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

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.