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依那普利治疗新西兰遗传性高血压大鼠对阻力动脉的重塑作用。

Remodelling of resistance arteries by treatment with enalapril in the New Zealand genetically hypertensive rat.

作者信息

Ledingham J M, Phelan E L, Cross M, Laverty R, Millar J A

机构信息

Department of Pharmacology, University of Otago Medical School, Dunedin, New Zealand.

出版信息

Clin Exp Pharmacol Physiol. 1994 Mar;21(3):235-7. doi: 10.1111/j.1440-1681.1994.tb02504.x.

DOI:10.1111/j.1440-1681.1994.tb02504.x
PMID:8076428
Abstract
  1. New Zealand genetically hypertensive (GH) rats were treated with enalapril from the age of 4 to 10 weeks and the effects of treatment on the structure of mesenteric resistance arteries (MRA) was measured by use of stereological analysis of stained sections and by myograph techniques. 2. Tail-cuff blood pressure (BP) was measured weekly and intra-arterial BP recorded just before MRA were either fixed by perfusion or mounted on a myograph. 3. Stereological techniques (Cavalieri and optical dissector) were used to determine media and lumen volume, fraction of smooth muscle (SM) within the media and SM cell density. For MRA mounted on the myograph, lumen diameter, media thickness, active tension and active pressure were recorded. 4. BP was significantly (P < 0.0001) lowered by enalapril throughout the experiment. Intraarterial BP and left ventricular (LV) mass were also significantly lower in the enalapril treated GH rats (P < 0.0001). 5. Stereological measurements showed that enalapril treatment significantly (P < 0.0001) reduced media volume by 50%, doubled lumen volume (P < 0.0001), reduced the fraction of SM in the media (P < 0.04), and had no effect on the number of SM cell layers or on SM cell density. 6. Myograph measurements showed a decrease in the ratio media thickness/lumen diameter which was accompanied by a decrease in maximum active tension and pressure development. 7. In the GH rat early treatment with enalapril causes a true loss of medial tissue that is not simply due to rearrangement of existing media around an enlarged lumen.(ABSTRACT TRUNCATED AT 250 WORDS)
摘要
  1. 对新西兰遗传性高血压(GH)大鼠从4周龄至10周龄给予依那普利治疗,并通过对染色切片进行体视学分析以及采用肌动描记法技术来测量治疗对肠系膜阻力动脉(MRA)结构的影响。2. 每周测量尾套血压(BP),并在MRA通过灌注固定或安装在肌动描记器上之前记录动脉内血压。3. 采用体视学技术(卡瓦列里法和光学分割器法)来确定中膜和管腔体积、中膜内平滑肌(SM)的比例以及SM细胞密度。对于安装在肌动描记器上的MRA,记录管腔直径、中膜厚度、主动张力和主动压力。4. 在整个实验过程中,依那普利使BP显著降低(P < 0.0001)。在接受依那普利治疗的GH大鼠中,动脉内血压和左心室(LV)质量也显著降低(P < 0.0001)。5. 体视学测量表明,依那普利治疗使中膜体积显著减少(P < 0.0001)达50%,管腔体积增加一倍(P < 0.0001),中膜内SM比例降低(P < 0.04),并且对SM细胞层数或SM细胞密度没有影响。6. 肌动描记法测量显示中膜厚度/管腔直径的比值降低,同时最大主动张力和压力的产生也降低。7. 在GH大鼠中,早期用依那普利治疗会导致中膜组织真正减少,这并非仅仅是由于围绕扩大的管腔对现有中膜进行重新排列所致。(摘要截短于250字)

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