RESUMO
OBJECTIVE: To study the influence of catecholamine on myocardium in rats with septic shock and its mechanism by biochemical and pathophysiological methods to evaluate the underlying pathophysiologic mechanism of myocardial damage and the influence of catecholamine on the myocardial injury. METHODS: Septic shock was replicated in rats by cecal ligation and puncture (CLP). Dobutamine (DB), norepinephrine (NE) and combination of DB and NE were used in the lowest dose. The rats were randomly divided into sham operations, CLP control group, CLP+DB group, CLP+NE group and CLP+DB+NE group, 8 rats in each group. Troponin I (cTnI) and total creatine kinase (CK) were measured, and myocardial tissue was examined under light microscopy and electron microscopy. RESULTS: An significantly increased cTnI level was found in CLP septic shock rats, compared with sham rats (P<0.05). In the present study, the use of DB or NE alone, or the combination of the two drugs, was not found to influence the cTnI levels. But, the total CK levels in catecholamine-treated group were significantly increased (P<0.05). There was no statistically significant correlation between cTnI and CK levels. Morphological study confirmed the results of cTnI. Findings that were common in the myocardium of CLP septic shock rats included extracellular and intracellular edema as well as mitrochondrial injury. However, no conclusive evidence was found for the influence of catecholamine on myocardial damage. CONCLUSION: No evidence of the influence of catecholamine on myocardial damage is found. Pathological study suggests that myocardial injury is the result of ischemia.