Laboratoire ORPHY EA 4324, Université Européenne de Bretagne, Université de Brest, France.
Crit Care Med. 2012 Mar;40(3):912-8. doi: 10.1097/CCM.0b013e3182373134.
The aim of this study was to highlight the link between induced hypothermia and increased survival duration as observed in the septic model developed by the laboratory. To reach this objective, survival duration and blood oxygen transport capacity were measured at two temperatures-38 °C (induced normothermia) and 34 °C (induced hypothermia)-in septic rats.
A prospective, randomized, experimental animal study.
University laboratory.
Forty-four male Sprague-Dawley rats (median weight, 232 g; range, 200-303 g).
After anesthesia and obtention of the temperature goal, sepsis was induced by cecal ligation and perforation.
Sepsis induction led to death 5 hrs 11 mins ± 0 hr 36 mins after cecal ligation and perforation at 38 °C. At this temperature, significant changes in blood oxygen transport capacity were observed in septic rats; Hill number decreased from 2.36 ± 0.10 (baseline group) to 1.99 ± 0.17 (septic group) (p = .008) and oxygen-hemoglobin affinity decreased and P50 increased from 41.40 ± 2.4 Torr (baseline group) to 51.17 ± 14.07 Torr (septic group). Furthermore, in normothermia, a significant increase of creatinine and albumin plasmatic concentrations was observed 4 hrs after sepsis induction. Survival duration was significantly higher in induced hypothermia (7 hrs 22 mins ± 0 hr 12 mins at 34 °C) compared with induced normothermia. At 34 °C, no significant change in blood oxygen transport capacity was observed. In the same way, exposure to 34 °C induced no change in measured plasmatic parameters except an increase in albumin concentration in septic rats compared with the baseline group.
Sepsis led to a decrease of both oxygen hemoglobin cooperativity and affinity at 38 °C. By contrast, no change in these parameters was observed when sepsis was induced during hypothermia. Taken together, these results could be interpreted in normothermia septic rats as an adaptive mechanism that could enhance the release of oxygen at the tissue level. Hypothermia by slowing down sepsis evolution could increase survival duration.
本研究旨在强调实验室建立的脓毒症模型中观察到的诱导性低温与存活时间延长之间的联系。为了达到这个目的,在 38°C(诱导正常体温)和 34°C(诱导低温)下测量了脓毒症大鼠的存活时间和血液氧运输能力。
前瞻性、随机、实验动物研究。
大学实验室。
44 只雄性 Sprague-Dawley 大鼠(中位数体重 232 克;范围 200-303 克)。
麻醉并达到体温目标后,通过结扎和穿孔盲肠诱导脓毒症。
在 38°C 时,盲肠结扎和穿孔后 5 小时 11 分钟±0 小时 36 分钟发生脓毒症诱导死亡。在这个温度下,脓毒症大鼠的血液氧运输能力发生了显著变化;Hill 数从 2.36±0.10(基础组)下降到 1.99±0.17(脓毒症组)(p=0.008),氧-血红蛋白亲和力下降,P50 从 41.40±2.4 托(基础组)增加到 51.17±14.07 托(脓毒症组)。此外,在正常体温下,脓毒症诱导后 4 小时观察到肌酐和白蛋白血浆浓度显著升高。与诱导正常体温(34°C 时 7 小时 22 分钟±0 小时 12 分钟)相比,诱导低温时的存活时间明显更长。在 34°C 时,血液氧运输能力没有显著变化。同样,在 34°C 下,暴露于低温不会改变测量的血浆参数,除了脓毒症大鼠的白蛋白浓度与基础组相比有所增加。
脓毒症导致 38°C 时氧血红蛋白协同性和亲和力下降。相比之下,在低温诱导脓毒症时,这些参数没有变化。这些结果可以解释为在正常体温的脓毒症大鼠中,这是一种适应性机制,可以增强组织水平的氧气释放。通过减缓脓毒症的发展,低温可以延长存活时间。