Hemodynamic effects of a ventriculocisternal perfusion of bupivacaine

Objectives: The cardiotoxic properties of bupivacain have been well documen ted under in-vitro, as well as under in-vivio conditions. A further mechani sm of cardiovascular impairment by bupivacaine via the central nervous syst em gained investigational interest in animal studies. The aim of our study was to demonstrate the effect of a ventriculocisternal perfusion of bupivac ain on systemic hemodynamic variabels and their reversability by wash-out w ith mock-CSF. Methods: After obtaining animal investional commitee consent, nine anaesthe tized and relaxated pigs were prepared fora ventriculocisternal perfusion ( VCP). Hemodynamic data were obtained by invasive blood pressure measurement s in the high and low pressure system as well as cardiac output (thermodilu tion technique), intracranial pressure and electrocardiogram. Systemic vasc ular 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 (KO 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 minu tes. After adminstration of 500 mu g bupivacaine data were collected (BU). The bupivacaine solution was replaced by mock-CSF and after twenty minutes hemodynamic measurement were repeated (K02). Results: The intravenous adminstration of 500 mu g bupivacaine had no effec t on all measured variables. VCP of the same dose resulted in significant i ncrease in heart rate, systolic, diastolic and mean arterial blood pressure s. Left and right heart filling pressures as well as systemic Vascular resi stance were not affected while the stroke volume decreased. After continuat ion of VCP with mock-CSF hemodynamic changes were reversed. Discussion: Our results demonstrate that bupivacaine initiates an indirect cardiovascular stimulating effect of a VCP with 500 mu g of bupivacaine via the central nervous system. The intravenous administration of the same dos e had no effect. The centrally mediated cardiovascular effect of bupivacain e was reversed by wash-out with mock-CSF. The cardiovascular stimulation ob served in this animal experiment may be of clinical relevance as a potentia l sign of toxic effects of bupivacaine on the CNS.