PATHOGENESIS OF HYPERTENSIVE RETINOPATHY - EXPERIMENTAL STUDY IN MONKEY
PATHOGENESIS OF HYPERTENSIVE RETINOPATHY - EXPERIMENTAL STUDY IN MONKEY
复制标题
DOI：
10.1136/bjo.59.1.3
复制
发表时间：
1975-01-01
影响因子：
4.1
通讯作者：
DOLLERY, CT
中科院分区：
文献类型：
--
作者：
GARNER, A;ASHTON, N;DOLLERY, CT
本文用活体检眼镜、彩色和荧光照相法，以及处死后的注射和消化液、光镜和电镜，观察了17只实验性高血压猴在加速性高血压时视网膜的变化。除三只猴子外，所有猴子都出现了棉絮状斑点。在高血压动物中，动脉变得扭曲和扩张，对光反射下降。最早的异常是在终末小动脉或小动脉上出现许多荧光素渗漏点。这种泄漏点总是与棉絮点有关，但并不局限于这些区域。未观察到动脉局灶性狭窄，但3只动物存在小动脉闭塞和远端节段逆行充盈。在5只动物中观察到浅表线性出血。光学显微镜检查发现棉絮样斑点，与在人体中观察到的斑点相同，有大量肿胀的轴突，其中含有染色密集的轴突核。通过电子显微镜对小动脉的研究显示了从正常到广泛坏死的结果。许多毛细血管前动脉收缩，有些几乎闭塞。许多收缩的小动脉壁中的平滑肌细胞存在退行性变化。许多动脉也显示出渗入肌层的血浆流入血管壁，有时甚至完全取代了平滑肌细胞。除了晚期坏死的小动脉外，没有迹象表明血浆溢出是如何发生的。两个广泛坏死的小动脉显示内皮细胞胞质内的断裂，可能发生了血浆蛋白的渗透。血管外组织显示无定形物质的集合，其中一种具有典型的纤维蛋白带状结构。提出的解释这些特征的事件序列如下：（1）随着压力升高，小动脉收缩，最有可能是血管自动调节的结果。这可能导致毛细血管前小动脉闭塞，并与血管平滑肌坏死有关。 (2)然后，血浆通过受损的内皮渗入无支撑的血管壁，从而发生扩张。这一阶段可能对应于自身调节的断点，并在临床上通过荧光素的局部渗漏来证明。(3)进行性血浆渗入血管壁，进一步肌肉坏死导致继发性闭塞和晚期纤维素样坏死的典型图像。
Retinal changes in accelerated hypertension were studied in seventeen monkeys with experimental hypertension by means of ophthalmoscopy and colour and flourescence photography during life, and by injection and digest preparations and light and electron microscopy after the animals had been killed. Cotton-wool spots developed in all but three monkeys. The arteries became tortuous and dilated and the light reflex decreased in those animals that became hypertensive. The earliest abnormality was a development of many points of fluorescein leakage on terminal arterioles or small arteries. Such leaking points were always present in relation to cotton-wool spots but were not confined to such areas. Focal narrowing of arteries was not observed but arteriolar occlusion and retrograde filling of the distal segment was present in three animals. Superficial linear haemorrhages were noted in five animals. Light microscopy revealed cotton-wool spots which were identical to those observed in man with a collection of swollen axons containing densely staining pseudonuclei. Study of the arterioles by electron microscopy showed findings ranging from normality to extensive necrosis. Many precapillary arteries were constricted and some were virtually occluded. Degenerative changes were present in smooth muscle cells in the wall of many of the constricted arterioles. Many arteries also showed insudation into their wall of plasma which had seeped into the muscular coat displacing and sometimes entirely replacing the smooth muscle cells. Except for arterioles with advanced necrosis, there was no indication of how plasma insudation occurred. Two arterioles with extensive necrosis showed a break within the endothelial cell cytoplasm through which penetration of plasma proteins had probably occurred. The extravascular tissues showed collections of amorphous material, sone of it with the typical banded configuration of fibrin. The sequence of events proposed to explain these features is as follows: (1) The arterioles constrict as the pressure rises, most likely as a result of vascular autoregulation. This may head to occlusion of the precapillary arterioles and is associated with necrosis of vascular smooth muscle. (2) Dilatation then occurs with insudation of plasma into the unsupported wall through a damaged endothelium. This stage probably corresponds to the autoregulatory break-point and is evidenced clinically by focal leakage of fluorescein. (3) Progressive plasma insudation into the vessel wall with further muscle necrosis results in secondary occlusion and the typical picture of advanced fibrinoid necrosis.