Cerebral metabolic protection in patients submitted to carotid tromboendoarterectomy (TEA) can be made by means of drugs, both in the clamping acute intraoperative phase and in the immediate post-operative period. The knowledge that DPH has the property of reducing CMRO2, the lactates production and of increasing the cerebral level of glucose, glycogen and phosphocreatinine, has persuaded us to use this drug instead of barbiturate, as a therapeutic protection to prevent hypoxic damages to the nervous cell. Our series include 12 patients submitted to carotid TEA in whom cerebral metabolic protection has been obtained by means of DPH at the dosage of 15-17 mg/kg body wt. injected intravenously in about 15' just before clamping. Using this type of pharmacologic protection, we have not observed any of the undesired effects in the cardiocirculatory system described in the literature. The prompt awakening, the absence of neurological deficits, the absence of side-effects suggest that DPH can be used to provide a cerebral metabolic protection during TEA.

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