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Effect of moderate hypothermia in the treatment of canine hemorrhagic shock.

机译:亚低温治疗犬失血性休克的效果。

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摘要

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.
机译:这项研究评估了中度低温治疗严重失血性休克的可能的保护和治疗作用。使用了改进的威格斯减震器。在失血性休克和复苏期间,常温犬(I组,N = 6)保持体温正常。在第二组中,失血性休克15分钟(N = 12)后开始进行体温过低,液体复苏后维持体温60分钟。然后将动物用接受碳酸氢钠的IIA组(N = 7)加热以纠正酸中毒,而使IIB组(N = 5)没有进行加热。对所有的狗进行额外的120分钟研究。在休克期间,两个低温组(IIA和IIB)的心率均低于正常体温犬(分别为85.0 +/- 3.9、77.7 +/- 4.6和136.7 +/- 4.2,p小于0.05),而+ dP / dt(mmHg / s)在所有狗中保持稳定。此外,在这段时间中,低温动物(IIA和IIB组)的pH值低于正常动物(IIA组:7.19 +/- 0.02,IIB组:7.13 +/- 0.02,而I组:7.24 +/- 0.02 )。低温出血性休克组IIA和IIB的动脉pCO2高于正常体温组(34.5 +/- 2.2,37.4 +/- 2.2 vs. 20.3 +/- 20,3 +/- 2.0,p小于0.05)降低体温的呼吸作用。在失血性休克期间,正常体温动物发生了较高的心肌氧气消耗量和心肌乳酸负平衡。复苏和加温后,与低温犬相比,持续存在酸碱紊乱的低温动物的中风量(mL /次)和心输出量(L / min)较低(分别为12.6 +/- 2.5、1.3 +/- 3.0)酸碱校正(20.1 +/- 3.3,2.2 +/- 0.3)和常温犬(24.6 +/- 3.0,3.0 +/- 0.3,p小于0.05),而心肌O2提取和心肌乳酸产生更高。结果表明,体温过低会降低失血性休克中的代谢需求并维持心肌收缩功能。体温过低可能具有有益的作用,并且通过酸碱平衡的正常化,对失血性休克具有治疗作用。

著录项

  • 作者

    Meyer, D M; Horton, J W;

  • 作者单位
  • 年度 1988
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  • 原文格式 PDF
  • 正文语种 en
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