, T.; Lechner, R.B.; Faden, A.I.; Holaday, J.W.
Circulatory Shock 7(1): 39-48
1980
ISSN/ISBN: 0092-6213 PMID: 6248265 Document Number: 168128
The endogenous opiate .beta.-endorphin is released by a variety of stressful situations. Since the cardiovascular system is sensitive to exogenous and endogenous opiates, endorphins may be involved in the pathophysiology of endotoxin = 6) 2 mg/kg i.v. as a bolus followed by 2 mg/kg .cntdot. h as an infusion i.v. until t = 4 h or saline (n = 14) in equivalent volumes. Etox decreased cardiac output (CO) to 1.1 .+-. 0.2 l/min, left ventricular contractility (LV dp/dtmax) from 2.2 .+-. 0.3 to 1.2 .+-. 0.1 .times. 103 mm Hg/sec and mean arterial pressure (MAP) from 139 .+-. 3 to 68 .+-. 8 mm Hg. Naloxone prevented the decrease in LV dp/dt, attenuated the decrease in MAP and reversed the fall in CO due to etox. Naloxone in non-endotoxic dogs had little or no effect on cardiovascular parameters except for a slight but significant increase in MAP (n = 5). Of the 6 dogs treated with naloxone at 2 mg/kg, 5 survived, compared to only 3 of 14 saline-treated dogs (P < 0.04). Naloxone at 1 mg/kg improved cardiovascular parameters but did not improve survival. The improved survival and cardiac performance in canine etox shock with naloxone suggests the involvement of endorphins or opiate receptors in the cardiovascular pathophysiology of etox shock.