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Experimental Study

Effect of Nicardipine on Basilar Artery Vasoactive Responses after Subarachnoid Hemorrhage

Pasqualin, Alberto M.D.; Tsukahara, Tetsuya M.D.; Kassell, Neal F. M.D.; Torner, James C. Ph.D.

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THE EFFECT OF the dihydropyridine calcium antagonist, nicardipine, on the vasoactive responses of the basilar artery was investigated after subarachnoid hemorrhage (SAH). Forty-five rabbits were separated into one control group and four groups receiving SAH (nine animals each). The SAH was induced by injecting 5 ml of autologous arterial blood into the cisterna magna. SAH animals were subjected to one of the following: 1) no treatment; 2) intravenous (i.v.) saline infusion (vehicle); 3) i.v. infusion of low-dose nicardipine (0.01 mg/kg/hr), or 4) i.v. infusion of high-dose nicardipine (0.15 mg/kg/hr). The i.v. infusions were started immediately after SAH and continued for 48 hours. Serotonin (5-HT) (10−8 to 10−5 mol/L) was used to evoke dose-dependent vasoconstriction of isolated rings of the basilar artery 2 days after SAH. Acetylcholine (ACh) (10−8 to 10−4) and adenosine-triphosphate (ATP) (10−8 to 10−4 mol/L) were applied after maximal contraction with 5-HT, to evoke a dose-dependent vasodilatation. Compared with controls, in animals subjected to SAH serotonin caused similar or slightly larger contractions; nicardipine infusion did not decrease the amount of contraction observed after SAH. ACh and ATP caused significantly less dilatation in animals submitted to SAH than in controls. After high-dose nicardipine, ACh- and ATP-induced dilatations were significantly more pronounced (57% and 68% of initial contractile tone) than in the other animals receiving SAH (36%-39% and 45%-55%, respectively). It is concluded that after SAH in rabbits, nicardipine infusion does not relieve the constrictor response of the basilar artery to 5-HT; however, it does enhance the vasodilatory response to ACh and ATP.

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