The effects of a calcium antagonist, nimodipine, upon physiological responses of the cerebral vasculature and its possible influence upon focal cerebral ischaemia.
The effects of a calcium antagonist, nimodipine, were tested on the response of the cerebral circulation to arterial pCO2 and blood pressure changes. The effects of reduced blood flow upon oedema formation and extracellular ion homeostasis under nimodipine preloading were studied. Both open and closed skull primate models were used, with alpha-chloralose anaesthesia. Nimodipine infusion increased basal blood flow in the open skull, but not the closed skull animals. Autoregulation to increased blood pressure was little affected. Responses to arterial pCO2 changes and autorerulation to reduced blood pressure were severely imparied. Residual blood flow after middle cerebral artery occlusion was significantly higher with nimodipine than in controls. The threshold levels of blood flow for the development of cortical oedema and for disturbance of ion homeostasis were, however, increased, suggesting that nimodipine interferes with cellular energy metabolism and increases the susceptibility of tissue to ischaemic damage.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001929:Brain Edema / Q000503:physiopathology; D002545:Brain Ischemia / Q000503:physiopathology; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D002245:Carbon Dioxide / Q000097:blood; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D004734:Energy Metabolism / Q000187:drug effects; D006706:Homeostasis / Q000187:drug effects; D009539:Nicotinic Acids / Q000494:pharmacology*; D009553:Nimodipine; D010215:Papio; D014882:Water-Electrolyte Balance / Q000187:drug effects
D002121:Calcium Channel Blockers; D009539:Nicotinic Acids; D002245:Carbon Dioxide; D009553:Nimodipine