Schäfer M K, Eberle B, Otto S, Jantzen J P, Dick W
Klinik für Anästhesiologie der Johannes Gutenberg-Universität, Mainz.
Anaesthesist. 1999 Apr;48(4):218-23. doi: 10.1007/s001010050693.
The cardiotoxic properties of bupivacain have been well documented under in-vitro, as well as under in-vivo conditions. A further mechanism of cardiovascular impairment by bupivacaine via the central nervous system gained investigational interest in animal studies. The aim of our study was to demonstrate the effect of a ventriculocisternal perfusion of bupivacain on systemic hemodynamic variables and their reversibility by wash-out with mock-CSF.
After obtaining animal investional committee consent, nine anaesthetized and relaxed pigs were prepared for a ventriculocisternal perfusion (VCP). Hemodynamic data were obtained by invasive blood pressure measurements in the high and low pressure system as well as cardiac output (thermodilution technique), intracranial pressure and electrocardiogram. Systemic vascular resistance and stroke volume were calculated using standard formulas. A second group of three animals were exposed to an intravenous infusion of the same dose of bupivacain over the same period of time to rule out direct cardiac effects. After instrumentation baseline data were obtained (K0 1) under VCP with mock-CSF for 30 minutes. The mock-CSF was replaced by 0.05% bupivacaine in mock-CSF and VCP was continued with 3 ml.h-1 for 20 minutes. After administration of 500 micrograms bupivacaine data were collected (BU). The bupivacaine solution was replaced by mock-CSF and after twenty minutes hemodynamic measurement were repeated (K02).
The intravenous administration of 500 micrograms bupivacaine had no effect on all measured variables. VCP of the same dose resulted in significant increase in heart rate, systolic, diastolic and mean arterial blood pressures. Left and right heart filling pressures as well as systemic vascular resistance were not affected while the stroke volume decreased. After continuation of VCP with mock-CSF hemodynamic changes were reversed.
Our results demonstrate that bupivacaine initiates an indirect cardiovascular stimulating effect of a VCP with 500 micrograms of bupivacaine via the central nervous system. The intravenous administration of the same dose had no effect. The centrally mediated cardiovascular effect of bupivacaine was reversed by wash-out with mock-CSF. The cardiovascular stimulation observed in this animal experiment may be of clinical relevance as a potential sign of toxic effects of bupivacaine on the CNS.