Takayasu M, Bassett J E, Dacey R G
Division of Neurological Surgery, University of North Carolina, Chapel Hill.
J Neurosurg. 1988 Jul;69(1):104-9. doi: 10.3171/jns.1988.69.1.0104.
There is no direct information on the effect of calcium antagonists on intracerebral penetrating arterioles, which are responsible for a significant part of total cerebrovascular resistance. In a study on rats, the effects of four calcium antagonists (diltiazem, verapamil, nifedipine, and nimodipine) on isolated intracerebral penetrating arterioles with mean resting diameters (+/- standard error of the mean) of 52.3 +/- 3.0 micron were investigated. Vessel diameters were monitored in vitro by means of a video microscope dimensional analyzer under constant transmural pressure (60 mm Hg) after cannulation. Each calcium antagonist produced maximal dilation of about 50% (diltiazem 46.4% +/- 5.6%, verapamil 53.1% +/- 6.0%, nifedipine 46.9% +/- 6.1%, and nimodipine 47.1% +/- 5.4%) with varied sensitivity (median effective dose (ED50): diltiazem 1.52 X 10(-6) M, verapamil 1.08 X 10(-7) M, nifedipine 8.65 X 10(-9) M, and nimodipine 1.62 X 10(-9) M). Dilation effects persisted for a significantly longer time after washout with calcium antagonists such as diltiazem (15.5 +/- 1.8 minutes), nifedipine (19.0 +/- 3.9 minutes), and nimodipine (30.0 +/- 1.6 minutes) than after washout with adenosine (8.5 +/- 1.0 minutes). It appeared that the magnitude of vasodilation was greater and the duration of dilation after washout longer in intracerebral penetrating arterioles than that reported for pial arterioles, although sensitivity to each calcium antagonist was quite similar to that reported for larger cerebral arteries. These data provide a possible explanation for the apparent disparity between clinical efficacy and angiographically determined vessel diameter when patients with cerebral vasospasm are treated with calcium antagonists. These agents may have a greater effect on intracerebral penetrating arterioles than on angiographically visible larger arteries.
关于钙拮抗剂对脑内穿通小动脉的影响尚无直接信息，而脑内穿通小动脉在总脑血管阻力中占很大一部分。在一项对大鼠的研究中，研究了四种钙拮抗剂（地尔硫卓、维拉帕米、硝苯地平、尼莫地平）对平均静息直径（±平均标准误差）为52.3±3.0微米的离体脑内穿通小动脉的影响。插管后，在恒定跨壁压力（60毫米汞柱）下，通过视频显微镜尺寸分析仪在体外监测血管直径。每种钙拮抗剂均产生约50%的最大扩张（地尔硫卓46.4%±5.6%，维拉帕米53.1%±6.0%，硝苯地平46.9%±6.1%，尼莫地平47.1%±5.4%），且敏感性各异（半数有效剂量（ED50）：地尔硫卓1.52×10⁻⁶M，维拉帕米1.08×10⁻⁷M，硝苯地平8.65×10⁻⁹M，尼莫地平1.62×10⁻⁹M）。用钙拮抗剂如地尔硫卓（15.5±1.8分钟）、硝苯地平（19.0±3.9分钟）和尼莫地平（30.0±1.6分钟）冲洗后，扩张效应持续的时间明显长于用腺苷冲洗后（8.5±1.0分钟）。似乎脑内穿通小动脉的血管扩张幅度更大，冲洗后的扩张持续时间更长，尽管对每种钙拮抗剂的敏感性与较大脑动脉的报道相当。这些数据为脑血管痉挛患者接受钙拮抗剂治疗时临床疗效与血管造影确定的血管直径之间明显的差异提供了一种可能的解释。这些药物对脑内穿通小动脉的作用可能比对血管造影可见的较大动脉的作用更大。
