中文摘要：

以往国内外普遍认为，烧伤休克主要是血管通透性增高所致的低血容量性休克，心脏不参与其发生。而对严重烧伤后心功能降低，大都归咎于有效循环血量减少和（或）心肌抑制因子等的作用。但是临床上有些严重烧伤患者，即使伤后立即给予补液治疗，休克的发生仍难以避免，而且有时还难以纠正。延迟复苏的严重烧伤患者休克难以纠正的现象更为常见，造成组织器官损害，

英文摘要：

Ischemia/hypoxia is one of the key clinical issues following severe burns, and ischemic/hypoxic damage of tissues and organs is still hard to be prevented or minimized by various fluid resuscitation regimens. To those who suffered severe burns, even though fluid replacement therapy is delivered promptly, ischemic/hypoxic damage of organs is still inevitable. Previously, blood flow in vital organs such as heart was considered not to be reduced because of blood redistribution under the circumstance of stress. The postburn 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, postburn 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 ischemic/hypoxic myocardial damage and functional impairment of myocardium due to activation of renin angiotensin system existing in the heart itself occur immediately after severe burns 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 burn shock and ischemic/hypoxic 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.