Schwartz A B, Boyle W, Janzen D, Jones R T
Department of Medicine and Anesthesia, U.C. Davis.
Can J Cardiol. 1988 May;4(4):188-92.
To evaluate the electrophysiologic and neurohumoral effects of cocaine on the sinus node, atrium, atrioventricular node, and His-Purkinje system, 14 conscious dogs were studied before and after an infusion titrated to maximum tolerance or to increase the systolic blood pressure by at least 15%. Plasma cocaine and catecholamine levels, blood pressure, surface and intracardiac electrograms were recorded. Programmed electrical stimulation was performed from the right atrium. The sinoatrial conduction time, paced PR interval, atrioventricular nodal conduction time, atrioventricular nodal effective refractory period and blood pressure increased. Plasma noradrenaline, adrenaline and dopamine increased and remained at two to three times control levels throughout the study although plasma cocaine levels declined. Adrenaline levels were strongly correlated with the hemodynamic response while plasma cocaine levels were not. No sustained spontaneous atrial or ventricular arrhythmias were recorded after cocaine infusion. Atrial fibrillation with a slow ventricular response was induced by pacing after cocaine in only three dogs. There were no significant changes in pacing threshold, right intra-atrial conduction time, infranodal conduction time, heart rate, QRS or QT. No pacing induced infranodal block occurred. The cocaine dose rate infused was 2.8 +/- 1.2 mg/kg; cocaine plasma levels were 1402 +/- 885 ng/mL immediately after the initial infusion and 525 +/- 321 ng/mL at the end of the study. It is concluded that in normal canine heart cocaine increases blood pressure, sinoatrial conduction time, atrioventricular nodal effective refractory period, paced PR interval, atrioventricular nodal conduction time, plasma catecholamines and susceptibility to atrial fibrillation. These findings cannot be explained solely by increased sympathetic nervous system activity and suggest participation of the parasympathetic nervous system.
为评估可卡因对窦房结、心房、房室结及希氏-浦肯野系统的电生理和神经体液效应，对14只清醒犬在输注可卡因至最大耐受量或使收缩压至少升高15%之前和之后进行了研究。记录血浆可卡因和儿茶酚胺水平、血压、体表和心内电图。从右心房进行程控电刺激。窦房传导时间、起搏PR间期、房室结传导时间、房室结有效不应期和血压升高。血浆去甲肾上腺素、肾上腺素和多巴胺升高，且在整个研究过程中维持在对照水平的两到三倍，尽管血浆可卡因水平下降。肾上腺素水平与血流动力学反应密切相关，而血浆可卡因水平则不然。输注可卡因后未记录到持续性自发性房性或室性心律失常。仅3只犬在输注可卡因后起搏诱发了伴有缓慢心室反应的心房颤动。起搏阈值、右心房内传导时间、结下传导时间、心率、QRS或QT无显著变化。未发生起搏诱发的结下阻滞。输注的可卡因剂量率为2.8±1.2mg/kg；首次输注后即刻血浆可卡因水平为1402±885ng/mL，研究结束时为525±321ng/mL。结论是，在正常犬心脏中，可卡因可升高血压、窦房传导时间、房室结有效不应期、起搏PR间期、房室结传导时间、血浆儿茶酚胺水平以及对心房颤动的易感性。这些发现不能仅用交感神经系统活动增强来解释，提示副交感神经系统也参与其中。
