Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fibromuscular dysplasia of renal arteries was the cause of hypertension in four consecutive children with renal artery stenosis. Two were asymptomatic, the third had had hypertension for seven years but had not been treated, and the fourth, a 9-month-old infant, presented with cardiac failure. Heart enlargement and left ventricular hypertrophy were present in all. Rapid sequence urograms demonstrated a smaller kidney and delayed appearance and disappearance of the contrast medium on the affected side in all. Angiograms showed left RAS in all. Peripheral plasma renin activity was elevated in only three of the four patients. Antihypertensive and diuretic drugs were not very effective therapeutically. Ischemia of the ipsilateral kidney probably prevented normal growth and led to shrinkage of the kidney in one patient. Following nephrectomy the BP has remained normal without any therapy for 24 to 64 months. With normalization of BP, accelerated growth ensued, the cardiomegaly regressed and the hypertensive retinopathy resolved. These patients demonstrate that: (1) FMD is an important cause of RAS. (2) the well-known radiologic feature of FMD, the beaded appearance, is usually not seen in children. (3) control of BP leads to normalization of linear growth, usually impaired in severe hypertension, and (4) target organ complications such as cardiomegaly, LVH, and hypertensive retinopathy are reversible in one to 10 months.
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PMID:Fibromuscular dysplasia of renal arteries: an important cause of renovascular hypertension in children. 15 54

Thirty patients who suffered from ocular involvement caused by toxemia of pregnancy were examined ophthalmologically during the nine-year period between 1980 and 1988 at Osaka Medical Center and Research Institute for Maternal and Child Health. The ophthalmoscopic findings were divided into the following five categories: cotton wool patches (CWP), retinal hemorrhages (RH), hard exudates (HE), yellowish opaque foci (YOF) and serous retinal detachments (SRD). Although the first three types of findings were recognized as hypertensive retinopathy (Keith-Wagener III or IV), the last two were recognized as choroidal vascular damage. Based on the frequency of fundus findings, patients were divided into three types: R-type mainly suffered from retinal vascular occlusion (CWP), C-type mainly suffered from choroidal vascular occlusion (YOF, SRD), and R + C-type consisted of mixed vascular occlusion. The maximum systolic blood pressure of C-type patients was significantly lower than that of R-type. The maximum diastolic blood pressure of C-type patients was also significantly lower than those of R-type and R + C-type. There were five C-type cases with systolic blood pressure of less than 160 mmHg in which the choroidal ischemia was concluded not to be hypertensive choroidopathy but a specific alteration characterized by toxemia of pregnancy (hypercoagulopathy).
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PMID:[Retinochoroidal changes in toxemia of pregnancy with the relation to hypertensive retinopathy and choroidopathy]. 223 51

We produced experimental renovascular malignant arterial hypertension by modified Goldblatt's procedures, in 60 rhesus monkeys. Hypertensive retinopathy was studied in detail (by ophthalmoscopy, and stereoscopic color fundus photography and fluorescein fundus angiography on long-term follow-up). Cotton-wool spots (CWSs) were found to be an important, early retinal lesion. On ophthalmoscopy, they had a characteristic appearance. Fluorescein fundus angiography of these lesions revealed focal retinal capillary nonperfusion. The CWSs usually lasted for over 3 weeks and resolved within 6 weeks, leaving permanent obliteration of the retinal capillaries in their distribution, secondary intraretinal microvascular abnormalities, and retinal nerve fiber loss. We discuss pathogenesis and other features of CWSs. There is overwhelming evidence that CWSs are due to occlusion of the terminal retinal arterioles, resulting in acute focal inner retinal ischemia; hence the scientifically valid term for them would be 'inner retinal ischemic spots'.
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PMID:Cotton-wool spots (inner retinal ischemic spots) in malignant arterial hypertension. 274 98

Experimental renovascular malignant arterial hypertension was produced, by modified Goldblatt's 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.
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PMID:Fundus lesions in malignant hypertension. VI. Hypertensive choroidopathy. 380 99

