Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been demonstrated in experiments on non-anesthetized rabbits that conjunctival injection of carnosine (beta-alanyl 1-histidine) caused a decrease in normal intraocular pressure and reduced prostaglandin-induced ocular hypertension. The rapid onset of the pressure response and the absence of papillary dilation in rabbits treated with carnosine were observed. It is concluded that L-carnosine can be used as a potent drug for the prevention of reactive hypertension syndrome.
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PMID:[Effect of carnosine on intraocular pressure]. 335 28

Computerized image analysis was used to measure changes in percent area of pallor of the optic disc in a retrospective study of a group of 16 normals and 39 untreated ocular hypertensives. The optic discs of the subjects were photographed on at least two visits at least one year apart (mean, 2 years). No significant changes in area of pallor for the normal group were observed between visits, except in the inferior quadrant of the left eye. The ocular hypertensive group showed a significant increase in area of pallor between visits for the total disc and for most quadrants of both eyes. Multiple regression analysis revealed that, in addition to ocular hypertension, the significant factors associated with a change in optic disc pallor were change of ocular pressure, standard deviation of the ocular pressures, presence of vascular hypertension, and standard deviation of vascular pulse pressures. Clinical implications of early detection of disc changes for follow-up and treatment of ocular hypertensives are discussed.
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PMID:Detection of increased pallor over time. Computerized image analysis in untreated ocular hypertension. 383 81

It has been demonstrated in experiments on unanesthetized rabbits that propranolol instilled into the eye conjunctival sac caused a decrease in normal intraocular pressure and reduced prostaglandin-induced ocular hypertension. Thymolol and atenolol decreased the normal ophthalmic tone but did no affect eye hypertension. Oxprenolol and talinolol did not affect the normal ophthalmic tone and did not remove the elevation of intraocular pressure induced by PGE2.
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PMID:[Effect of beta-adrenoblockers on prostaglandin-induced ocular hypertension in rabbits]. 613 8

A series of 24 eyes in 23 patients is described showing solitary silent venous papillary loops. These loops are usually associated with a considerable degree of ocular hypertension, presenting when this hypertension is being investigated. They are silent, usually with no previous ocular history, single with a large diameter, affecting veins at the optic disc and not extending into the vitreous. The optic disc is cupped, but usually not more than 0.6 disc diameter, there is good central vision and either a full visual field or only early field loss. Fluorescein angiography shows the loops to be competent with no evidence of any other retinal vascular abnormality. Rarely loss of central vision may occur due to progression to advanced glaucoma. The condition is distinct from prepapillary vascular arterial papillary loops, neovascularization at the optic disc and optociliary shunt vessels. It is also distinct from the venous collateral vessels which develop at the optic disc after acute central or branch retinal vein occlusion. These collaterals are usually multiple, the accompanying ocular hypertension is of lesser degree, cupping of the disc and field loss are usually much more advanced and, while visual acuity may be normal, it is often grossly reduced. On fluorescein angiography all these cases of venous collaterals after retinal vein occlusion showed evidence of other retinal vascular dysfunction. Solitary silent venous papillary loops appear to develop from venules on the optic disc as a bypass to a low grade venous occlusion which is seldom clinically manifest. They form a distinct entity with a good prognosis if the accompanying ocular hypertension is carefully controlled.
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PMID:Solitary silent venous papillary loops and ocular hypertension. 652 79

Forty-four unselected patients with amaurosis fugax (AF) have been followed for 4.6 years (mean 2.6). Thirty per cent had atheromatous lesions, 20% had miscellaneous diagnoses (temporal arteritis 5, transitory ocular hypertension 2, glaucomatous iritis 1, benign intracraniel hypertension 1), 50% consisted of young, mainly women, in whom no cause was found. Prior to AF 2 had hemiplegia, 4 TCI, one optic atrophy and suspicion in 3. None died, one developed hemiparesis and one macular degeneration. An individual conservative attitude to AF seems justified in this material.
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PMID:Amaurosis fugax. A unselected material. 663 19

