Gaevyĭ M D, Pavlova L I
Biull Eksp Biol Med. 1978 Apr;85(4):434-6.
Acute experiments were conducted on anesthetized cats; verapamil in a dose of 0.05, 0.1, 0.5, and 1 mg/kg, injected intravenously, caused a reduction of the tone of the cerebral vessels and of the general arterial pressure. Changes in the volume velocity of the cerebral circulation were phasic in character and depended on the tone of the cerebral vessels and the arterial pressure level. The circulation increased more in the cerebral cortex than in the reticular formation; PO2 correlated with the circulation in the cerebral cortex. The diameter of the pial arteries became greater both in case of the intravascular verapramil administration and its local application. The block of beta-adrenoceptors, M-cholinoreceptors, histamine receptors and preliminary administration of the sympatholytic failed to eliminate the vasodilatory action of verapamil. It is supposed that vasodilation was myotropic in character, and was possible connected with the electrolyte metabolism.
在麻醉猫身上进行了急性实验;静脉注射剂量为0.05、0.1、0.5和1毫克/千克的维拉帕米,可导致脑血管张力和全身动脉压降低。脑循环容积速度的变化具有阶段性,取决于脑血管张力和动脉压水平。大脑皮质的循环增加比网状结构更多;PO2与大脑皮质的循环相关。无论是血管内给予维拉帕米还是局部应用,软脑膜动脉的直径都会变大。阻断β-肾上腺素能受体、M-胆碱能受体、组胺受体以及预先给予交感神经阻滞剂均未能消除维拉帕米的血管舒张作用。据推测,血管舒张具有肌源性特征,可能与电解质代谢有关。