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JYMS : Journal of Yeungnam Medical Science

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HOME > J Yeungnam Med Sci > Volume 10(2); 1993 > Article
Original Article The effect of lidocaine dose and pretreated diazepam on cardiovascular system and plasma concentration of lidocaine in dogs ansthetized with halothane-nitrous oxide
Kyeong Sook Lee, Sae Yeon Kim, Dae Pal Park, Jin Mo Kim, Chung Gil Chung
Journal of Yeungnam Medical Science 1993;10(2):451-474
Published online: December 31, 1993
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Lidocaine if frequently administered as a component of an anesthetic: for local or regional nerve blocks, to mitigate the autonomic response to laryngoscopy and tracheal intubation, to suppress the cough reflex, and for antiarrhythmic therapy. Diazepam decrease the potential central nervous system (CNS) toxicity of local anesthetic agents but -may modify the stimulant action of lidocaine in addition to their own cardiovascular depressant. The potential cardiovascular toxicity of local anesthetics may be enhanced by the concomitant administration of diazepam. This study was designed to investigate the effects of lidocaine dose and pretreated diazepam to cardiovascular system and plasma concentration of lidocaine. Lidocaine in 100 mcg/kg/min, 200 mcg/kg/min, and 300 mcg/kg/min was given by sequential infusion to dogs anesthetized with halothane-nitrous oxide (Group I). And in group II, after diazepam pretreatment, lidocaine was infused by same way when lidocaine was administered in 100 mcg/kg/min, the low plasma levels (3.97+/-0.22-4.48+/-0.36 mcg/ml) caused a little reduction in cardiovascular hemodynamics. As administered in 200 mcg/kg/min, 300 mcg/kg/min, the higher plasma levels (7.50+/-0.66-11.83+/-0.59 mcg/ml) reduced mean arterial pressure (MAP), cardiac index (CI), stroke index (SI), left ventricular stroke work index (LVSWI), and right ventricular stroke work index (PVSWI) and increased pulmonary artery wedge pressure (PAWP), central venous pressure (CVP), systemic vascular resistance index (SVRI), but was associated with little changes of heart rate (HR), mean pulmonary artery pressure (MPAP), and pulmonary vascular resistance index (PVM). When lidocaine with pretreated diazepam was administered in 100 mcg/kg/min, the low plasma level, the lower level than when only lidocaine administered reduced MAP, but was not changed other cardiovascular hemodynamics. While lidocaine was infused in 200 mcg/kg/min, 300 mcg/kg/min in dogs pretreated diazepam, the higher plasma level (7.64+/-0.79-13.79+/-0.82 mcg/ml) was maintained and was associated with reduced CI, SI, LVSWI and increased PAWP, CVP, SVRI but was a little changes of HR, MPAP, PVRI. After CaCl2 administration, CI, SI, SVRI, LVSWI was recovered but PAWP, UP was rather increased than recovered. The foregoing results demonstrate that pretreated diazepam imposes no additional burden on cardiovascular system when an infusion of large dose of lidocaine is given to dogs anesthetized with halothane and nitrous oxide. But caution may be advised if the addition of lidocaine is indicated in subjects who have impaired autonomic nervous system and who are in hypercarbic, hypoxic, or acidotic states.

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