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Cardiovascular Research 1998 38(1):107-115; doi:10.1016/S0008-6363(97)00284-8
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

The effect of brain death on cardiovascular function in rats. Part II. The cause of the in vivo haemodynamic changes

Paul Herijgers and Willem Flameng*

Centre for Experimental Surgery and Anaesthesiology, K.U. Leuven, Provisorium I, Minderbroedersstraat 17, B-3000 Leuven, Belgium

* Corresponding author. Tel.: +32 (16) 337298; Fax: +32 (16) 337855.

Objective: Brain death-induced haemodynamic collapse in rats is not caused by intrinsic myocardial damage as shown in the accompanying paper. We investigated whether this collapse could be caused by the withdrawal of the basal adrenergic tone. Methods: Heart rate and blood pressure variability was studied in rats before and after brain death. The effect of high doses of phentolamine, propranolol or their combination administered before or after brain death was assessed. Results: Heart rate variability in the respiratory frequency range significantly increased, whereas in the low-frequency range it tended to decrease after brain death. Systolic and diastolic blood pressure variability up to 0.18 Hz largely disappeared, but stayed unchanged in the respiratory frequency range. High-dose combined phentolamine and propranolol pretreatment induced a haemodynamic picture comparable to the situation seen after brain death without pharmacological intervention. Brain death did not further deteriorate the haemodynamic situation after combined pretreatment. On the other hand, once the haemodynamic collapse after brain death had settled, adrenergic blockade had no important influence any more. Conclusion: We conclude that the haemodynamic situation seen after brain death is one of profound sympathetic withdrawal.

KEYWORDS Rat; Brain death; Haemodynamic collapse; Adrenergic system; Autonomic nervous system; Heart rate variability


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