Retinal ischemia results in the loss of vision in a number of ocular diseases including acute glaucoma, diabetic retinopathy, hypertensive retinopathy and retinal vascular occlusion. Recent studies have shown that most of the neuronal death that leads to loss of vision results from apoptosis. XIAP-mediated gene therapy has been shown to protect a number of neuronal types from apoptosis but has never been assessed in retinal neurons following ischemic-induced cell death. We injected an adeno-associated viral vector expressing XIAP or GFP into rat eyes and 6 weeks later, rendered them ischemic by raising intraocular pressure. Functional analysis revealed that XIAP-treated eyes retained larger b-wave amplitudes than GFP-treated eyes up to 4 weeks post-ischemia. The number of cells in the inner nuclear layer (INL) and the thickness of the inner retina were significantly preserved in XIAP-treated eyes compared to GFP-treated eyes. Similarly, there was no significant reduction in optic nerve axon numbers in XIAP-treated eyes. There were also significantly fewer TUNEL (TdT-dUTP terminal nick end labeling) positive cells in the INL of XIAP-treated retinas at 24 h post-ischemia. Thus, XIAP-mediated gene therapy imparts both functional and structural protection to the retina after a transient ischemic episode.
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PMID:XIAP-mediated neuroprotection in retinal ischemia. 1630 1

Systemic hypertension affects approximately 25 % of the population worldwide and is the most important preventable risk factor for cardiovascular diseases. Hypertension-related fundus abnormalities can be classified into hypertensive retinopathy, choroidopathy, and optic neuropathy. Hypertensive retinopathy causes vascular constriction of retinal arterioles and typical fundus findings, such as blot hemorrhages, hard exudates and cotton wool spots resulting from ischemia within the nerve fiber layer. The use of a detailed grading system based on the severity of vascular constriction is not practicable as arteriosclerotic changes are common among elderly people. Therefore, early stages with pure vascular pathology should be differentiated from severe forms of hypertensive retinopathy with parenchymal changes of the fundus. Screening the retina for hypertensive changes is essential in cases of severe systemic hypertension, acute visual impairment, diabetes mellitus and pregnancy.
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PMID:[Hypertensive changes of the fundus]. 2412 78

Systemic hypertension is widely spread in the general population. It is recognised as a major risk factor for cardiovascular morbidity and mortality. Hypertensive retinopathy is the most common manifestation. Initial changes are retinal arteriolar vasoconstriction and findings such as flame or blot hemorrhages, cotton wool spots and hard exsudates resulting from localised retinal ischemia. Ocular complications of high blood pressure (HBP) are subconjunctival hemorrhages and retinal vein occlusions. Hypertensive retinopathy contributes to worsening of diabetic retinopathy. Less common but more threatening are ischemic optic neuropathy and retinal arterial occlusions. Screening is recommended in case of severe systemic hypertension, diabetes, or any complain of recent visual disturbances.
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PMID:[Hypertension and the eye]. 2685 52

The pathogenesis of visual dysfunction in stroke remains unclear. The objective of this study was to explore retinal damage in stroke spontaneously hypertensive rats (SHR) and evaluate the role of curcumin in the retinal injury after stroke. Mature male SHR were used as the animal model for hypertension and age-matched male Wistar-Kyoto (WKY) rats as the normotensive controls. The rat model of stroke was made by bilateral vertebral artery electrocoagulation combined with transient bilateral common carotid artery ligation. The animals were randomly divided into sham group, ischemia/reperfusion group, solvent control group, and curcumin treatment group. Each group was subdivided into 2 h, 6 h, 24 h, 72 h, and 7 day after reperfusion. Blood pressure was measured in SHR and WKY rats. Eye fundus was examined in living animals, and then, tissue specimens were collected for histologic examination, terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate nick end labeling, and immunohistochemistry. Retinopathy, induced by I/R, was more serious in rats with hypertension than that in normotensive rats (retinal thickness index, p = 0.004). The number of apoptosis in retinal capillary cells and neurons reduced significantly in the curcumin-treated groups. Curcumin treatment inhibited phosphorylated c-Jun N-terminal kinase (JNK) expression in SHR after retinal I/R injury. Thus, hypertension aggravated retinal I/R injury after stroke. Curcumin, a specific inhibitor of JNK, can prevent the development of hypertensive retinopathy after I/R injury by inhibiting apoptosis in retinal capillary cells and neurons.
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PMID:Curcumin protects against hypertension aggravated retinal ischemia/reperfusion in a rat stroke model. 2867 31

Severe systemic hypertension can cause significant damage to the eye. Although hypertensive retinopathy is a well-known complication, hypertensive optic neuropathy and hypertensive choroidopathy are much less common. The aim of this article is to report an unusual case of hypertensive choroidopathy with bullous exudative retinal detachments in both eyes. The retinal detachments spontaneously resolved after blood pressure was controlled. However, multiple large retinal pigment epithelial (RPE) rips were found in both eyes. These RPE rips may be related to severe choroidal ischemia, and their locations may be compatible with the watershed zones of the choroidal perfusions.
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PMID:Bilateral retinal pigment epithelial rips in hypertensive choroidopathy. 2901 32