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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Symptomatic neonatal hypertension, defined as a mean arterial blood pressure (MAP) greater than 70 mm Hg for 3 separate determinations, was observed in 2% of all admissions (20 of 988) to the intensive and intermediate care nurseries. Evidence of renal dysfunction occurred in 85% of these infants, including increased plasma renin, abnormal renal scintiscans, and pathologic evidence of renal vascular embolism or thrombus in 13 of 20. Cardiac complications were present in 55% of affected patients, and features of hypertensive retinopathy were noted in 53% of those examined. Medical management during the neonatal period successfully controlled hypertension in all infants. Higher than usual doses of three or more antihypertensive medications were necessary in 15 of 18 treated patients. The infants requiring these high doses did not develop adverse side effects. In light of the fact that 80% of our affected patients had indwelling umbilical arterial catheters whose tips were in the thoracic aorta, the possible role of catheter management, position, or placement in the pathogenesis of this disorder is suggested.
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PMID:Epidemiology and management of severe symptomatic neonatal hypertension. 371 46

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

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.
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PMID:Fundus lesions in malignant hypertension. III. Arterial blood pressure, biochemical, and fundus changes. 395 16

Experimental renovascular malignant arterial hypertension was produced in 57 rhesus monkeys by a modified Goldblatt's procedure and their eyes were studied by serial ophthalmoscopy, by stereoscopic color fundus photography, and by fluorescein fundus angiography over a period of months or years. A very common, and one of the earliest, lesions in hypertensive retinopathy was focal intraretinal periarteriolar transudates (FIPTs). In the past, FIPTs have been described erroneously as "cotton-wool spots." The two types of lesions differ very much in shape, size, color, location, fluorescein fundus angiographic pattern, resolution pattern, life cycle, and pathogenesis. FIPTs, on ophthalmoscopy, usually are pinpoint to pinhead size, round or oval, dull white in color, and situated in deeper layers of the retina and beside the major retinal arteries and their main branches. On fluorescein angiography, FIPTs show multiple punctate foci of fluorescein leakage from dilated precapillary retinal arterioles, and there is no focal retinal capillary obliteration. They usually last for two to three weeks, and on resolution leave no ophthalmoscopic, angiographic, or microvascular abnormality. Cotton-wool spots are seen in a variety of retinopathies; FIPTs, however, are a specific retinal lesion of malignant arterial hypertension only. They develop due to breakdown of blood-retinal barrier in pre-capillary retinal arterioles, due to dilatation of the arterioles from failure of autoregulation (caused by severe rise of blood pressure).
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PMID:Fundus lesions in malignant hypertension. IV. Focal intraretinal periarteriolar transudates. 395 17

Hypertension (blood pressure greater than 70 mm Hg on three days) was noted in 1.2% of all neonatal admissions to the intensive and intermediate care nurseries. During this investigation of neonatal hypertension, a retinopathy identical to that seen in hypertensive adults was noted. Indirect ophthalmoscopy was performed in 21 neonates with elevated blood pressure. Eleven of these patients demonstrated some or all of the following abnormalities: increased ratio of venous to arterial caliber, vascular tortuosity (including arteriovenous crossing changes), superficial and deep hemorrhages, and exudates. These findings appeared to resolve after control of the hypertension. The specificity of this constellation of lesions for hypertensive retinopathy and their possible clinical significance are explained in light of what is known about hypertensive retinopathy in adults.
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PMID:Hypertensive retinopathy in the newborn infant. 663 11

Retinal blood vessels differ from most other vessels in the body (with the exception of those in the brain) in two important respects. The first is the presence of blood-retinal barriers, best illustrated by fluorescein angiography. The second important difference is that retinal vessels do not have sympathetic innervation and blood flow is modulated by autoregulation mechanisms. In 1939 Keith, Wagener and Barker proposed a classification system for hypertensive retinopathy which was innovative and of prognostic importance at that time. However, the different features of hypertensive and arteriosclerotic vasculopathies are not adequately distinguished by this classification system. Clinical features of accelerated hypertension are retinal haemorrhages, cotton wool-spots, hard exudates, papilloedema and increased vascular permeability. These must be differentiated from features associated with arteriosclerosis which are arteriovenous crossing changes and arterial constriction. The advantages of the Hogan classification system, based up on histopathologic and pathogenetic considerations are discussed. Other retinal vascular diseases associated with hypertension are also mentioned. Such as toxaemia of pregnancy, arterial macroaneurysm and anterior ischaemic optic neuropathy. Retinal branch vein occlusion is rather associated with arteriosclerosis than with hypertension.
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PMID:[Hypertensive retinopathy]. 667 24

