The effects of a calcium antagonist (nimodipine) on basal cerebral blood flow and reactivity to various agonists.
In vitro studies suggest that cerebrovascular contraction is more dependent on the influx of calcium to smooth muscle than general systemic arteries. The present study tested the in vivo effects of a calcium influx blocker (nimodipine) on cerebral blood flow and metabolism in 16 baboons. The 133xenon clearance technique was used together with careful control of EEG and blood gases. With normal blood gases intravenous nimodipine infusion (1 microgram/kg/min) produced an 18% increase in cerebral blood flow with no alteration in cerebral oxidative metabolism or blood pressure. Higher doses (above 10 micrograms/kg/min) resulted in a decreased arterial blood pressure and a return to control cerebral flow. Infusion of the dose producing maximal increase in flow, decreased the cerebral reactivity to altered PCO2 (n = 5). These results suggest that nimodipine may be a relatively selective cerebrovascular dilator.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001921:Brain / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D002245:Carbon Dioxide / Q000502:physiology; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D004569:Electroencephalography; D006985:Hyperventilation / Q000503:physiopathology; D009539:Nicotinic Acids / Q000494:pharmacology*; D009553:Nimodipine; D010101:Oxygen Consumption / Q000187:drug effects; D010215:Papio; D012701:Serotonin / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects
D002121:Calcium Channel Blockers; D009539:Nicotinic Acids; D002245:Carbon Dioxide; D012701:Serotonin; D009553:Nimodipine; D002118:Calcium