For the elucidation of mechanism of circulatory collapse in acute venom intoxication, an experimental :studies was carried out for the cardiotoxic effect of rat myocardium using the venom of "<4gkistrodon saxatilis. The rat used were adults weighing between 200---250 gm. 40 mg of freeze dried venom was diluted to 12 ml of normal saline, and 0. 4 ml of this solution was administrated intravenously through´ tail vein to each rat.
The rats were sacrificed serially with time interval; after venom administration 1 hour; 3 hours, 6 hours, 1 day, 4 days and 7 days, respectively. The hearts were immediately prepared for light and electron microscopy. Additionally serum enzymes, namely glutamic oxaloacetic transaminase(GOT), lactic dehydro-_genase(LDH) and creatinine phosphokinase(CPK) were measured for the associated changes.
The results obtained were as follows:
1. _.Light microscopic changes in the heart revealed moderate to marked congestion, edema and hemorrhage in the ventricular and subendocardial myocardium with coagulation necrosis of myocardial muscles in the hemorrhagic areas in I hour after venom administration. Congestion and edema were reduced but hemorrhagic areas were infiltrated with a few inflammatory cells in 3^-6 hours. Thereafter fibrosis was due in the areas of necrosis.
2. Early electron microscopic changes in the myocardium revealed marked intracellular edema with lifting, bleb formation and rupture of sarcolemma as well as separation of myofilaments and focal random loss of myofilaments. Mitochondrial swelling and vacuolar changes were also seen.
3. Serum levels of GOT were significantly elevated in 3 hours to 312. 5+213. 6IU/1 (p<0, 05) until 6 hours to 376.7283.5IU;l(p<0.01).
4. Serum levels of LDH were significantly reduced in 24 hours to 508. 1269.OIU/1 (p<0.01) until 4 days to 453.4190.3IU/1 (p<0.O1).
5. Serum levels of CPK were significantly reduced in 24 hours to 306.1+205. 1 IU/l(p<0.O1) until 4 days 532.1457.8IU/l(p<0.05).
Summarizing the above results, it was suggested that cardiotoxicity of the venom of Agkistrodon saxatilis, characterized by marked myocardial edema and hemorrhage with necrosis, could play a role in explaining acute circulatory collapse in rats. It was also interesting to note that the extent of myocardial damage did not parallel to the levels of serum glutamic oxaloacetic transaminase, lactic dehydrogenase and creatinine phosphokinase.
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