EFFECTS OF ACUTELY RAISING INTRACRANIAL-PRESSURE ON CARDIAC SYMPATHETIC EFFERENT NEURON FUNCTION

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 v ascular pressure on heart rate, left atrial and left ventricular chamb er pressures, as well as right and left ventricular intramyocardial pr essures, were studied following removal of the adrenal glands from the circulation. Cardiac effects induced by systemic administration of ni cotine, tyramine or isoproterenol were investigated before and after r aising intracranial pressure: (1) in 9 dogs with neurally intact heart s in which cardiac release of catecholamines and intrinsic cardiac neu ronal activity were studied; (2) in another 8 dogs in which intrathora cic autonomic neurons were disconnected from central neurons; (3) in a nother 8 dogs after decentralizing intrathoracic sympathetic but not p arasympathetic neurons; (4) in 2 animals after decentralizing intratho racic parasympathetic, not sympathetic neurons. Results: Increasing in tracranial pressure in neurally intact preparations induced ventricula r augmentation followed by depression such that after 12 min of cerebr al ischemia left ventricular systolic pressure was 62 +/- 5 mmHg. Isop roterenol and tyramine augmented right ventricular inotropism similarl y before and after raising intracranial pressure, their effects on lef t ventricular systolic pressures being reduced secondary to the system ic vascular hypotension. Although nicotine excited intrinsic cardiac n eurons similarly before and after raising intracranial pressure, it fa iled to enhance cardiac liberation of noradrenaline after compared to before raising intracranial pressure. Nicotine-induced ventricular aug mentation was obtunded after brain death despite the fact that ventric ular myocytes underwent no detectable histological changes. In contras t, nicotine induced similar cardiac augmentation before and after rais ing intracranial pressure when intrathoracic autonomic neurons or when intrathoracic sympathetic, not parasympathetic neurons, were decentra lized. Conclusion: Cardiac sympathetic efferent neuronal function is o btunded by acutely raising intracranial pressure.