Physiologic and Neuropathologic Aspects of Hypothermic Circulatory Arrest in Newborn Dogs
Physiologic and Neuropathologic Aspects of Hypothermic Circulatory Arrest in Newborn Dogs
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新生犬低温循环骤停的生理和神经病理学方面
DOI：
10.1203/00006450-199010000-00011
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发表时间：
1990
影响因子：
3.6
通讯作者：
R. Vannucci
中科院分区：
文献类型：
--
作者：
D. Mujsce;J. Towfighi;R. Vannucci
摘要：在新生犬中建立了低温停循环模型。用氟烷麻醉10只幼犬，使其麻痹，并用70%一氧化二氮30%氧气人工通气至动脉氧压>8.0 kPa（60 mm Hg），动脉二氧化碳压为4.4-5.6 kPa（33-42 mm Hg），动脉pH值为7.35-7.42。将动物表面冷却至20°C，之后用静脉内KCl产生心脏骤停。犬在无通气的情况下保持心搏停止1.0（n = 4）、1.5（n = 3）或2.0（n = 3）次，通过闭胸按压、机械通气、静脉注射肾上腺素和NaHCO 3并复温至37°C完成复苏。休息后恢复维持3-4 h;此后，对幼犬进行脑灌注固定，进行病理学分析。低温心脏停搏期间血糖（对照组= 8.3 mmol/L）略微升高（+36%），但在休息后15 min显著升高（20 mmol/L）。血乳酸（对照组= 1.1 mmol/L）在低温停循环期间增加近200%，在停循环后15 min进一步升高至9.0 mmol/L。此后，乳酸在1小时的逮捕狗蝙蝠增加进行性的其他组。平均动脉血压在休息后15分钟恢复到基线（73 mm Hg），在1 h组犬中保持稳定，但在3 h时1.5 h和2.0 h组分别降至62和34 mm Hg。在幼犬被捕1小时，而所有的pnppies逮捕1.5或2小时有不同程度的大脑皮层和海马损伤的神经病理学改变。因此，新生狗耐受1小时的低温停循环而无脑损伤，此后有分级的神经元损伤。该实验模型具有直接的临床意义，可用于研究脑、心脏和其他器官在长时间缺血期间的细胞损伤机制。
ABSTRACT: A modle of hypothermic circulatory arrest has been developed in the newborn dog. Ten puppies were anesthetized with halothane, paralyzed, and artificially ventilated with 70% nitrous oxide 30% oxygen to arterial oxygen pressure >8.0 kPa (60 mm Hg), arterial carbon dioxide pressure of 4.4–5.6 kPa (33–42 mm Hg), and arterial pH of 7.35–7.42. Animals were surface cooled to 20°C, after which cardiac arrest was produced with i.v. KCI. Dogs remained asystolic without ventilation for 1.0 (n = 4), 1.5 (n = 3), or 2.0 (n = 3) th Rescucitation was accomplished with closed-chest compression, mechanical ventilation, i.v. epinephrine and NaHCO3, and rewarming to 37°C. Postarrest recovery was maintained for 3–4 h; thereafter, the puppies underwent perfusion-fixation of their brains for pathologic analysis. Plasma glucose (control = 8.3 mmol/L) increased slightly during hypothermic cardiac arrest (+36%) but was markedly elevated at 15 min postarrest (20 mmol/L). Blood lactate (control = 1.1 mmol/L) increased almost 200% during hypothermic circulatory arrest, with a further rise to 9.0 mmol/L at 15 min postarrest. Thereafter, lactate decreased in the 1-h arrested dogs bat increased progressively in the other groups. Mean arterial blood pressure returned to baseline (73 mm Hg) by 15 min postarrest, remained stable in the 1-h dogs, but fell at 3 h to 62 and 34 mm Hg in the 1.5-and 2.0-h groups, respectively. No neuropathologic alterations were seen in puppies arrested for 1 h, whereas all pnppies arrested for 1.5 or 2 h had varying degrees of cerebral cortical and hippocampal damage. Thus, newborn dogs tolerate 1 h of hypothermic circulatory arrest without brain damage, with graded neuronal injury thereafter. The experimental model has direct clinical relevance and can be used to study mechanisms of cellular injory in brain, heart, and other organs during prolonged ischemia.