Perdrizet G A
Department of Surgery, Hartford Hospital, CT 06102-5037, USA.
New Horiz. 1995 May;3(2):312-20.
Tissue injury, resulting from ischemia and reperfusion, is a common theme seen in many clinical disease processes. Conditions ranging from hemorrhagic shock in the young trauma victim to myocardial infarction in the elderly have, as part of their pathophysiology, some degree of ischemia and reperfusion. The conditions typical of modern organ preservation are extremely stressful and injurious to living tissues. Organ preservation is a model of ischemia and reperfusion unique to the medical field as it permits the opportunity for preventive interventions. The established fields of thermotolerance and heat-shock biology have focused their studies upon the understanding of the cellular response to hyperthermia. The knowledge gained from these two disciplines shows that the cellular response to heat is an example of a more generalized stress response. Following the acute heat-shock response, the cell rapidly acquires a state of temporary protection against injury due to heat and other noxious conditions such as ischemia and reperfusion. The studies described here illustrate that the purposeful induction of the heat-shock response in whole organs prior to procurement and preservation can successfully protect these tissues against preservation (ischemia) and transplantation (reperfusion) injuries.
由缺血和再灌注导致的组织损伤是许多临床疾病过程中常见的现象。从年轻创伤受害者的失血性休克到老年人的心肌梗死等病症，在其病理生理学中都存在一定程度的缺血和再灌注。现代器官保存的典型条件对活体组织极具压力且会造成损伤。器官保存是医学领域特有的一种缺血和再灌注模型，因为它为预防性干预提供了机会。已确立的耐热性和热休克生物学领域将研究重点放在了对细胞对高温反应的理解上。从这两个学科获得的知识表明，细胞对热的反应是更普遍的应激反应的一个例子。在急性热休克反应之后，细胞迅速获得一种针对热以及其他有害条件（如缺血和再灌注）所致损伤的临时保护状态。此处所述的研究表明，在获取和保存之前对整个器官有目的地诱导热休克反应能够成功保护这些组织免受保存（缺血）和移植（再灌注）损伤。
