Response Of Retinal Vessels Research Articles

Retinal vessel responses to passive tilting

Alterations in retinal vessel calibre on changing posture may indicate an autoregulatory response to changing perfusion pressure. The effect of passive tilting on retinal response in healthy individuals was investigated. Subjects were supported on a specially constructed tilting table. The control measurements were taken with the body in a 30 degrees head up position. Red-free fundus photographs were taken before, during and after a three minute period of 30 degrees head down tilting. Ten subjects were assessed (mean age 29 years: range 18-38). A total of 92 arteriolar and 86 venular sites were measured. On tilting to the head down position arterioles showed an early and significant decrease in calibre: mean -3.1% (p less than 0.001). Venules showed an increase of 3.7% (p less than 0.001). The response was not sustained throughout the period of tilting despite a maintained increase in ocular perfusion pressure, which was estimated in six of the subjects.

The effect of cervical sympathectomy on retinal vessel responses to systemic autonomic stimulation

The retinal vessel calibre responses to systemic sympathetic stimulation, were studied in nine patients (eight male; mean age: 31.7 years; range: 19-58 years) with unilateral disruption of their cervical sympathetic tract. All patients had ipsilateral decreased/absent facial sweating and a Horners syndrome, evidence of unilateral sympathetic denervation. Both eyes of each patient were studied and the results were analysed in two groups: the group of nine sympathectomised eyes and the control group of unaffected fellow eyes. During handgrip contraction there was a significant difference in the mean retinal arteriolar constriction (mean +/- SEM) between the group of sympathectomised eyes (4.6 +/- 0.89%) and control eyes (7.1 +/- 1.13%), p less than 0.01. Similarly, there was a significant difference in mean venule constriction during sustained handgrip contraction between the group of sympathectomised eyes (1.5 +/- 0.67%) and control eyes (4.9 +/- 0.98%), p less than 0.05. There was no significant difference in the mean rise in diastolic blood pressure between the two groups: control eyes +27.9 +/- 2.38 mmHg and sympathectomised eyes +27.8 +/- 2.25 mmHg. There was no correlation between the blood pressure and retinal vessel responses in either group. These results suggest that the sympathetic nervous system plays an integral role in retinal blood flow regulation.

Impaired autoregulation of the retinal vasculature and microalbuminuria in diabetes mellitus

The relationship between microalbuminuria and retinal vessel responses to sustained handgrip contraction was studied in a group of 20 diabetic patients. The diabetics were divided into two groups based on their albumin excretion rates (AER): Group 1 (AER less than or equal to 10 mcg/min) consisted of ten diabetic patients, mean age 55.8 +/- 3.9 years (mean +/- SEM); five IDDM and five NIDDM. Group 2 (AER greater than 10 mcg/min) comprised ten diabetic patients: mean age 56.8 +/- 3.04 years; six IDDM and four NIDDM. Both groups were similar in that there were no significant differences between mean age, type of diabetes, mean duration of diabetes, glycaemic control or mean resting blood pressures. Group 2 diabetics had a higher incidence of autonomic dysfunction than Group 1, based on the results of four standard tests of autonomic nerve function. There were significantly decreased retinal vessel responses to sustained handgrip contraction in Group 2 diabetics (mean arteriolar constriction 0.1 +/- 0.32%, and mean venule constriction 1.0% +/- 0.99%) compared with Group 1 diabetics (mean arteriolar constriction 6.9 +/- 1.69%, and mean venule constriction 4.2 +/- 0.05%). Retinopathy was slightly worse in Group 2. The implications of the association of microalbuminuria (AER greater than 10 mcg/min) and loss of retinal vessel reactivity to sustained handgrip contraction are discussed.

Retinal vessel responses to systemic autonomic stimulation in fellow eyes of patients with retinal vein occlusion

The retinal vessel calibre responses to systemic autonomic stimulation were studied in fellow eyes of 11 patients with central retinal vein occlusion (CRVO) and 10 patients with branch retinal vein occlusion (BRVO), using sustained isometric muscle contraction as the stimulus. These vessel responses were compared to those of a control group of 11 subjects of similar ages. The changes in retinal vessel calibre were measured using the Quantimet Image Analyser. There was no significant difference in mean arteriolar constriction during isometric muscle contraction (mean +/- SEM) between the CRVO group (6.0 +/- 1.34%) and the BRVO group (5.4 +/- 0.31%), (p greater than 0.05), and between either of these groups compared with the control group (7.4 +/- 1.20%), (p greater than 0.50). Similarly there was no significant difference in mean venule responses between the groups (CRVO 4.9 +/- 0.48%; BRVO 4.6 +/- 0.63%; control subjects 3.8 +/- 0.90%; p greater than 0.05). The diastolic blood pressure responses were similarly not significantly different between the 3 groups (CRVO 22.3 +/- 1.27, range + 17 to 29 mmHg; BRVO 25.8 +/- 2.9 mmHg, range 18 to 45 mmHg; control subjects 21.3 +/- 1.7 mmHg, range 16 to 35 mmHg), (p greater than 0.10). The implications of the results are discussed.

Retinal vessel responses to exercise and hypoxia before and after high altitude acclimatisation.

