Boylan J F, Cheng D C, Sandler A N, Carmichael F J, Koren G, Feindel C, Boylen P
Department of Anaesthesia, University of Toronto, Toronto Hospital, Ontario, Canada.
J Cardiothorac Vasc Anesth. 1996 Oct;10(6):772-7. doi: 10.1016/S1053-0770(96)80204-7.
Increasing numbers of people use cocaine recreationally and may require anesthesia care, having recently abused the drug. However, no data currently exist concerning potential interactions between toxic levels of cocaine and volatile anesthetic agents. This study investigated the effects of cocaine infusion on systemic hemodynamics, myocardial metabolism, and regional organ blood flow in relation to depth of isoflurane anesthesia.
Prospective, randomized, controlled trial.
A laboratory at a university medical center.
Twelve miniature pigs.
An open-chest swine model was used. Isoflurane (ISO) was the sole anesthetic, administered at 0.75 and 1.5 minimum alveolar concentration (MAC), and cocaine was infused (n = 6) at a rate of 0.5 mg/kg/min. Control animals (n = 6) received an equivalent amount of normal saline.
Systemic and pulmonary arterial pressures and thermodilution cardiac output data were collected at 0.75 MAC and 1.5 MAC ISC. Regional myocardial and blood flows to other organs were measured using radiolabeled microspheres. Arrhythmias and altered ventricular conduction were noted only in the cocaine group, along with significant elevations in diastolic arterial pressure, coronary perfusion pressure, and systemic vascular resistance. Increased subendocardial blood flow occurred during cocaine infusion (p = 0.03); subepicardial perfusion was unchanged. Cerebral (p < 0.01) and spinal cord (p < 0.05) blood flows were reduced in animals receiving cocaine. Other organ blood flows were unchanged with depth of anesthesia or cocaine administration, with the exception of splenic blood flow (p < 0.04).
Moderately toxic cocaine levels occurring during isoflurane at 0.75 MAC and 1.5 MAC are associated with hemodynamic abnormalities, a marked increase in systemic vascular resistance, and a tendency to produce cardiac arrhythmias. A reversal of endo/epicardial myocardial perfusion ratio occurs associated with cocaine infusion during ISO anesthesia. This is probably not related to a primary redistribution of subendocardial blood flow and may be related to a combination of increased myocardial oxygen demand and epicardial coronary vasoconstriction. The reductions in cerebral and spinal cord perfusion observed may explain, in part, the neurologic sequelae of cocaine toxicity.
越来越多的人将可卡因用于消遣，这些人在近期滥用该药物后可能需要接受麻醉护理。然而，目前尚无关于可卡因中毒水平与挥发性麻醉剂之间潜在相互作用的数据。本研究调查了可卡因输注对与异氟烷麻醉深度相关的全身血流动力学、心肌代谢和局部器官血流的影响。
前瞻性、随机、对照试验。
一所大学医学中心的实验室。
12只小型猪。
采用开胸猪模型。异氟烷（ISO）作为唯一麻醉剂，以0.75和1.5最低肺泡浓度（MAC）给药，可卡因以0.5mg/kg/min的速率输注（n = 6）。对照动物（n = 6）输注等量生理盐水。
在0.75MAC和1.5MAC异氟烷时收集全身和肺动脉压以及热稀释心输出量数据。使用放射性微球测量局部心肌血流和其他器官的血流。仅在可卡因组中观察到心律失常和心室传导改变，同时舒张压、冠状动脉灌注压和全身血管阻力显著升高。可卡因输注期间心内膜下血流增加（p = 0.03）；心外膜灌注无变化。接受可卡因的动物脑血流（p < 0.01）和脊髓血流（p < 0.05）减少。除脾血流外（p < 0.04），其他器官血流不受麻醉深度或可卡因给药影响。
在0.75MAC和1.5MAC异氟烷麻醉期间出现的中度可卡因中毒水平与血流动力学异常、全身血管阻力显著增加以及产生心律失常的倾向相关。在异氟烷麻醉期间，可卡因输注会导致心内膜/心外膜心肌灌注比值逆转。这可能与心内膜下血流的原发性重新分布无关，可能与心肌需氧量增加和心外膜冠状动脉血管收缩的综合作用有关。观察到的脑和脊髓灌注减少可能部分解释了可卡因中毒的神经后遗症。
