An Experimental Study on the Pressor Effect of Naloxone-HCI and the Changes of Plasma Beta-Endorphin Level in Shock .
10.4097/kjae.1982.15.4.409
- Author:
Doo Ik LEE
1
;
Kwang II SHIN
Author Information
1. Department of Anesthesiology, College of Medicine, Kyung Hee University, Seoul, Korea.
- Publication Type:Original Article
- MeSH:
Rabbits;
Animals
- From:Korean Journal of Anesthesiology
1982;15(4):409-422
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
It is known that the cardiovascular system is extremely sensitive to the effect of both exogenous and endogenous opiates. In rabbits, less than 1% of the usual morphine dose necessary to produce antinociception results in significant hypotension and bradycardia. The endozenous opiate, beta-endorphin, is stored along with pitulatary adrenocorticotorphin(ACTH), and the action of stressors seems to result in the release of both peptides. Therefore it seems likely that beta-endorphin is released during stress such as shock and that it might contribute to the hypotension. In order to probe this hypothesis, hypovolemic and endotoxin shock model were produced in rabbits. If these hemorrhage and endotoxin induced hypotension were mediated through the beta-endorphin release, the blockade of beta-endorphin should reverse such hypotension. Using the specific opiate antagonist, Naloxone-HCl, these hypotensions could be reversed and prevented as following results show, 1) As compared with the saline control, the hypovolemic shock experiment had a 36.49+/-14.44% increase in mean arterial pressure(MAP) within 2 to 3 minutes and the endotoxin shock had a 52.43+/-23.66% increase in MAP within 5 to 6 minutes after naloxone treatment (0.4mg/kg). 2) AS compared with the saline control, in both hypovolemic and endotoxin shock naloxone pretreatment(0.4mg/kg) could prevent the decrease of MAP significantly. 3) No significant difference were seen in heart rate between the control and both experimental groups. And plasma bets-endorphin was measured by radioimmunoassay(RIA), using beta-endorphin kit(Immunonucler corportion, Stillwater, Minnesota, USA) and Beckman 8,000 tau-Counter, in these shock model with following results. 1) Hemorrhage and endotoxin induced shock produced a significant increase in plasma beta-endorphin to about 3 times control and reversed by naloxone treatment(0.4mg/kg) significantly as compared with saline control. 2) AS compared with the saline control, in both hypovolemic and endotoxin experiments naloxone pretreatment(0.4mg/kg) could prevent the increase of plasma beta-endorphin significantly.
