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Richard M. Lehman

The rapid advances in the technology of, and accumulation of pertinent data in, electrophysiological testing has increased exponentially in the past decade. This is attributable to continued advances in computer technology, biomedical engineering, and now the coregistration of the electrophysiological data with neuroimaging results. Knowledge of normal function and electrophysiological response at rest or on stimulation of the central and peripheral nervous systems is important to the neurosurgeon. Only by a basic understanding of normal and abnormal recordings may diagnoses and localizations be achieved. Intraspinal and intracranial surgical procedures are predicated on nontrauma to the neuraxis. This can be accomplished by performing electrophysiological testing to monitor the function of the spinal and cranial nerves, spinal cord, brainstem, basal ganglia, and cerebrum. If the surgeon cannot delineate critical cortex or pathways, he or she will be unable to avoid these areas in the patient.

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Shigeru Fujiwara, Neal F. Kassell, Tomio Sasaki, Tadayoshi Nakagomi and Richard M. Lehman

✓ The effect of hemoglobin on endothelium-dependent vasodilation of the isolated rabbit basilar artery was examined using an isometric tension recording method. Acetylcholine (ACh) (10−7−10−4 M) evoked a dose-dependent vasodilation of isolated rabbit basilar artery previously contracted by 10−6 M serotonin. This vasodilating action disappeared after removal of the endothelium. The ACh-induced vasodilation of rabbit basilar artery is thought to be strictly endothelium-dependent. Hemoglobin (10−7-10−5 M) inhibited this ACh-induced endothelium-dependent vasodilation conditional upon the dose. Adenosine triphosphate (ATP, 10−7-10−4 M) also relaxed isolated rabbit basilar artery already contracted by 10−6 M serotonin. This vasodilating action was slightly inhibited by adenosine antagonist, 8-phenyltheophylline (8-PT), and markedly attenuated by removal of the endothelium. This ATP-induced vasodilation is thought to be composed of ATP itself (endothelium-dependent) and ATP degradation products (endothelium-independent) such as adenosine monophosphate or adenosine. Hemoglobin markedly inhibited ATP-induced vasodilation, but there still remained a small vasodilation, which was blocked by 8-PT. Papaverine-induced vasodilation was not affected by removal of the endothelium, and hemoglobin did not inhibit the papaverine-induced vasodilation. These results suggest that rabbit basilar artery has endothelium-dependent vasodilating mechanisms induced by ACh and ATP, and that hemoglobin selectively blocks the endothelium-dependent vasodilation. This finding may relate to the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage: there is a possibility that the presence of hemoglobin released from lysed erythrocytes inhibits the endothelium-dependent vasodilation of cerebral arteries; furthermore, the endothelial degeneration following subarachnoid hemorrhage may impair the vasodilating mechanisms of cerebral artery smooth-muscle cells.