Effects Of Renin-angiotension System On Prompt Reduction Of Cardiac Function And Organ Blood Perfusion At Early Stage Following Severe Burn In Rats

Background and ObjectiveMyocardial damage and functional impairment occurs immediately following severe burns even before significant reduction in blood volume secondary to increase of capillary permeability, which is also a precipitating factor for burn shock and ischemic/hypoxic injury of systemic tissues and organs, so called"shock heart"hypothesis. It is important to elucidate the mechanism of prompt ischemic/hypoxic injury of heart at early stage following severe burn in rats.The renin-angiotensin axis appears to play a critical role in the pathophysiology of thermal injury according to many researches. Local renin-angiotensin system (RAS) existing in heart can synthesize and release angiotensin, which can regulate myocardial regional blood flow, vascular tone and myocardial contractility. The local and systemic RAS may play an important role in prompt myocardial ischemic injury during early postburn stage.The purpose of the present study is to observe the changes of RAS components and its effects on heart function and organ perfusion, and to reveal the mechanism of heart damage and endogenous protection at early stage postburn by regulating RAS.Materials and Methods1. Rats inflicted with 30% TBSA of full-thickness burns were used. Cardiac local RAS and systemic RAS components were detected at 10min, 30min, 1h, 3h and 6h after burn. At the same time points, cardiac function and organ perfusion were observed as well2. Rats inflicted with 30% TBSA of full-thickness burns were used. ACEI Enalaprilat was used to regulate the renin-angiotensin axis. Hemodynamics were observed consecutively and organ blood perfusion were assayed at appropriate time points.Results:1. RAS components in myocardial and serum increased rapidly at 10min, and kept rising till 6h postburn.2. LVSP, LV±dp/dtmax and heart blood flow decreased significantly 10min after burn, then began to recover until 1h and decreased again, while the heart rate showed a sustained decline after 1.5h postburn. However, LVEDP have no obvious change.3. The organ blood perfusion of kidneys, spleen, stomach and ileum declined 10min postburn, then reached a bottom 1h or 3h postburn, and had a little recovery at 6h postburn. The perfusion of brain maintained at normal level during the experiment period4. Compared with burn group, cardiac function and heart blood flow in ACEI group improved significantly at early stage following severe burn. ACEI can also increase blood perfusion of other organs at 3h postburn.Conclusion:1. As an important regulating system of circulation, cardiac local RAS and systemic RAS were activated rapidly and promptly at early stage postburn(10min), and kept rising till 6h.2. Heart dysfunction and decrease of heart blood flow occurred immediately following severe burns, which proved the"shock heart"theory of ischemic/hypoxic injury.3. Cardiac function and heart blood flow were improved significantly by initiatively regulating the imbalance of RAS, indicating that the activation of RAS was one of the important reasons for prompt myocardial ischemic injury at early stage postburn.