Stroke, Vol 17, 82-85, Copyright © 1986 by American Heart Association
LA Fernandez, DD Spencer and T Kaczmar Jr
Evidence indicates that after vascular occlusion, infusion of angiotensin
II restores blood supply to ischemic tissues by stimulating the development
of collateral circulation through a mechanism independent of the mechanical
effects of increased blood pressure. To test this effect in focal cerebral
ischemia, angiotensin II was intravenously administered for four hours to
gerbils immediately after unilateral carotid ligation. Three different
pressor doses, 50, 250, and 500 ng/kg/min, were used, and mortality rate
was evaluated at 1 and 2 days after vascular occlusion. Two additional
groups similarly prepared were infused either with saline or with the
pressor agent metaraminol. There was a significant inverse relationship
between the infusion dose of angiotensin II and mortality: the greater the
infusion dose of angiotensin II, the lower the mortality rate. Infusion of
metaraminol, at the dose chosen to mimic the pressor effect of the highest
angiotensin II dose, yielded a mortality rate which was statistically
indistinguishable from that obtained with saline infusion. It is concluded
that the mortality rate after unilateral carotid occlusion is significantly
reduced by intravenous administration of angiotensin II through mechanisms
unrelated to its hypertensive action. Evidence suggests that this may occur
by the enhancement of the development of collateral circulation and
therefore the reduction of the severity of brain ischemia.
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Angiotensin II decreases mortality rate in gerbils with unilateral carotid ligation
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