The Effect of Naloxone on the Reversal of Hypovolemic Shock in Rats / 대한마취과학회지

ABSTRACT

The effects of morphine in bringing sleep and an end to pain have been known from the beginning of recorded history. But the existence of endogenous opiates(endorphin) has been demonstrated only in the last decade. Endorphin bind to opiate receptors and exhibit potent opiate-like activity. In the corticotroph cells of the anterior lobe of pitultary, ACTH and beta-endorphin are synthesized simultaneously. There is a hypothalamic releasing factor which causes the secretion both beta-endorphin and ACTH, but ACTH and beta-endorphine are also released simultaneously by stress. Endorphins adversely affect the circulatory status and these effects are reversed by the intravenous injection of the narcotic antagonist, naloxone. The author studied Dirksen's hypothesis that endorphins may be involved in the pathophysiology of hemorrhagic shock. In this experiment, the author divided in the pathophysiology of hemorrhagic shock. In this experiment, the author divided laboratory animals into 3 groups and administered normal saline, salicylate or hyprocortisone, respectively. l. normal saline pretreated group. ll. salicylate pretreated group. lll. hydrocortisone pretreated group. Each group was then divided into 4 subgroups and treated as follows 1) hypovolemic shock + normal saline. 2) hypovolemic shock + naloxone. 3) hypovolemic shock + hydrocortisone. 4) hypovolemic shock + PGE1. The following results were obtained 1) MAP was significantly increased after naloxone and PGE1 adminitration in the normal saline pretreated group. 2) MAP was not changed in the salicylate pretreated group. 3) MAP was significantly increased after naloxone and PGE1 administration in the hydrocortisone pretreated group. 4) Pulse pressure was significantly increased after anloxone, hydrocortisone and PGE1 administration in the normal saline and hydrocortisone pretreated groups. From the above experiment, it may be inferred that endorphins and prostaglandin may play a role in the pathophysiology of hypovolemic shock.