[Protective effect of labetalol on cardiovascular consequences of brain death in the swine]

Abstract

Objective: Assessment of the preventive effect on cardiovascular changes following experimental brain death (BD) in the pig by pretreatment with labetalol, an alpha and beta adrenoreceptor blocking agent.

Study design: Experimental study.

Animals: Ten 25-35 kg domestic pigs allocated either in the control group (n = 5) or the labetalol group (n = 5).

Methods: BD was achieved in anaesthetized animals by the rapid inflation of a Foley catheter inserted into the sub-dural space. In the labetalol group, the agent (total: 10 +/- 3 mg.kg-1) was administered immediately before BD and thereafter over a 20-min period, in order to maintain haemodynamic parameters at control values. The following haemodynamic data were recorded over a 3 hour period after BD: heart rate (HR), dP/dtmax, mean arterial pressure (MAP), pulmonary capillary wedge pressure (PCWP), cardiac output (CO) and left anterior descending coronary artery blood flow (CBF). Afterwards, a dynamic loading test with 500 mL of dextran over 20 min was performed.

Results: In the control group, BD elicited a significant increase in HR (from de 96 +/- 9 to 176 +/- 11 b.min-1), dP/dtmax (from 1,960 +/- 123 to 4,904 +/- 930 mmHg.s-1), MAP (from 88 +/- 5 to 119 +/- 11 mmHg), CO (from 2.4 +/- 0.2 to 3.6 +/- 0.7 L.min-1) and CBF (from 45 +/- 6 to 73 +/- 7 mL.min-1) respectively. Apart from a slight increase in HR and a significant increase in CBF (from 34 +/- 4 to 55 +/- 6 mL.min-1), no other modifications occurred in the labetalol group. Following volume expansion, the labetalol group animals experienced a significant increase in CO (from 2.3 +/- 0.3 to 3.7 +/- 0.2 L.min-1), dP/dtmax (from 1,400 +/- 91 to 2,100 +/- 212 mmHg.s-1) and MAP (from 55 +/- 5 to 70 +/- 5 mmHg). In the opposite, a significant decrease in dP/dtmax (from 1,645 +/- 450 to 628 +/- 152 mmHg.s-1) occurred in the control group.

Conclusion: The protective effect of labetalol confirms the role played by the activation of the cardiac sympathetic nervous system in the cardiocirculatory changes following BD.