Анналы клинической и экспериментальной неврологии (Mar 2018)
Pharmacological correction of cerebrovascular disorders in various experimental pathological conditions
Abstract
Abstract Introduction. In the treatment of patients with cerebrovascular disorders, pharmacological correction of cerebral circulation largely depends on the character and the state of the pathological process. This determines the need to study the pharmacological regulation of the cerebral blood supply in various pathological conditions. Objective. To study the effects of oxymethylethylpiridine succinate, nicotinoyl gamma-aminobutiric acid, nimodipine, amlodipine besylate and S-amlodipin nicotinate on the cerebral circulation of intact and ischemic rats, and to assess the effects of oxymethylethylpiridine succinate and nimodipine in experimental myocardial infarction and combined vascular pathology of the brain and heart. Materials and methods. The cerebral circulation was evaluated using the laser Doppler flowmetry technique. Global transient ischemia was caused by occlusion of both common carotid arteries with simultaneous decrease in arterial pressure by bleeding and subsequent reinfusion. Experimental myocardial infarction was modeled by occlusion of the left coronary artery. Results. Oxymethylethylpiridine succinate significantly increases blood supply to the brain in rats under conditions of global transient ischemia of the brain and combined vascular pathology of the brain and heart, in contrast with intact animals and animals with experimental myocardial infarction. Nicotinoyl gamma-aminobutiric acid equally increased blood circulation of the intact and the ischemic brain. Nimodipine equally increased cerebral blood flow in intact rats and in rats underwent brain ischemia, whereas this effect was significantly weakened in experimental myocardial infarction and disappeared in combined vascular pathology. S-amlodipin nicotinate and, to a lesser extent, amlodipine bisilate increased blood supply to the ischemic brain. The vasodilating effects of oxymethylethylpiridine succinate, nicotinoyl gamma-aminobutiric acid and S-amlodipin nicotinate, but not of nimodipine, were eliminated by GABAA receptor blockers. Conclusions. The dependence of the vasodilating effect of the studied drugs on the initial state of the organism was revealed. This phenomenon should be taken into account in prescribing target pathogenetic therapy of ischemic stroke.
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