Kambam J, Mets B, Hickman R, Janicki P, James M F, Kirsch R
Department of Anesthesiology, Vanderbilt University Hospital, Nashville, TN 37232-2125.
J Lab Clin Med. 1993 Aug;122(2):188-96.
We investigated systemic effects and possible mechanisms for lethality of intravenously infused cocaine in spontaneously breathing and mechanically ventilated unconscious Landrace male pigs weighing about 26 kg (25.75 +/- 0.25 kg) that were pretreated with either saline solution (groups 1 and 3) or iso-ompa (tetraisopropyl pyrophosphoramide), a specific plasma cholinesterase inhibitor (groups 2 and 4). Pigs were made unconscious with sodium thiopental and ventilated with 70% nitrous oxide and 30% oxygen. A carotid arterial cannula and a Swan-Ganz catheter were inserted for hemodynamic monitoring. Pigs in groups 1 and 2 were then allowed to breathe spontaneously and groups 3 and 4 were mechanically ventilated. After obtaining a stable state, as judged by cardiovascular and respiratory parameters, the pigs were infused intravenously with cocaine hydrochloride (0.8 mg/kg/min) until the time of cardiac arrest. Respiratory and cardiovascular parameters, blood temperature, and sodium and potassium levels were monitored. The times of occurrence of respiratory arrests (RA), cardiac arrests (CA), and convulsions were recorded. Our results showed that RA is the primary cause of death in spontaneously breathing pigs and that mechanical ventilation significantly delayed the occurrence of CA (p < 0.05). Significant decreases in cardiac output, mean blood pressure, and heart rate as well as significant increases in systemic and pulmonary vascular resistances, central venous and pulmonary wedge pressures, and blood K+ levels were noted in mechanically ventilated pigs (p < 0.05). Variable hemodynamic responses were noticed in spontaneously breathing pigs. Our results also showed that no significant changes occurred in blood catecholamine levels when compared with baseline values associated with the infusion of toxic doses of cocaine.(ABSTRACT TRUNCATED AT 250 WORDS)
我们研究了静脉注射可卡因对体重约26千克(25.75±0.25千克)的自发呼吸和机械通气的无意识长白雄性猪的全身影响及致死的可能机制。这些猪预先用生理盐水(第1组和第3组)或异奥芬(四异丙基焦磷酸酰胺)进行预处理,异奥芬是一种特异性血浆胆碱酯酶抑制剂(第2组和第4组)。用硫喷妥钠使猪失去意识,并用70%氧化亚氮和30%氧气进行通气。插入颈动脉插管和Swan - Ganz导管进行血流动力学监测。然后第1组和第2组的猪允许自发呼吸,第3组和第4组的猪进行机械通气。在根据心血管和呼吸参数判断达到稳定状态后,给猪静脉输注盐酸可卡因(0.8毫克/千克/分钟)直至心脏骤停。监测呼吸和心血管参数、体温以及钠和钾水平。记录呼吸骤停(RA)、心脏骤停(CA)和惊厥发生的时间。我们的结果表明,RA是自发呼吸猪死亡的主要原因,并且机械通气显著延迟了CA的发生(p<0.05)。在机械通气的猪中,心输出量、平均血压和心率显著降低,全身和肺血管阻力、中心静脉压和肺楔压以及血钾水平显著升高(p<0.05)。在自发呼吸的猪中观察到血流动力学反应各不相同。我们的结果还表明,与输注毒性剂量可卡因相关的基线值相比,血儿茶酚胺水平没有显著变化。(摘要截断于250字)