Morphometric study of mesenteric arteries from genetically hypertensive Dahl strain rats.
Morphometric study of mesenteric arteries from genetically hypertensive Dahl strain rats.
复制标题
遗传性高血压达尔品系大鼠肠系膜动脉的形态测量研究。
DOI：
10.1159/000158642
复制
发表时间：
1986
期刊：
影响因子：
--
通讯作者：
C. Triggle
中科院分区：
文献类型：
--
作者：
R. M. Lee;C. Triggle
在给予高盐（8%）或低盐（0.4%）饮食6-7周的盐敏感（DS）和耐盐（DR）Dahl大鼠中，对不同动脉进行光学显微镜水平的形态测量和肠系膜动脉的超微结构研究。给予高盐饮食(DS-H)的DS大鼠产生高血压，而给予低盐饮食(DS-L)的DS大鼠仅产生中度高血压。然而，给予高盐（DR-H）和低盐（DR-L）的 DR 大鼠的血压是正常的。 DS-H大鼠的肠系膜上动脉（弹性动脉）、肠系膜大动脉（肌性动脉）和肠系膜小动脉（肌性小动脉或小动脉）的中膜横截面积显着增加。在所有血管类型中，这种增加与血压的增加呈正相关。在肠系膜上动脉中，内壁增大可能是由于细胞间隙增大和/或平滑肌细胞肥大。同样，肠系膜小动脉中膜的增加可能是由于平滑肌细胞肥大所致。相反，肠系膜大动脉中膜的增加与平滑肌细胞的增生有关。 DS-H 的 3 种血管类型均发现内皮细胞损伤。各组大鼠肠系膜上动脉均发现由肌内膜细胞组成的内膜病变。我们的结果表明，这些病变形成的发生率按以下顺序较高：DS-H大于DS-L大于DR-H大于DR-L，这表明高血压程度（DS与DR大鼠）和饮食中的盐含量（DR-H与DR-L）可能是导致这些病变发生的一些因素。我们得出的结论是，由于内侧平滑肌质量（例如肌性动脉）增加而导致的动脉过度反应，和/或由于内皮细胞损伤而可能损害 DS-H 大鼠的动脉舒张能力，可能导致遗传性高血压 Dahl 模型中血压升高。
Morphometric measurements on different arteries at the light-microscopic level and ultrastructural studies of the mesenteric arteries were carried out in salt-sensitive (DS) and salt-resistant (DR) Dahl rats given a high-salt (8%) or low-salt (0.4%) diet for 6-7 weeks. Hypertension was produced in DS rats given high-salt diet (DS-H), while only moderate hypertension was produced in DS rats given low-salt diet (DS-L). Blood pressure in DR rats given high salt (DR-H) and low salt (DR-L), however, was normal. Cross-sectional area of the media was increased significantly in the superior mesenteric artery (an elastic artery), large mesenteric arteries (muscular arteries) and small mesenteric arteries (small muscular arteries or arterioles) from DS-H rats. In all the vessel types, this increase was positively correlated with the increase in blood pressure. In the superior mesenteric artery, medial wall increase was probably due to an increase in intercellular space, and/or hypertrophy of the smooth muscle cells. Similarly, increase in the media of small mesenteric arteries was probably due to hypertrophy of the smooth muscle cells. In contrast, increase in the media of large mesenteric arteries was related to hyperplasia of the smooth muscle cells. Damage to endothelial cells was noted in the 3 vessel types from DS-H. Intimal lesions composed of myointimal cells were found in the superior mesenteric arteries of all the rat groups. Our results showed that the incidence of these lesion formations was higher in the following order: DS-H greater than DS-L greater than DR-H greater than DR-L, suggesting that the degree of hypertension (DS vs. DR rats) and the amount of salt in the diet (DR-H vs. DR-L) may be some of the factors contributing to the development of these lesions. We conclude that hyperreactivity of the arteries due to increase in medial smooth muscle mass (e.g. muscular arteries), and/or probably impaired relaxation capability of the arteries in the DS-H rats due to endothelial cell damage, may contribute to the elevation of BP in the Dahl model of genetic hypertension.