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

To determine the effects of a chronic pressure load on cardiac function and morphology, spontaneously hypertensive rats (SHR) and two normotensive strains of Wistar rats (WKY and NWR) were studied under ether anesthesia at 13, 25, 52, and 90 wk of age. Although resting cardiac index of the SHR was comparable to that of WKY and NWR at all ages, the peak cardiac output and peak stroke volume per gram of left ventricle determined during a rapid intravenous infusion of Tyrode solution was markedly reduced in the SHR only at 90 wk of age. Autonomic inhibition did not alter the peak stroke volume attained, but reduced peak cardiac output at all ages in each of the strains. Absolute left ventricular dimensions in the SHR increased out of proportion to body growth, consistent with concentric hypertrophy. As peak pumping ability markedly declined from 52 to 90 wk of age in the SHR, the free wall of the left ventricle greatly thickened whereas the septum remained unchanged. At this time the right ventricle also hypertrophied. This disproportionate thickening of the walls of the left ventricle and the hypertrophy of the right ventricle were reflected in measurements of their fiber diameters. These alterations in ventricular architecture may contribute to the decrease in pumping ability observed in long-standing hypertension.
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PMID:Cardiac function and morphology with aging in the spontaneously hypertensive rat. 49 31

In order to investigate the vasopressor role of ADH in the regulation of blood pressure, passive immunization experiments with an antibody to AVP were carried out in experimentally hypertensive rats. In hypertensive rats treated with deoxycorticosterone acetate (DOCA), spontaneously hypertensive rats (SHR) and spontaneously hypertensive stroke-prone rats (SHR-sp), the intravenous injection of a specific vasopressin antibody resulted in a transient fall of blood pressure of 11 approximately 25mmHg, while in rats with two-kidney Goldblatt hypertension and normal rats, the blood pressure was not affected. This strongly suggests that ADH contributed to systemic vaso-constriction in DOCA hypertension and spontaneous hypertension in rats.
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PMID:[The vasopressor role of ADH in the maintenance of blood pressure in experimentally hypertensive rats (author's transl)]. 49 16

Thirty-nine thrombosed arterial segments of the branches of the circle of Willis were studied by a complete serial section technique. Twenty-two patients had been hypertensive and 8 had hypercholesterolemia before the onset of cerebral artery thrombosis. The histological characteristics of the thrombosed arterial segments were intramural hemorrhage in 28 segments, superficial edema of the fibrous cap of the atheroma of fibrous plaque in 4, rupture of the atheromatous plaque in 1, superficial accumulation of foam cells in the atheroma in 1 and an atheroma or fibrous plaque without any other changes in 5. They were many intramural small blood vessels in the atheroma or fibrous plaques of 22 segments with intramural hemorrhage. Fibrinoid degeneration of these small blood vessels was noted in 5. These findings suggested that intramural hemorrhage from the intramural small blood vessels was the major cause of cerebral artery thrombosis and that persistent hypertension not only promoted cerebral atherosclerosis but also induced hemorrhage from the intramural small blood vessels.
Stroke
PMID:Cerebral artery thrombosis and intramural hemorrhage. 50 77

Intravenously injected metaraminol induced a larger blood pressure increase in spontaneously hypertensive rats (SHR) than in normotensive controls (NR) when the pressure was raised from the same starting level. Cerebral blood flow (CBF) response in NR was either perfect autoregulation, partial autoregulation or "break-through." When present, the autoregulatory response was very rapid, i.e. the flow returned to the initial value within 10-15 sec. All SHR showed an initial prompt vasoconstrictor response which was followed after 30-40 sec by a gradual flow increase. The blood pressure elevation was highest in SHR when hypertension was induced by compression of the aorta, which supports the hypothesis that the enhanced response is, at least in part, a consequence of an increased vessel wall to lumen ratio. The characteristic CBF pattern observed in SHR after a metaraminol-induced rise in blood pressure was not seen when the blood pressure was increased by aortic compression, which suggests an effect of the drug separate from its pressor effect. During maximum vasodilatation the cerebrovascular resistance (CVR) was considerably higher in SHR than in NR. Assuming an equivalent vessel density in the 2 groups, our results suggest that structural changes in resistance vessels in SHR encroach on the lumen.
Stroke
PMID:Cerebral vasomotor reactivity in normotensive and spontaneously hypertensive rats. 50

