Journal of neurosurgery
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Nitroglycerin was given intravenously to five anesthetized, hyperventilated (PaCO2 25 to 30 torr) patients during craniotomy, to facilitate surgery by creating a relatively bloodless field, and to decrease the potential need to blood transfusion. A subarachnoid screw and an indwelling radial artery catheter were inserted to monitor intracranial pressure (ICP) and mean arterial pressure (MAP). ⋯ Cerebral perfusion pressure decreased from 90.2 +/- 3.6 (SEM) to 38.2 +/- 2.3 torr (p < 0.0005). We attribute this nitroglycerin-induced ICP increase to capacitance vessel dilation within the relatively noncompliant cranial cavity, with subsequent cerebral blood volume increase.
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Journal of neurosurgery · Sep 1980
Case ReportsElectrophysiological evaluation of phrenic nerve function in candidates for diaphragm pacing.
The electrophyisological status of phrenic nerve function has been determined by an assessment of the conduction time and diaphragm muscle action potential in patients who were being evaluated as candidates for diaphragm pacing, or who were being studied for suspected phrenic nerve injury or disease. The conduction time and muscle action potential were evoked by transcutaneous phrenic nerve stimulation or by stimulation with a permanently implanted diaphragm pacemaker. In normal volunteers the conduction time was found to be 8.40 msec +/- 0.78 msec (SD). ⋯ In patients who were selected for implantation of a diaphragm pacemaker, a conduction time that was prolonged (10 to 14 msec) preoperatively did not preclude successful diaphragm pacing. Postoperatively, a prolonged (> 10 msec) conduction time was associated with severe systemic disease or local nerve injury caused by trauma or infection. The elucidation of phrenic nerve function by such electrophysiological studies serves as a valuable adjunct to the selection and management of patients undergoing diaphragm pacing.
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Journal of neurosurgery · Sep 1980
Spinal cord energy metabolism following compression trauma to the feline spinal cord.
The purpose of this study was to determine the spinal cord metabolic state for 24 hours after compression trauma to the feline spinal cord. Cats were anesthetized with pentobarbital and injured by placing a 190-gm weight on the spinal cord for 5 minutes. Biochemical analysis of the injured segment revealed a significant depletion in the levels of adenosine triphosphate (ATP), phosphocreatine (P-creatine), and total adenylates for the entire 24-hour recovery period. ⋯ This sequence of metabolic changes suggested that metabolism was probably not homogeneous throughout the injured segment, and that tissue metabolic rate was depressed for the initial 4 hours after trauma then increased in metabolically active tissue for the remainder of the 24-hour recovery period. This model of spinal cord trauma results in a severe, prolonged ischemia and metabolic injury to the affected tissue. Whether these metabolic changes results from or cause the tissue damage and irreversible paraplegia associated with this type of spinal cord injury remains to be determined.