Ischemic/hypoxic myocardial damage and functional impairment of the myocardium occurs immediately after major burns. This experimental study investigated whether the prompt cardiac dysfunction initiates hepatic, renal, and intestinal injuries soon after a severe burn.
Wistar rats were randomized to a sham burn group, a burn group (subjected to 30% total body surface area third-degree burn) that was subdivided into two groups: a simple burn group, observed at 0.5 hour, 1 hour, 3 hours, 6 hours, 12 hours, 24 hours postburn and a group medicated with propranolol (a cardiac inhibitor), cedilanid (a cardiotonic agent), enalaprilat (an angiotensin converting enzyme inhibitor), and cedilanid plus enalaprilat injected at 0.5 hour postburn and observed at 6 hours later. Serum cardiac troponin I, total bile acid, beta2-microglobulin concentrations, and diamine oxidase activity were measured to reflect the severity of cardiac, hepatic, renal, and intestinal injuries that were confirmed by histopathologic observations. Cardiac function and organs' blood flow were also recorded.
Histopathologic changes and serum cardiac troponin I increase occurred significantly earlier than the other organs, and the organ damage developments followed a similar pattern. Myocardial injury was significantly aggravated in rats treated with propranolol, with further decreases in myocardial function, blood flow to the liver, kidneys, and intestines significantly decreased, and injuries were aggravated. In contrast, these conditions were greatly improved in the rats treated with enalaprilat, cedilanid, or with both.
The prompt cardiac dysfunction has some initiating effects on ischemic/hypoxic injury to organs such as the liver, kidneys, and intestines soon after a severe burn.