Meyer D M, Horton J W
Department of Surgery, University of Texas Health Science Center, Dallas 75235-9031.
Ann Surg. 1988 Apr;207(4):462-9. doi: 10.1097/00000658-198804000-00015.
This study evaluated a possible protective and therapeutic effect of moderate hypothermia in the treatment of severe hemorrhagic shock. A modified Wiggers shock preparation was used. Normothermic dogs (Group I, N = 6) were maintained at normal body temperature throughout hemorrhagic shock and resuscitation. In Group II, hypothermia was initiated after 15 minutes of hemorrhagic shock (N = 12) and maintained for 60 minutes after fluid resuscitation. Animals were then rewarmed with Group IIA (N = 7) receiving sodium bicarbonate to correct acidosis, while Group IIB (N = 5) did not; all dogs were studied for an additional 120 minutes. During shock heart rate was lower in both hypothermic groups (IIA and IIB) compared to normothermic dogs (85.0 +/- 3.9, 77.7 +/- 4.6 vs. 136.7 +/- 4.2, respectively, p less than 0.05), while +dP/dt (mmHg/s) remained stable in all dogs. Furthermore, pH was lower in the hypothermic (Groups IIA and IIB) compared to normothermic animals at this time period (Group IIA: 7.19 +/- 0.02, Group IIB: 7.13 +/- 0.02 vs. Group I: 7.24 +/- 0.02). Arterial pCO2 was higher in the hypothermic hemorrhagic shock Groups IIA and IIB compared to normothermic group (34.5 +/- 2.2, 37.4 +/- 2.2 vs. 20.3 +/- 20,3 +/- 2.0, p less than 0.05) due to hypothermia-depressed respiration. A higher myocardial O2 consumption and a negative myocardial lactate balance occurred in the normothermic animals during hemorrhagic shock. After resuscitation and rewarming, stroke volume (mL/beat) and cardiac output (L/min) were lower in hypothermic animals with persistent acid-base derangements (12.6 +/- 2.5, 1.3 +/- 3.0, respectively) compared to hypothermic dogs with acid-base correction (20.1 +/- 3.3, 2.2 +/- 0.3) and normothermic dogs (24.6 +/- 3.0, 3.0 +/- 0.3, p less than 0.05), while myocardial O2 extraction and myocardial lactate production were higher. Results suggest hypothermia decreases the metabolic needs and maintains myocardial contractile function in hemorrhagic shock. Hypothermia may have a beneficial effect and, with normalization of acid-base balance, a therapeutic role in hemorrhagic shock.
本研究评估了中度低温在治疗严重失血性休克中的潜在保护和治疗作用。采用改良的维格斯休克模型。正常体温的犬（I组，N = 6）在失血性休克和复苏过程中维持正常体温。在II组中，失血性休克15分钟后开始降温（N = 12），液体复苏后维持60分钟。然后对动物进行复温，IIA组（N = 7）接受碳酸氢钠以纠正酸中毒，而IIB组（N = 5）不接受；所有犬再研究120分钟。在休克期间，两个低温组（IIA和IIB）的心率均低于正常体温的犬（分别为85.0±3.9、77.7±4.6与136.7±4.2，p<0.05），而所有犬的+ dP/dt（mmHg/s）保持稳定。此外，在此时间段内，低温组（IIA和IIB）的pH低于正常体温的动物（IIA组：7.19±0.02，IIB组：7.13±0.02与I组：7.24±0.02）。由于低温抑制呼吸，低温失血性休克IIA组和IIB组的动脉pCO2高于正常体温组（34.5±2.2，37.4±2.2与20.3±2.0，p<0.05）。在失血性休克期间，正常体温的动物心肌氧耗较高，心肌乳酸平衡为负。复苏和复温后，持续存在酸碱紊乱的低温动物的每搏量（mL/搏）和心输出量（L/分钟）低于酸碱纠正的低温犬（分别为12.6±2.5，1.3±3.0）和正常体温的犬（24.6±3.0，3.0±0.3，p<0.05），而心肌氧摄取和心肌乳酸生成较高。结果表明，低温可降低代谢需求并在失血性休克中维持心肌收缩功能。低温可能具有有益作用，并且随着酸碱平衡的正常化，在失血性休克中具有治疗作用。
