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Protective effects of thiopental, mannitol, and glycerol on global cerebral ischemia were neu rophysiologically investigated.<BR> Global cerebral ischemia was produced for 20 or 30 minutes in cats by temporary intrathoracic clamping of the innominate and left subclavian arteries following previous ligation of the mammary arteries and simultaneous lowering of the systemic arterial blood pressure. Thiopental, mannitol, or glycerol was rapidly given by intravenous infusion over 20 minutes; two thirds of the total dosage prior to ischemia and the remaining one third during ischemia. The measurement of recovery of neuronal functions after ischemia was assessed by electroencephalograms (EEG), somatosensory evoked potentials (SEP), and neurologic conditions. All 6 animals which received no treatment and were subjected to is chemia for 20 or 30 minutes did not show any recovery of neurologic condition after cerebral ischemia, showed no reappearance of EEG activity or discernible response of SEP, and died within 2 hours following cerebral ischemia. In contrast, about half of the 28 animals which were treated with these agents and subjected to ischemia for 20 (n = 12) or 30 (n = 1) minutes significantly recovered all parameters of neuronal functions monitored, which was Grade 3 or better. There was little difference in neuronal recovery among these agents, and neuronal functions recovered better with thiopental-mannitol or thiopental-glycerol combinations than with thiopental alone. Thiopental, mannitol, and glycerol had neurophysiologically significant protective effects on cerebral ischemia.

Protective Effects of Barbiturate, Mannitol and Glycerol on Experimental Global Cerebral Ischemia (Part II)