Takei Kazuo, Araki Nobuo, Ohkubo Takeshi, Tamura Naotoshi, Yamamoto Toshimasa, Furuya Daisuke, Yanagisawa Chiaki Takano, Shimazu Kunio
Department of Neurology, School of Medicine, Saitama Medical University.
Intern Med. 2009;48(16):1357-61. doi: 10.2169/internalmedicine.48.2158. Epub 2009 Aug 17.
It is known that the risk of cerebral stroke recurrence in post-stroke patients is comparatively higher than in normal subjects, and it is suggested that autonomic nervous system dysfunctions elevate this risk. We investigated the anti-hypertensive effects of cilnidipine, a Ca antagonist which suppresses sympathetic nerve activation, in hypertensives with chronic-stage cerebrovascular disease in a comparison with amlodipine.
Amlodipine 5-7.5 mg/day, or cilnidipine 5-10 mg/day was administered to 78 hypertensive subjects (greater than 140 mmHg systolic, or 90 mmHg diastolic) undergoing outpatient treatment. Amlodipine or cilnidipine was also administered similarly, to 30 subjects having hypertension associated with a cerebral infarct which occurred more than one month earlier due to cerebral thrombosis or embolism. After 3 months administration, the subjects' blood pressures and pulse rates were recorded with an ambulatory blood pressure monitor over 24 hours.
No difference was recognized in patient age, gender, and systolic and diastolic blood pressure before treatment between the groups. In the cilnidipine groups, no difference in average 24-hour or waking systolic blood pressure values was seen between cerebrovascular disease (CVD) subjects and non-CVD subjects, although in the amlodipine groups, CVD subjects had significantly higher blood pressure values than non-CVD subjects. In the cilnidipine group, the coefficient of variation values of pulse rate were significantly higher in CVD subjects than in non-CVD subjects (p<0.05).
In patients with recent stroke, a Ca antagonist with no sympathetic nerve suppression had weaker blood pressure-lowering effects. Significantly increased pulse rate variability, shown in the CVD subjects administered cilnidipine, suggests that cilnidipine enhanced the parasympathetic function in hypertensive patients with CVD.
已知中风后患者脑卒中超复发风险较正常受试者相对更高，且提示自主神经系统功能障碍会增加此风险。我们研究了西尼地平（一种抑制交感神经激活的钙拮抗剂）对患有慢性期脑血管疾病的高血压患者的降压作用，并与氨氯地平进行比较。
对78名接受门诊治疗的高血压受试者（收缩压大于140mmHg或舒张压大于90mmHg）给予氨氯地平5 - 7.5mg/天或西尼地平5 - 10mg/天。对30名因脑血栓形成或栓塞导致脑梗死发生超过1个月且患有高血压的受试者也同样给予氨氯地平或西尼地平。给药3个月后，使用动态血压监测仪记录受试者24小时的血压和脉搏率。
两组之间患者年龄、性别以及治疗前收缩压和舒张压均无差异。在西尼地平组中，脑血管疾病（CVD）受试者与非CVD受试者之间24小时平均收缩压或清醒时收缩压值无差异，而在氨氯地平组中，CVD受试者的血压值显著高于非CVD受试者。在西尼地平组中，CVD受试者的脉搏率变异系数值显著高于非CVD受试者（p<0.05）。
在近期中风患者中，不具有交感神经抑制作用的钙拮抗剂降压效果较弱。给予西尼地平的CVD受试者中显著增加的脉搏率变异性表明，西尼地平增强了患有CVD的高血压患者的副交感神经功能。
