Naloxone이 저혈량성 Shock에 미치는 영향

Abstract

스트레스나 shock을 받게되면 뇌하수체선에서 부신피질자극 호르몬과 함께 β-endorphin이 유리된다. β-endorphin은 내인성 opiate 유사물질로 morphine과 같은 약리적 작용을 나타낸다. Dirksen 등 (1981)은 β-endorphin이 모세순환과 심장박출에 관여하는 prostaglandin E-_1(이하 PGE_1으로 약함)과 카테콜라민의 작용을 억압함으로써 혈압하강을 일으킨다고 하였다. 본 연구자는 "endorphin stress system"에 착안하여 normal saline, salicylate 및 hydrocortisone으로 전처치한 흰쥐에 실혈을 일으킨 후 naloxone, hydrocortisone 및 PGE_1을 투여하여 저혈량성 shock에서 혈압하강 기전의 일부를 규명하고 아울러 혈압하강 치료 지침에 도움이 되고자 실험에 착수하여 다음과 같은 결과를 얻었다. 1. Normal saline 전처치군에서 실혈 후 naloxone 및 PGE_1을 투여하여 평균동맥압이 의의있게 상승하였다. 2. Salicylate 전처치군에서 실혈 후 naloxone, hydrocortisone 및 PGE_1을 투여하여도 평균동맥압의 변화는 없었다. 3. Hydrocortisone 전처치군에서 실혈 후 naloxone 및 PGE_1을 투여하여 평균동맥압이 의의있게 증가하였다. 4. Normal saline 전처치군과 hydrocortisone 전처치군에서 실혈 후 naloxone, hydrocortisone 및 PGE_1을 투여하여 맥압이 의의있게 증가하였다. 5. Salicylate 전처치군에서 실혈 후 naloxone, hydrocortisone 및 PGE_1을 투여하여도 맥압의 변화가 없었다. 이상의 결과로 보아 저혈량성 shock의 혈압하강에는 β-endorphin이 관여하며, 이는 내인성 PGE_1의 작용을 억압하기 때문이다. Naloxone은 β-endorphin의 작용을 억제하여 내인성 PGE_1의 작용을 활성화시켜 모세순환 및 혈류를 증가시켜 혈압을 상승시키는 것으로 생각된다. ; The effects of morphine in bringing sleep and an end to pain have been known from beginning of record history. But the existence of endogenous opiates(endorphins) has been demonstrated only in the last decade. Endorphins bind to opiate receptors and have potent opiate-like activity. In the corticotroph cells of anterior lobe of pituitary, ACTH and β-endorphin are synthesized simultaneously within proopiocortin. There is a hypothalamic releasing factor which causes the secretion both β-endorphin and ACTH. Also, ACTH and β-endorphin are released simultaneously by stress. Endorphins adversely affect circulatory status and these effects were reversed by the intravenous injection of narcotic antagonist, naloxone. The author studied the Dirksen s hypothesis that endorphins may be involved in the pathophysiology of hemorrhagic shock. In this experiment, the author divided animals in 3 groups according to pretreated drugs. I. normal sline pretreated group II. salicylate pretreated group III. hydrocortisone pretreated group And each group was divided into 4 subgroups according to treated drugs. 1. hypovolemic shock + normal saline 2. hypovolemic shock + naloxone 3. hypovolemic shock + hydrocortisone 4. hypovolemic shock + shock + PGE_1 The following results were obtained: 1. MAP was significantly increased after naloxone and PGE_1 administration in the normal saline pretreated group. 2. MAP was not changed in the salicylate pretreated group. 3. MAP was significantly increased after naloxone and PGE_1 administration in the hydrocortisone pretreated group. 4. Pulse pressure was significantly increased after naloxone, hydrocortisone and PGE_1 administration in the normal saline and hydrocortisone pretreased group. From the above experiment, it may be inferred that endorphins and prostaglandin may play a role in the pathophysiology of hypovolemic shock.