Machuganska A
Acta Physiol Pharmacol Bulg. 1986;12(1):62-9.
The development of an acute hemorrhagic shock in rats with hereditary diabetes insipidus (DI), lacking vasopressin, is very dramatic, compared to rats of the parent strain Long Evans (LE). After removal of 50% of the circulating blood for LE, and 30% for DI, the mortality for both LE and DI groups was 50%, the shock index being 0.049 and 0.028, respectively. Infusion of either vasopressin (107 mU/100 g) or naloxone (0.2 mg/100 g) in DI rats, prevented the progression of hemorrhagic shock into irreversible stage, and augmented survival up to 66% and 57%, respectively. The specific opioid antagonist naloxone exerted a therapeutic effect on rats with hemorrhagic shock by antagonism of opioid receptors, without influencing ACTH and aldosterone secretion in DI rats. This is another evidence for the role of beta-endorphin in the pathogenesis of hemorrhagic shock.
与亲代品系朗·埃文斯(LE)大鼠相比,缺乏血管加压素的遗传性尿崩症(DI)大鼠急性失血性休克的发展非常显著。对于LE大鼠,去除50%的循环血量,对于DI大鼠,去除30%的循环血量后,LE组和DI组的死亡率均为50%,休克指数分别为0.049和0.028。给DI大鼠输注血管加压素(107 mU/100 g)或纳洛酮(0.2 mg/100 g),可防止失血性休克发展为不可逆阶段,生存率分别提高至66%和57%。特异性阿片类拮抗剂纳洛酮通过拮抗阿片受体对失血性休克大鼠发挥治疗作用,且不影响DI大鼠促肾上腺皮质激素和醛固酮的分泌。这是β-内啡肽在失血性休克发病机制中作用的又一证据。