Heat shock and tissue protection.
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.
Perdrizet
G A
GA
Department of Surgery, Hartford Hospital, CT 06102-5037, USA.
D000818:Animals; D006360:Heat-Shock Proteins / Q000502:physiology*; D006358:Hot Temperature; D006801:Humans; D007511:Ischemia / Q000503:physiopathology; D009926:Organ Preservation; D051381:Rats; D015427:Reperfusion Injury / Q000517:prevention & control; D013312:Stress, Physiological / Q000503:physiopathology*; D013552:Swine
D006360:Heat-Shock Proteins