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自发性高血压大鼠红细胞滤过功能受损的研究:镍滤过技术的应用。

Impaired erythrocyte filterability of spontaneously hypertensive rats: investigation by nickel filtration technique.

机构信息

Department of Medicine & Biosystemic Science, Kyushu University, Japan.

出版信息

Circ J. 2010 Jan;74(1):129-36. doi: 10.1253/circj.cj-09-0252. Epub 2009 Dec 2.

DOI:10.1253/circj.cj-09-0252
PMID:19952438
Abstract

BACKGROUND

Deformability of erythrocytes plays a key role in the impairment of the microcirculation in hypertension. However, erythrocyte deformability in spontaneously hypertensive rats (SHR) during development of hypertension has not been fully investigated so far.

METHODS AND RESULTS

Erythrocyte filterability (whole cell deformability) was investigated in relation to blood pressure measured by the tail-cuff method in SHR and age-matched Wistar-Kyoto rats (WKY), using a highly sensitive and reproducible nickel mesh filtration technique. Impaired erythrocyte filterability was marked (37.0+/-17.5%) in prehypertensive young SHR (7 weeks of age) and sustained (51.6+/-13.3%) in hypertensive mature SHR (18 weeks of age), when compared with that of age-matched WKY (62.1+/-7.2% in 7 weeks of age, P<0.005, and 71.1+/-3.9% in 18 weeks of age, P<0.005, respectively). This impairment in SHR could not be explained by the mean corpuscular volume or mean corpuscular hemoglobin concentration of erythrocytes, but the erythrocyte count was significantly (P<0.005) greater in SHR than in the age-matched WKY.

CONCLUSIONS

Although the precise mechanisms remain to be elucidated, markedly impaired erythrocyte filterability in SHR is considered to contribute to the development and maintenance of genetic hypertension. (Circ J 2010; 74: 129 - 136).

摘要

背景

红细胞的变形能力在高血压患者的微循环损伤中起着关键作用。然而,目前为止,自发性高血压大鼠(SHR)在高血压发展过程中的红细胞变形能力尚未被充分研究。

方法和结果

采用高度敏感和可重复的镍网过滤技术,在 SHR 和年龄匹配的 Wistar-Kyoto 大鼠(WKY)中,通过尾套法测量血压,研究红细胞滤过性(全细胞变形能力)与血压的关系。在年轻的预高血压 SHR(7 周龄)中,红细胞滤过性受损明显(37.0+/-17.5%),在高血压成熟 SHR(18 周龄)中持续受损(51.6+/-13.3%),与年龄匹配的 WKY 相比(7 周龄时为 62.1+/-7.2%,P<0.005,18 周龄时为 71.1+/-3.9%,P<0.005)。这种 SHR 中的红细胞滤过性受损不能用红细胞的平均细胞体积或平均细胞血红蛋白浓度来解释,但 SHR 的红细胞计数明显(P<0.005)高于年龄匹配的 WKY。

结论

尽管确切的机制仍有待阐明,但 SHR 中明显受损的红细胞滤过性被认为有助于遗传高血压的发展和维持。(Circ J 2010; 74: 129 - 136)。

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