© 1995 by European Society of Cardiology
Copyright © 1995, European Society of Cardiology
Effects of acutely raising intracranial pressure on cardiac sympathetic efferent neuron function
aDepartment of Surgery, Faculty of Medicine, Dalhousie University, Halifax, N.S., B3H 4H7, Canada
bDepartment of Clinical Chemistry, Faculty of Medicine, Dalhousie University, Halifax, N.S., B3H 4H7, Canada
cDepartment of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, N.S., B3H 4H7, Canada
* Corresponding author. Tel.: (+ 1-902) 494 3517; fax: (+ 1-902) 494 1685.
Objective: To determine whether acutely raising intracranial pressure modifies the function of cardiac efferent autonomic neurons. Methods: The effects of suddenly raising intracranial pressure above systemic vascular pressure on heart rate, left atrial and left ventricular chamber pressures, as well as right and left ventricular intramyocardial pressures, were studied following removal of the adrenal glands from the circulation. Cardiac effects induced by systemic administration of nicotine, tyramine or isoproterenol were investigated before and after raising intracranial pressure: (1) in 9 dogs with neurally intact hearts in which cardiac release of catecholamines and intrinsic cardiac neuronal activity were studied; (2) in another 8 dogs in which intrathoracic autonomic neurons were disconnected from central neurons; (3) in another 8 dogs after decentralizing intrathoracic sympathetic but not parasympathetic neurons; (4) in 2 animals after decentralizing intrathoracic parasympathetic, not sympathetic neurons. Results: Increasing intracranial pressure in neurally intact preparations induced ventricular augmentation followed by depression such that after 12 min of cerebral ischemia left ventricular systolic pressure was 62 ± 5 mmHg. Isoproterenol and tyramine augmented right ventricular inotropism similarly before and after raising intracranial pressure, their effects on left ventricular systolic pressures being reduced secondary to the systemic vascular hypotension. Although nicotine excited intrinsic cardiac neurons similarly before and after raising intracranial pressure, it failed to enhance cardiac liberation of noradrenaline after compared to before raising intracranial pressure. Nicotine-induced ventricular augmentation was obtunded after brain death despite the fact that ventricular myocytes underwent no detectable histological changes. In contrast, nicotine induced similar cardiac augmentation before and after raising intracranial pressure when intrathoracic autonomic neurons or when intrathoracic sympathetic, not parasympathetic neurons, were decentralized. Conclusion: Cardiac sympathetic efferent neuronal function is obtunded by acutely raising intracranial pressure.
KEYWORDS Adrenergic receptors; Brain death; Cardiac neurons; Isoproterenol; Nicotine; Tyramine; Dog, anesthetized
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