Prem Singh Virdi

Fundus Lesions in Malignant Hypertension: VI. Hypertensive Choroidopathy

Experimental renovascular malignant arterial hypertension was produced, by modified Goldblatts procedures, in 60 rhesus monkeys, and hypertensive fundus changes were studied in detail (by serial ophthalmoscopy and fluorescein fundus angiography in all monkeys on a long-term follow-up, and pathologically in 29 eyes). In hypertensive choroidopathy, retinal pigment epithelial (RPE) lesions and serous retinal detachment (RD) were the classic ophthalmoscopic lesions, whereas fluorescein fundus angiography and histopathologic studies revealed marked abnormalities in the choroidal vascular bed, in addition to the changes in the RPE. The RPE lesions could be subdivided into initial acute focal lesions (due to focal RPE infarction), and degenerative lesions, which developed later and were progressive in nature, maximally involving the macular and peripheral regions of the fundus. The RD developed most commonly in the posterior pole and infrequently involved the peripheral retina. The choroidal vascular bed showed impaired circulation and extensive occlusive and ischemic changes. These studies revealed that hypertensive choroidopathy is as important a fundus change as hypertensive retinopathy. The pathogenesis of hypertensive choroidopathy is discussed in detail; the evidence indicates that it is due to choroidal ischemia, and that hypertensive choroidopathy and retinopathy are two independent and unrelated manifestations of renovascular malignant hypertension.

Fundus lesions in malignant hypertension. V: Hypertensive optic neuropathy

We produced experimental renovascular arterial hypertension in 57 rhesus monkeys by modified Goldblatts procedures. Hypertensive fundus changes were studied in detail by serial ophthalmoscopy and fluorescein fundus angiography in all animals on a long-term follow-up, and pathologically in 23 eyes. Initial evidence of hypertensive optic neuropathy was optic disc edema which developed at the median blood pressure (BP) of 190 mmHg (normal BP, 120 mmHg). On follow-up, mild to marked pallor of the optic disc developed. The optic disc changes were correlated with BP and other fundus changes. Pathogenesis of hypertensive optic neuropathy, which has been highly controversial so far, is discussed at length in the light of the findings of the present study and other recent evidence. All the available clinical and pathologic findings in the present study indicate that hypertensive optic neuropathy represents a form of anterior ischemic optic neuropathy, and that hypertensive optic neuropathy is a distinct entity. A caution is given against a precipitous reduction of BP in patients with hypertensive optic neuropathy because that may cause complete, permanent blindness.

Anterior segment ischemia after recession of various recti: an experimental study

In 40 normal adult cynomolgus monkey eyes, recession of various recti in different combinations was done to evaluate their effects on the anterior segment. These procedures were done as primary, secondary, tertiary, and fourth procedures (each separated by several weeks or months), ultimately involving all four recti in the eyes. In 11 eyes, posterior ciliary arteries (PCAs) were occluded to determine its effects on the anterior segment. All eyes were examined by slit lamp, color photography, and fluorescein angiography of the anterior segment, and tonometry, before surgery and serially thereafter during the follow-up period. These studies showed that recession of two or three recti simultaneously in different combinations produced no serious permanent anterior segment changes, although initially in some of the eyes there was transient mild-to-moderate anterior segment ischemia. Recession of four recti simultaneously as a primary procedure produced serious permanent ocular and anterior segment changes; however, when this was done as a secondary or tertiary procedure after previous recessions of three or four recti, anterior segment changes were much fewer and milder than when it was a primary procedure. Occlusion of all the posterior ciliary arteries in itself produced no important changes in the anterior segment, but when combined with simultaneous recession of both the horizontal recti, it produced serious anterior segment changes. In the light of these findings, the pattern of arterial blood supply of the anterior segment is discussed.

Fundus Lesions in Malignant Hypertension: III. Arterial Blood Pressure, Biochemical, and Fundus Changes

Malignant (accelerated) renovascular arterial hypertension was produced in 57 adult rhesus monkeys by clamping the renal artery (one-kidney model in 25 animals and two-kidney model in 32). The animals were investigated before renal artery clamping and serially thereafter by recording systolic arterial blood pressure (BP), biochemical changes, and changes in the fundus of the eye; the latter was evaluated by ophthalmoscopy, stereoscopic color fundus photography, and fluorescein fundus angiography. All of the animals developed arterial hypertension. The data on BP, biochemical, and fundus findings were analyzed and correlated. The findings of this study clearly showed that the various fundus lesions seen in these hypertensive animals fall into three distinct categories: (1) hypertensive retinopathy, (2) hypertensive choroidopathy, and (3) hypertensive optic neuropathy. The appearance of the retinopathy was significantly earlier than that of the choroidopathy or optic neuropathy (P less than 0.01), but the difference between the times of appearance of the choroidopathy and neuropathy was not significant. There was no significance in the order in which the three types of fundus changes reached their maximum severity. There was no significant difference between the mean BPs when the retinopathy, choroidopathy, or optic neuropathy first appeared, nor between the BPs at the time of their appearance and at the time when they were most marked. In monkeys of the one-kidney model, the rise in BP developed significantly (P = 0.01) faster and the fundus lesions appeared significantly (P = 0.00001) earlier than in those with the two-kidney model.

Macular lesions in malignant arterial hypertension.

We produced experimental renovascular malignant arterial hypertension by a modified Goldblatts procedure in 60 rhesus monkeys (25 one-kidney model and 35 two-kidney model), and studied various macular lesions by detailed serial ophthalmoscopy, and stereoscopic color fundus photography and fluorescein fundus angiography on a long-term follow-up. The various lesions which developed in the macular region included retinal edema, cystic retinal changes, serous retinal detachment, retinal pigment epithelial changes (initially acute focal and later degenerative lesions), and lipid deposits. In addition to these, the usual retinal lesions associated with hypertensive retinopathy, e.g., focal intraretinal periarteriolar transudates, cotton-wool spots and retinal hemorrhages, were also frequently seen in the macular retina. Findings on the various lesions are described in detail, and the pathogenesis of macular edema in malignant arterial hypertension is discussed.

Effects of Pilocarpine, Timolol, Epifrin and Thymoxamine on iris vessels in rhesus monkeys

In 24 normal eyes of healthy adult rhesus monkeys, the effects of 1% Pilocarpine, 0.5% Timolol, 0.5% levoepinephrine (Epifrin) and 0.5% Thymoxamine were tested on the iris vessels, intraocular pressure and pupil size. Fluorescein iris angiography and applanation tonometry were performed on the eyes before the use of any drug, and then 2–4 h after topical instillation of each drug; all drugs were used in all the eyes, an interval of one week being left after the use of each drug. The findings of this study suggest that Pilocarpine and Timolol produced vasodilation. Epifrin and Thymoxamine seemed to have no appreciable effect. Pilocarpine produced miosis while other drugs had no significant effect on pupil size. Pilocarpine, Timolol and Epifrin each produced a significant fall in the intraocular pressure. The mechanisms of vascular changes are discussed. The various limitations of fluorescein iris angiography in such a study are stressed.