The prevalence of glaucoma and ocular hypertension was investigated in an epidemiological study of diabetics traced by registration of prescriptions on insulin and oral hypoglycaemic agents (OHA) on the island of Falster (inhabitants 44 498), Denmark. Among 533 diabetics (227 insulin- and 306 OHA-treated) the prevalence rate of primary open angle glaucoma and ocular hypertension was 6.0% and 3.0%, respectively. Neovascular glaucoma occurred in 2.1% of all diabetics and in 21.3% of diabetics with proliferative retinopathy. Open angle glaucoma was more prevalent (P less than 0.01) in type 2 diabetes mellitus compared with type 1 diabetes mellitus. No difference in the prevalence of neovascular glaucoma was found between type 1 and type 2 diabetics. The occurrence of open angle glaucoma correlated positively (P less than 0.01) to the current age (greater than 65 years) in both groups and the diabetes onset age (greater than 40 years) in insulin-treated diabetics. Neovascular glaucoma correlated positively (P less than 0.05) with diabetic macrovascular complications in total (myocardial infarction, ischemic heart disease, arterial hypertension, cerebrovascular stroke, gangrene/amputation), neuropathy and severe microvascular complications (proliferative retinopathy, retinovascular occlusion). Diabetics with open angle glaucoma and ocular hypertension showed a higher frequency (P less than 0.05) of ischemic heart disease, arterial hypertension and retinovascular occlusion compared with diabetics without glaucoma or ocular hypertension.
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PMID:The prevalence of glaucoma and ocular hypertension in type 1 and 2 diabetes mellitus. An epidemiological study of diabetes mellitus on the island of Falster, Denmark. 663 28

The prognosis of traumatic hyphemias in general is favorable, the blood being resorbed spontaneously in a short period. The case is different, however, where hemorrhage is abundant, and the condensed blood in the anterior chamber coagulates; here, the angle is often blocked with fibrin, the intraocular pressure rises considerably, accompanied always with severe pain. The arrest of aqueous circulation by the consolidated clot suppresses the process of resorption; thereafter, local and general therapeutic measures become ineffective. The state of "malignant hypertension" once established, surgical intervention becomes imperative. In this study are given the results of 10 cases of traumatic hyphemia complicated by malignant hypertension, treated by ultrasonic irradiation. The results are obviously favorable: rapid fall of ocular hypertension with prompt disappearance of subjective symptoms; revelation of signs of liquefaction and resumption of processes of resorption in 9 patients. Under continued treatment, complete resorption of the hyphemia was attained with accelerated pace. In one case, however, unrelenting hypertension persisted to the 12th day, despite the complete liquefaction of the coagulum. A phakotopic factor lying under the hyphemia was suspected. The visual recuperation was remarkable in 7 cases free from posterior segment alterations.
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PMID:[Ultrasonic decompression of malignant ocular hypertension secondary to traumatic hyphema]. 686 25

The distribution of fluorescein introduced into the vitreous or respectively the anterior chamber with and without induced ocular hypertension was investigated. In frozen sections it can be seen clearly that with induced hypertension fluid is forced out of the vitreous into the anterior chamber. An important point is that there was no direct discharge of fluorescein into the choroid.
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PMID:[Induced ocular hypertension: experimental investigations on rabbit eyes]. 713 88

In 148 healthy volunteers and 75 older patients the physiological aqueous humor secretion was calculated during the afternoon hours (13.00 to 20.00 hours) using the anterior chamber protocol of Fluorotron Master II (Coherent, Palo Alto, USA). Fluorescein eye drops were applied topically to each eye five times, 5 h before measurements. Healthy volunteers as well as patients had no history of ocular pathology, surgery or laser treatment. Further exclusion criteria were hypertension, diabetes, local and systemic drug therapy, neoplasia, kidney or liver diseases, contact lens, ocular trauma. Mean age of volunteers was 26.5 +/- 3.8 years; mean age of patients was 65.5 +/- 10.5 years. The aqueous humor flow in healthy volunteers (mean +/- standard deviation) was 2.26 +/- 1.0 microliters/min and in the older patients 1.91 +/- 1.1 microliters/min. Correlation coefficient between right and left eyes in the younger volunteers: r = 0.8; in the older patients: r = 0.54. The Mann-Whitney-U-test revealed a significant difference comparing mean aqueous humor flow in healthy volunteers with the mean aqueous humor flow in older patients (P < 0.01). The results in our study underline that the mean aqueous secretion does decrease with age of about 2.5% per decade. However, to date we do not know whether eyes with primary open-angle glaucoma or ocular hypertension show such a decrease in aqueous humor flow with age or whether there is an autoregulation mechanism in eyes with primary open-angle glaucoma that decreases aqueous humor secretion in relation to an increase of outflow facility.
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PMID:[Physiologic aging in aqueous humor minute volume of the human eye]. 781 85

The changes of 10 enzymatic activities of cat retinas and their blood vessels under acute ocular hypertension were systematically observed by enzyme histochemical methods. These changes were induced by the damage caused by retinal ischemia-reperfusion. The activities of the free radical scavengers, catalase and hydrogen peroxidase, were decreased, demonstrating that the excess of free radicals is one of the essential causes of the injury. The principles of treatment are besides lowering of intraocular hypertension, during retinal ischemic stage, oxygen and nutrients needed urgently should be supplied through extra-vascular route and during reperfusion stage, free radical scavengers ought to be given.
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PMID:[Experimental studies on changes in retinal enzyme activities under acute ocular hypertension in cat eyes]. 784 15


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