Computerised microdensitometry was used to study diameter changes in 93 arterial and 91 venous vessel sites in the retinas of four mountain climbers before and after spending seven weeks in the Himalaya mountains. The vascular response to short-term strenuous exercise was measured at sea level, to acute hypoxia of simulated altitude of 15,000 ft (4,572 m) at rest, and to strenuous exercise while acutely exposed to the same hypoxic condition. Before the mountain exposure, retinal vessels constricted during exercise -1.9% (arteries); -3.3% (veins) and dilated in acute hypoxia 9.4% (arteries); 8.1% (veins). Superimposed exercise on hypoxic dilated arteries reduced the vasodilation (9.4% to 6%). After acclimatisation, the same physical work load at sea level constricted the arteries more (-5.4% vs -1.9%) but did not constrict the veins (0.2% vs -3.3%). Superimposed exercise on hypoxic dilated vessels, excessively dilated both arteries (8.4% vs 6.0%) and veins (13.7% vs 8.4%), compared to changes seen before the mountain sojourn. This study shows that physical conditioning and long adaptation to hypoxia, significantly change the vascular response of the retina to physical activity both in normal atmospheric conditions and during hypoxic stress. High altitude retinal hemorrhages (HARH) were present in one climber, and the study may indicate why HARH is seen often in young and physical well-trained subjects.

Hypothesis: vasoconstriction contributes to amaurosis fugax.

Platelets play a critical role in the pathophysiology of amaurosis fugax. Emboli to retinal vessels apparently produce amaurosis but, in addition, we propose that augmented vasoconstrictor responses and vasospasm may contribute to amaurosis. In this study we tested the hypothesis that constrictor responses of retinal vessels to serotonin, which is released when platelets aggregate, are potentiated in experimental atherosclerosis. Blood flow to the retina was measured in normal and atherosclerotic cynomolgus monkeys. In normal monkeys, infusion of serotonin did not alter flow to the retina. In atherosclerotic monkeys, infusion of serotonin reduced retinal blood flow (in milliliters per minute per 100 g) from 66 +/- 7 (mean +/- SE) to 5 +/- 2. Infusion of serotonin in atherosclerotic monkeys abolished the retinal response to light. Thus, atherosclerosis greatly potentiates constrictor responses to serotonin in the retinal circulation and produces a profound but reversible impairment of retinal function. We propose that altered responses to vasoactive substances that are released by platelets may contribute to the pathogenesis of amaurosis fugax.

Responses of the retinal circulation to systemic autonomic stimulation in diabetes mellitus.

The retinal vessel calibre responses to systemic sympathetic stimulation, were studied in 22 randomly selected diabetic patients (mean age +/- SEM: 54.7 +/- 2.59 years, range 25-73; 13 IDDM, 9 NIDDM; 4 females), using sustained isometric muscle contraction as the stimulus. At a different session the integrity of the autonomic nerve function in these diabetic patients was assessed using 3 standard tests of autonomic nerve function, based on cardiovascular reflexes. Diabetic patients with an intact autonomic nervous system: Group 1, (n = 11, mean age: 54.9 +/- 4.55 years, 7 IDDM 4 NIDDM) showed a mean arteriolar constriction of 9.2% (SEM 2.89, p less than 0.01) and a mean venule constriction of 5.1% (SEM 1.73, p less than 0.02), for a mean rise in diastolic blood pressure of 23.7 mmHg (SEM 2.19 range: 13-33). There were no significant mean retinal vessel responses however, in diabetics with autonomic dysfunction (Group 2): mean arteriolar constriction of 1.2% (SEM 1.38 p greater than 0.05) and venule constriction of 2.1% (SEM 1.38, p greater than 0.05); for a mean rise in diastolic blood pressure of 19.8 mmHg (SEM 4.49, range: 2-50). There was no correlation between the rise in diastolic blood pressure and the retinal arteriolar constriction in the 2 groups (Group 1:r = 0.45, p greater than 0.01 and Group 2: r = 0.56, p greater than 0.05). Duration, type and control of diabetes were not significantly different between the 2 groups. The severity of retinopathy was slightly worse in Group 2 compared to Group 1. These results point to an association between autonomic neuropathy and failure of regulation of retinal blood flow.

Talc retinopathy in primates: a model of ischemic retinopathy. III. An electron microscopic study.

Electron microscopic study of experimental talc retinopathy provides an opportunity to study the basic cytologic response of retinal and choroidal vessels to small, relatively inert emboli. Occlusion of the retinal and choroidal capillaries resulted primarily from the cellular reaction to, rather than directly from, the emboli. Mitotic figures in pericytes were observed. Even though we failed to produce retinal neovascularization (as is sometimes seen in human talc retinopathy) in this experimental model, our observations suggest that proliferation of pericytes may be an initial step in the process of retinal neovascularization.

Experimental Retinal Neovascularization Induced by Intravitreal Tumors

Adult rabbit retinal vessels underwent neovascularization in response to tumor implantation within the vitreous body. The neovascular response was presumably elicited by the tumor angiogenesis factor (TAF). The response of adult retinal vessels to an angiogenic stimulus raises the possibility that a similar substance may cause retinal neovascularization in humans, and that in normal conditions the vitreous may be able to suppress angiogenic activity.

The response of normal retinal blood vessels to angiotensin and noradrenaline.

The response of normal retinal blood vessels to angiotensin and noradrenaline.

Retinal vascular reactivity in patients with diabetes mellitus and with atherosclerosis.

By means of fundus photography, a comparative study has been made of the constrictor response of retinal vessels to the inhalation of oxygen in 47 control subjects, 50 diabetic patients, and 15 persons with atherosclerosis unassociated with hypertension or diabetes. The diabetic group showed decreased reactivity of both arteries and veins, as indicated by a decreased constrictor response to oxygen. Retinal arterial reactivity was significantly reduced in diabetic subjects, even in the absence of retinopathy or hypertension. With the appearance of retinopathy, arterial reactivity was still further reduced. The patients with uncomplicated atherosclerosis did not show significant changes in retinal vascular reactivity.

Response of normal and diseased retinal vessels to changes in blood oxygen tension

Response of normal and diseased retinal vessels to changes in blood oxygen tension