[Experimental study of the cerebrovascular effects of sodium nitroprusside in the baboon Papio papio. Its action on the experimental vasospasm].
Sodium nitroprusside (SNP) has been suggested as hypotensive agent in the surgery of cerebral aneurysms. As a preliminary step to neurosurgery, a study of its cerebro-vascular and EEG action had been carried out in 42 papio-papio baboons. On the unanaesthetized analgesic-free animal, doses below 20 mumg/kg/min. induce only a moderate decrease of mean arterial blood pressure (MABP), a slight rise of intracranial pressure (ICP) and a neat fall of cerebro-vascular resistance (CVR) without EEG modifications. Doses above 50 mumg/kg/min. induce a neat fall of MABP with a rise of cerebral blood flow (CBF), of ICP and signs of poisoning with metabolic acidosis and prolonged EEG disturbances. Beyond 90 mumg/kg/min. irreversible hypotension occured accompanied by metabolic acidosis and progressive abolition of cerebral electrogenesis. The hypotensive action of SNP is potentiated by neuroleptanalgesic drugs (phenoperidine and dehydrobenzoperidol). Using this combination marked hypotension was achieved with non toxic doses of SNP (6 to 10 mumg/kg/min.). During those hypotensions cerebral auto-regulation was maintained up to a MABP of 50 mmHg. Deeper brief hypotensions up to a MABP of 25 to 45 mmHg induce a 23% fall of CBF (p less than 0, 05) but without major EEG alterations. During experimental arterial spasms induced by injection of blood in the cisterna magna or serotonin infusion, SNP has a vasodilating action. It induces a significant rise of CBF (p less than 0, 01) for doses between 8 and 19 mumg/kg/min.