A toxemia-like syndrome was induced in pregnant beagles by intraperitoneal inoculation of concentrates prepared from placentas of patients with preeclampsia-eclampsia and hydatidiform mole, which contained an agent, Hydatoxi lualba, that stained in a unique fashion with toluidine blue-O-. The pregnant dogs inoculated with either of these concentrates progressively developed hypertension, eyeground changes consistent with hypertensive retinopathy, proteinuria, disseminated intravascular coagulation, and hepatic dysfunction in addition to intrauterine growth retardation and intrauterine fetal death. Hepatic periportal hemorrhage and glomeruloendotheliosis, lesions usually seen in preeclampsia-eclampsia, were also noted to occur in pregnant beagles inoculated with these concentrates. A significant increased sensitivity to angiotensin II infusion was also noted. The toxemia-like syndrome did not develop in pregnant beagles when inoculated in a similar fashion with concentrates prepared from placentas from normal term pregnancies which were free of Hydatoxi lualba or in nonpregnant beagles inoculated with concentrates containing Hydatoxi lualba. Although the agent was not injected in pure form, the inoculation of concentrates containing Hydatoxi lualba appears to be required for the manifestation of the toxemia-like syndrome.
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PMID:Experimental induction of a toxemia-like syndrome in the pregnant beagle. 684 42

In 1898 Marcus Gunn described the changes in retinal vessels noted with hypertension. Arteriolar narrowing, caliber irregularity, alterations of the light reflex, and hiding of the arterial blood column were noted. Arteriovenous crossing changes and capillary bed abnormalities, such as cotton-wool spots, retinal hemorrhages, and retinal edema were also mentioned, as well as blurred discs. In the 83 intervening years, little has been added to the description of hypertensive retinopathy, but our understanding has increased. Retinal vessels respond to elevations of systemic blood pressure by generalized arteriolar constriction. This can lead to arteriolar necrosis, retinal edema, cotton-wool spots, hemorrhage, and disc edema. If the blood pressure is controlled, or slow rising, or if arteriolar sclerosis is present in the retinal arteries, then a picture of arteriolar irregularity will be noted and, depending upon the ability of the retinal vessels to contract, segmental constriction will be seen. In separating hypertensives from nonhypertensives, the most consistent ophthalmoscopic finding is arteriolar narrowing with focal irregularity. In prognosticating for survival, the best method available is the Keith-Wagener-Barker classification. However, the difficulty in separating Groups 1 and 2 of this classification has lead to numerous modifications that make comparisons from one study to another difficult.
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PMID:Hypertensive retinopathy. Description, classification, and prognosis. 715 23

The effects of systemic hypertension on the posterior segment of the eye are discussed under the headings of hypertensive choroidopathy, hypertensive retinopathy, and hypertensive optic disc edema. The sympathetic nervous control and autoregulatory mechanisms of the retinal and choroidal vasculatures are briefly reviewed. In hypertensive choroidopathy focal occlusion of choriocapillaris leads to necrosis of retinal pigment epithelium (Elschnig spots). Hypertensive retinopathy is described in vasoconstrictive, exudative, and sclerotic phases, followed by complications of the sclerotic phase. Hypertensive optic disc edema is influenced by the blood supply and extracellular tissue fluid pressure of the optic nervehead. In baboons with hypertensive disc edema, accumulation of axoplasmic components is observed in the optic nervehead.
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PMID:Pathophysiology of hypertensive retinopathy. 715 24

The hypotensive effect of nifedipine (a Ca2+-antagonist) was studied in acute tests and during the long-term administration of the drug together with propranolol. Nifedipine (10 mg, sublingually) decreased blood pressure from 174/102 to 136/82 mmHg with increase in heart rate and plasma renin activity. The combination of nifedipine (10 mg, sublingually) and propranolol (0.2 mg/Kg body weight, intravenously) decreased blood pressure from 168/104 to 131/86 mmHg with decrease in heart rate and plasma renin activity. Twenty-five hypertensive patients were treated with nifedipine and propranolol (10 mg x 3 to 4/day) together with or without diuretic for long-term. With the combination therapy, blood pressure of Group I (11 hypertensive patients with coronary heart disease) fell from 211/129 to 140/85 mmHg, blood pressure of Group II (9 severe hypertensive patients without coronary heart disease) from 230/137 to 139/84 mmHg, and blood pressure of Group III (5 established hypertension) from 182/107 to 134/83 mmHg. With this treatment regimen, heart rate and plasma renin activity decreased, and abnormal electrocardiographic findings, hypertensive retinopathy, and renal dysfunction were improved. Nifedipine, in combination with propranolol and a diuretic, is considered an effective treatment of hypertension either with or without coronary heart disease.
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PMID:Hypotensive action of nifedipine (Ca2+-antagonist) and propranolol in acute trials and its long-term therapy of hypertensive coronary heart disease patients. 730 28


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