Deshpande G G, Heidemann S M, Sarnaik A P
Wayne State University School of Medicine and Children's Hospital of Michigan, Detroit, Michigan 48201, USA.
Crit Care. 2000;4(1):45-9. doi: 10.1186/cc649. Epub 2000 Jan 24.
Elevated plasma lactate has been shown to correlate with mortality in patients with septic shock. Heat stress prior to sepsis has resulted in reduction in acute lung injury and mortality. We investigated whether heat stress resulted in decreased plasma lactate concentration and protected the lung by decreasing the inflammatory response to sepsis.
Plasma lactate concentration was elevated in septic rats without prior heat stress. Lactic acid levels were significantly lower in heat-treated septic rats (P < 0.05) and were not significantly different when compared with control rats. Septic rats with or without heat pretreatment had significantly higher myeloperoxidase activity in the lung than did control groups. Heat pretreatment did not prevent neutrophil infiltration or inflammatory mediator production in the lung.
Prior heat stress ameliorates lactic acidemia in rat sepsis. Heat stress did not attenuate the pulmonary inflammatory process. The mechanism of heat-induced protection from lactic acidemia in sepsis needs to be further explored.
血浆乳酸水平升高已被证明与感染性休克患者的死亡率相关。败血症发生前的热应激已导致急性肺损伤减轻和死亡率降低。我们研究了热应激是否会导致血浆乳酸浓度降低，并通过减少对败血症的炎症反应来保护肺部。
未进行热应激预处理的脓毒症大鼠血浆乳酸浓度升高。热预处理的脓毒症大鼠乳酸水平显著降低（P < 0.05），与对照组相比无显著差异。有或无热预处理的脓毒症大鼠肺组织中的髓过氧化物酶活性均显著高于对照组。热预处理并不能阻止中性粒细胞浸润或肺部炎症介质的产生。
热应激预处理可改善大鼠脓毒症中的乳酸血症。热应激并未减轻肺部炎症过程。热诱导保护脓毒症中乳酸血症的机制有待进一步探索。
