Stroke, Vol 13, 759-766, Copyright © 1982 by American Heart Association
RJ Harris, NM Branston, L Symon, M Bayhan and A Watson
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.
ARTICLES
The effects of a calcium antagonist, nimodipine, upon physiological responses of the cerebral vasculature and its possible influence upon focal cerebral ischaemia
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