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高血压性血管病变的形态发生

Morphogenesis of hypertensive vascular lesions.

作者信息

Nemes Z, Mann J F, Dietz R, Lüth J B

出版信息

Br J Exp Pathol. 1982 Oct;63(5):490-500.

PMID:7171473
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2040768/
Abstract

Accelerated hypertension is a convenient model for studying the pathomechanism of hypertensive vascular lesions. It has not been settled, however, whether such lesions are really equivalent to those developing slowly in the course of experimental hypertensive vascular disease. In the present study, early vascular lesions of accelerated hypertension have been compared with those of hypertensive vascular disease by using two complementary techniques: small-molecule plasma-protein label (Ferrlecit) and a macromolecular tracer protein (horse ferritin). Two kinds of vascular lesions have been distinguished. Non-destructive vascular lesions exhibit necrotic smooth-muscle cells with intracellular deposition of Ferrlecit-labelled plasma proteins and intact basement-membrane barrier to the macromolecular tracer. Destructive vascular lesions, in turn, are characterized by the breakdown of the basement-membrane barrier to the macromolecular tracer. Incipient destructive lesions are identified as dissecting microaneurysms initiated by small ruptures of the basement membrane framework. Both non-destructive vascular lesions and incipient destructive vascular lesions end in confluent medial destruction that precedes the formation of fibrinoid necrosis. The localization and morphology of vascular lesions is identical both in hypertensive vascular disease and in accelerated hypertension. Circumstantial evidence strongly suggests that non-destructive vascular lesions are caused by arterial contraction. Nevertheless, the possibility that non-destructive lesions are but abortive forms of destructive ones cannot be excluded.

摘要

急进性高血压是研究高血压性血管病变发病机制的一个便利模型。然而,此类病变是否真的等同于实验性高血压性血管疾病过程中缓慢发展的病变,这一点尚未明确。在本研究中,通过使用两种互补技术:小分子血浆蛋白标记物(Ferrlecit)和大分子示踪蛋白(马铁蛋白),对急进性高血压的早期血管病变与高血压性血管疾病的早期血管病变进行了比较。区分出了两种血管病变。非破坏性血管病变表现为坏死的平滑肌细胞,细胞内有Ferrlecit标记的血浆蛋白沉积,且对大分子示踪物有完整的基底膜屏障。相反,破坏性血管病变的特征是对大分子示踪物的基底膜屏障破坏。初期破坏性病变被确定为因基底膜框架小破裂引发的夹层微动脉瘤。非破坏性血管病变和初期破坏性血管病变最终都会导致融合性中层破坏,这先于纤维蛋白样坏死的形成。高血压性血管疾病和急进性高血压中血管病变的定位和形态是相同的。间接证据有力地表明,非破坏性血管病变是由动脉收缩引起的。然而,非破坏性病变只是破坏性病变的未遂形式这种可能性也不能排除。

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本文引用的文献

1
ACUTE HYPERTENSIVE VASCULAR DISEASE. 2. STUDIES ON VASCULAR REACTION PATTERNS AND PERMEABILITY CHANGES BY MEANS OF VITAL MICROSCOPY AND COLLOIDAL TRACER TECHNIQUE.急性高血压性血管疾病。2. 运用活体显微镜和胶体示踪技术对血管反应模式及通透性变化的研究。
Acta Pathol Microbiol Scand. 1964;62:497-515. doi: 10.1111/apm.1964.62.4.497.
2
ISOPROTERENOL-INDUCED MYOCARDIAL NECROSIS. A HISTOCHEMICAL AND ELECTRON MICROSCOPIC STUDY.异丙肾上腺素诱导的心肌坏死。一项组织化学和电子显微镜研究。
Am Heart J. 1964 Jul;68:71-90. doi: 10.1016/0002-8703(64)90242-x.
3
ANGIOTENSIN AND RENAL VASCULAR DAMAGE.
血管紧张素与肾血管损伤。
Br J Exp Pathol. 1964 Feb;45(1):7-12.
4
Effect of angiotensin on juxtaglomerular cells and vessels of the kidney.血管紧张素对肾脏球旁细胞和血管的作用。
Circ Res. 1962 Dec;11:955-60. doi: 10.1161/01.res.11.6.955.
5
Pathologic changes induced by 1-norepineprine: quantitative aspects.
Am J Cardiol. 1960 May;5:619-27. doi: 10.1016/0002-9149(60)90127-2.
6
L-Norepinephrine myocarditis.左旋去甲肾上腺素性心肌炎
Am J Clin Pathol. 1958 Nov;30(5):425-34. doi: 10.1093/ajcp/30.5.425.
7
Vasoconstriction and increased blood pressure in the development of accelerated vascular disease.血管收缩与血压升高在加速性血管疾病发展过程中的作用。
Virchows Arch A Pathol Anat Histol. 1980;386(2):161-73. doi: 10.1007/BF00427228.
8
Medial changes in arterial spasm induced by L-norepinephrine.L-去甲肾上腺素诱导的动脉痉挛的内侧变化。
Am J Pathol. 1981 Dec;105(3):212-22.
9
Investigations of the permeability changes of the vascular wall in experimental malignant hypertension by means of a colloidal iron preparation.用胶体铁制剂对实验性恶性高血压血管壁通透性变化的研究。
Br J Exp Pathol. 1969 Feb;50(1):13-6.
10
Calcium as mediator of isoproterenol-induced myocardial necrosis.钙作为异丙肾上腺素诱导心肌坏死的介质。
Am J Pathol. 1972 Dec;69(3):459-70.