Moore F A, Moore E E
Denver General Hospital, Colorado.
Surg Clin North Am. 1995 Apr;75(2):257-77. doi: 10.1016/s0039-6109(16)46587-4.
Early epidemiologic studies concluded that infection with systemic sepsis was the common pathway for the development of ARDS and eventual MOF. As a consequence, research investigation from 1977 to 1987 focused on later clinical events (e.g., immunosuppression, persistent hypercatabolism, and bacterial translocation). Now, it is believed that an initial massive traumatic insult can create severe SIRS independent of infection (one-hit model). Alternatively, a less severe traumatic insult can create an inflammatory environment (i.e., primes the host) such that a later, otherwise innocuous, secondary inflammatory insult precipitates severe SIRS (two-hit model). As a result of these newer inflammatory models, research interest during the last 5 years has shifted to investigating earlier clinical events (e.g., unrecognized flow-dependent oxygen consumption, ischemia/reperfusion, and priming/activation of the inflammatory response).
早期的流行病学研究得出结论，全身性脓毒症感染是急性呼吸窘迫综合征（ARDS）和最终多器官功能衰竭（MOF）发生发展的常见途径。因此，1977年至1987年的研究调查集中在后期临床事件（如免疫抑制、持续高分解代谢和细菌移位）上。现在，人们认为最初的严重创伤性损伤可引发独立于感染的严重全身炎症反应综合征（SIRS）（单次打击模型）。或者，较轻的创伤性损伤可营造一种炎症环境（即致敏宿主），使得随后发生的、原本无害的继发性炎症损伤引发严重SIRS（双次打击模型）。由于这些更新的炎症模型，过去5年的研究兴趣已转向调查早期临床事件（如未被认识到的血流依赖性氧消耗、缺血/再灌注以及炎症反应的致敏/激活）。
