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卡托普利对自发性高血压大鼠遗传性高血压的血管影响

[Vascular effects of captopril in the prevention of genetic hypertension in the spontaneously hypertensive rat].

作者信息

Freslon J L, Arbeille-Brassart B, Giudicelli J F

出版信息

Arch Mal Coeur Vaiss. 1982 Jun;75 Spec No:45-9.

PMID:6214232
Abstract

Captopril (100 mg/kg, q.d., orally, from the 6th week of age) strongly inhibits genetic hypertension development (GHD) and this effect persists up to 12 weeks after treatment discontinuation. However, during these 12 weeks, systolic blood pressure and heart weight/body weight ratio (HW/BW) show a similar trend to slowly increase. We have investigated whether identical phenomena develop at the vascular level. Captopril strongly increased vascular mesenteric compliance, reduced aortic wall weight, mesenteric arterial wall lumen ratio and active contractile ability during treatment period and these effects were still observed up to 7 weeks after treatment interruption although there was a slight but progressive reduction in their intensity. Thus captopril opposes the structural and functional vascular and cardiac alterations which accompany GHD and this effect contributes to a large extent to the long-lasting preventive effects of the drug against GHD.

摘要

卡托普利(100毫克/千克,每日一次,口服,从6周龄开始)强烈抑制遗传性高血压的发展(GHD),且这种作用在停药后持续长达12周。然而,在这12周内,收缩压和心脏重量/体重比(HW/BW)呈现出缓慢上升的相似趋势。我们研究了在血管水平是否会出现相同的现象。在治疗期间,卡托普利显著增加了肠系膜血管顺应性,降低了主动脉壁重量、肠系膜动脉壁腔比和主动收缩能力,尽管这些作用的强度有轻微但逐渐的降低,但在治疗中断后长达7周仍可观察到。因此,卡托普利对抗了伴随GHD的血管和心脏结构及功能改变,并且这种作用在很大程度上促成了该药物对GHD的长期预防效果。

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