PATHOGENESIS OF EXPERIMENTAL SHOCK

Abstract

Fatal shock was produced in animals by rotational trauma, occlusion of the superior mesenteric artery, and bacterial endotoxin. Experiments were also carried out with animals rendered tolerant to trauma or pretreated with cortisone. Release of beta glucuronidase and cathepsins from the large granule fraction of liver homogenates was increased during traumatic and endotoxin shock in the rat. Circulating levels of acid phosphatase and beta glucuronidase were increased during traumatic shock in rats and rabbits, and during endotoxin shock in rats. Tolerance to traumatic injury prevented the increase in levels of circulating acid phosphatase normally observed after stress, and was associated with an increased stability of hepatic lysosomal particles . Cortisone also reduced the increase in plasma acid phosphatase brought about by endotoxin and trauma. It is suggested that: a) Disruption of lysosomes may occur in liver and intestine of shocked animals. b) This process may play a role in exacerbating tissue injury and accelerating irreversibility during shock. c) Increased stability of lysosomes of tolerant and of cortisone-treated animals may be a component of the resistance of these animals to shock.