[The postburn "shock heart"].
OBJECTIVE
To investigate the pathogenesis of postburn "shock heart".


METHODS
A combined serial studies in both animal experiments and prospective clinical investigation were carried out with the determination of indices reflecting myocardial injury, such as cardiac function, myocardial injury parameters, cytoplasmic and cytoskeletal structure injury, myocardial biomechanics and pathomorphological changes. The pathogenesis was also explored by the evaluation of myocardial nutritional blood flow (NBF), cardiac myocytic oxygen consumption, energy metabolism and cytokines released from cardiac myocytes.


RESULTS
Cardiac function, myocardial biomechanics, NBF, the oxygen consumption, energy metabolism and the viscoelastic properties of cardiac myocytes decreased significantly postburn, and myocyte cytoplasm and cytoskeleton were damaged after burn. Furthermore, focal dissolution and fragmentation of myocardiac fibers were observed. In the meantime the plasma levels of CM -- LC, TnT and myocardial tissue cytokines increased markedly.


CONCLUSIONS
These results suggest that organic damage of cardiac myocytes occurred during postburn shock stage. The principle pathogenesis might be related to ischemic -- reperfusion injury, inability of oxygen utility and energy metabolism in cardiac myocytes, as well as myocardial edema and uncontrolled inflammatory response.
Huang
Y
Y
Institute of Burn Research, Southwestern Hospital, The Third Military Medical University, Chongqing 400038, P.R. China.
Yang
Z
Z
Chi
L
L
D000818:Animals; D002056:Burns / Q000473:pathology* / Q000503:physiopathology; D004487:Edema / Q000209:etiology; D006439:Hemodynamics; D006801:Humans; D015428:Myocardial Reperfusion Injury / Q000209:etiology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D009504:Neutrophils / Q000502:physiology; D010101:Oxygen Consumption; D051381:Rats