| Summary: | 博士 === 慈濟大學 === 醫學研究所 === 90 === Major trauma associated with hemorrhagic shock is one of the most common and important causes of death in emergency room. Hemorrhagic shock disturbs cell metabolism and makes cell hypoperfusion and hypoxia in circulation system. Multiple organ failure is a frequent complication after hemorrhagic shock and accounts for a high incidence of mortality. The study explores the relationship between multiple organ failure and hemorrhagic shock. We used male Spague-Dawely (SD) rat weighing 380-440g (n=8). Femoral artery was catheterized to monitor blood pressure and heart rate. Femoral arterial bleeding of 50% total blood volume (11-13ml) induced hemorrhagic shock. Supplement of fluid was not given. Blood samples were collected before shock, and 30 min, 1, 3, 6, 9,12, 18, 24, 48 hr after shock. Lymphocyte and white blood cell (WBC), glutamic-oxaloacetic transamonase (sGOT), glutamic pyruvic transminase (sGPT), lactic acid dehydrogenase (LDH), creatine phosphokinase (CPK), amylase, lipase, blood urea nitrogen (BUN), creatinie were determined. Some rats were sacrificed by decapitation at 48 and 72 hr after hemorrhagic shock to collect organs such as brain, liver, heart, pancreatic, renal, spleen and intestine. Laboratory data showed that GOT and GPT were elevated after 3 hr, LDH and CPK were elevated after 6 hr and decreased after 24 hr. Lipase was elevated, and amylase was decreased after 30 min in shock. Heart rate and mean arterial pressure were decreased after 30 min and elevated after 1 hr. Nitrates/Nitrites were elevated after 30 min and peak after 3 hr. Methyl Guanidine was decreased after 30 min and elevated after 3 hr. Pathological picture conservative of liver, brain, heart showed mild necrosis in 48 and 72 hr. There are no significant change in pathology of pancreatic, renal, spleen and intestines. Hemorrhagic shock causes cerebral, hepatic, and myocardial injuries.
|
|---|
