Isehemia/hypoxia is one of the key clinical issues following severe burns, and isehemic/hypoxic damage of tissues and organs is still hard to be prevented or minimized by various fluid resuscitation regimens . To those who suffered severe bums, even though fluid replacement therapy is delivered promptly, isehemic/hypoxie damage of organs is still inevitable. Previously, blood flow in vital organs such as heart was eonsidered not to be reduced because of blood redistribution under the circumstance of stress. The postbum cardiac dysfunction has been mainly attributed to the reduced blood flow returned to the heart due to decreased blood volume caused by increased capillary permeability. Therefore, postbum cardiac dysfunction has been considered to be the result of burn shock. During the past two decades, we have performed serial studies on severe burns, and found that isehemie/hypoxie myocardial damage and functional impairment of myocardium due to activation of reninangio tensin system existing in the heart itself occur immediately after severe bums even before significant reduction in blood volume secondary to an increase of capillary permeability . Such prompt myocardial damage leads to cardiac deficiency, and it is also a precipitating factor for bum shock and isehemic/hypoxie injury of systemic tissues and organs. Therefore, we called it " shock heart" in our reports. The cellular and molecular mechanisms leading to myocardial damage were systematically investigated. Strategies for prevention of early postburn myocardial damage and dysfunction, and a new effective burn shock resuscitation regimen "volume replacement" plus "dynamic support" (cardiac support and myocardial protection) have been proposed based on our previous studies.