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Effects of AE0047, a calcium antagonist, on cerebral circulation and brain edema formation after middle cerebral artery occlusion in cats
AE0047 (AE) is a new type of dihydropyridine calcium anatagonist with long lasting antihypertensive effects. We examined the effects of AE on the hemodynamic consequences of and edema formation after middle cerebral artery occlusion (MCAO) in anesthetized cats, and compared its efficacy with that of...
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Published in: | Japanese Journal of Pharmacology 1994, Vol.64 (suppl.1), p.132-132 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Citations: | Items that cite this one |
Online Access: | Get full text |
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Summary: | AE0047 (AE) is a new type of dihydropyridine calcium anatagonist with long lasting antihypertensive effects. We examined the effects of AE on the hemodynamic consequences of and edema formation after middle cerebral artery occlusion (MCAO) in anesthetized cats, and compared its efficacy with that of nilvadipine (NIL) and nicardipine (NIC). Cortical blood flow (CBF) was measured by the H_2 clearance method at 5 ipsilateral and 1 contralateral sites in the area served by the MCA before and during 4 h of ischemia. CBF was classified according to the severity of CBF reduction at 15 min after MCAO (i.e., ischemic or oligemic area). Water content (WC) of the cortical tissue around each electrode was estimated by the dry weight method after killing the animal. Both AE (10 μg/kg) and NIL (30 μg/kg), given iv 20 min after MCAO, caused an approximate 10% hypotensive response and significantly increased CBF, in ischemic and oligemic areas as well as in contralateral areas, compared to the vehicle group. However, NIC (5 μg/kg bolus followed by infusion of 3 μg/kg/min) failed to mitigate the reduction of CBF, despite a marked increase in the CBF of the contralateral cortex. In addition, AE prevented an increase in cortical WC in ischemic areas, whereas the WC in both the NIL and NIC groups increased. These results demonstrate that administration of AE, after induction of ischemia by MCAO, ameliorates the reduction in CBF without concomitant aggravation of the brain edema. AE may prevent the development of brain edema through a mechanism independent of its hemodynamic effects. |
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ISSN: | 0021-5198 |
DOI: | 10.1016/S0021-5198(19)50169-X |