Ischemic optic neuropathy and retinal arterial occlusion are 2 forms of arterial occlusive disease affecting the eye. Reports in the literature suggest platelet hyperactivity in acute arterial occlusive diseases affecting other organ systems. Therefore, 14 patients with ischemic optic neuropathy and 17 patients with central or branch retinal artery occlusion were studied to determine whether platelets have a role in the pathogenesis of these vascular occlusive disorders. The results of the following investigations were no different in these patients compared with those in 18 control patients with non-vascular eye diseases: prothrombin times, partial thromboplastin times, plasma fibrinogen, factor V, factor VIII, platelet counts and threshold concentrations of ADP, epinephrine and collagen resulting in secondary platelet aggregation and serotonin release. In contrast, platelet coagulant activities concerned with the early stages of intrinsic coagulation were significantly increased in patients with retinal artery occlusion without hypertension or type IV hyperlipoproteinemia, but generally normal in patients with ischemic optic neuropathy and in patients with retinal artery occlusion associated with hypertension, type IV hyperlipoproteinemia, diabetes mellitus and generalized atherosclerosis. These results are consistent with a platelet contribution to retinal arterial occlusive disease in patients without other known contributing factors such as hypertension, serum lipid abnormalities, diabetes mellitus and generalized atherosclerosis and may have implications regarding prophylaxis.
Stroke
PMID:Platelet coagulant activities in arterial occlusive disease of the eye. 50 1

Eighteen patients with idiopathic optic neuropathy lacked symptoms and signs of cardiovascular and cerebrovascular disease, especially when compared to three groups of patients with sudden visual loss caused by retinal infarction, transient ischemia, and cerebral infarction. Many patients in the latter groups had hypertension, carotid bruits, heart disease, transient ischemic attack, and stroke. But among the patients with ischemic optic neuropathy, hypertension was the only evidence of cardiovascular disease, affecting 44% of the patients. We argue that, in many cases, ischemic optic neuropathy represents a direct and early complication of hypertension arterial disease affecting small arterioles supplying the anterior part of the optic nerve. The pathologic process may thus be similar or identical to lacunar infarction of the brain.
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PMID:Ischemic optic neuropathy as a possible early complication of vascular hypertension. 51 8

Seven cases of SLE with concomitant neurological syndromes are reported. In 2 cases brain stroke with right-sided hemiplegia and aphasia developed, in the remaining cases brain-stem stroke with subarachnoid haemorrhage, progressive hemiparesis and signs of intracranial hypertension, chorea, status epilepticus in terminal uraemia were observed. In one case myasthenia coexisted. Severe neurological syndromes were preceded by signs of involvement of other organs and in most cases by low-grade signs of central nervous system involvement. Treatment with corticosteroids and immunosuppressants resulted in significant improvement without complete remission. A retrospective survey of clinical material showed that modern therapeutic methods have improved the prognosis in systemic lupus erythematosus independently of central nervous system involvement.
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PMID:[Neurological syndromes in the course of systemic lupus erythematosus]. 52 35

The common carotid arteries of normotensive non-arteriosclerotic Sprague-Dawley (S-D) rats, mildly hypertensive but arteriosclerotic breeder S-D rats, severely hypertensive but non-arteriosclerotic virgin spontaneously hypertensive rats (SHR), and severely hypertensive breeder SHR were ligated to induce injury. Three weeks post-ligation, the animals were killed and histopathological sections of the ligated artery demonstrated myointimal proliferation without occlusion in the normotensive S-D rats but myointimal proliferation with occlusion in the severely hypertensive SHR. Breeder S-D rats with moderate hypertension manifested a high incidence of total occlusion by combined myointimal proliferation and thrombosis. Severely hypertensive breeder SHR manifested a high incidence of massive thrombi containing cholesterol clefts causing total occlusion of the injured artery. It is suggested that the severity of the hypertension and the hormonal-metabolic milieu conditions the morphologic response of the arterial wall to injury.
Stroke
PMID:Histopathological reactivity of carotid arteries of normotensive Sprague-Dawley vs spontaneously hypertensive rats to ligation injury. 52 7

This study has identified all persons in the population of Rochester, Minnesota, who had a diagnosis of cerebral infarction during the period Jan. 1, 1970, through Dec. 31, 1974, and has confirmed the continuing decline in the incidence rate previously reported. The decline in the rate has been accelerating, with a relatively greater reduction occurring in women and in the more elderly age groups. There has been a decline in the prevalence rate in women which was not seen in men. The over-all impact of cerebral infarction was to reduce the proportion of those persons who were completely independent from 57% before cerebral infarction to 16% after infarction. Comparison of survival among patients with cerebral infarction occurring in the two quinquennia 1945--49 and 1970--74 showed only a 2% increased probability of survival at 30 days; the difference in survival increased progressively to 16% at 5 years. The reason for the declining incidence and increased survival in cerebral infarction in this population has not been established, but evidence of increased community surveillance and treatment of hypertension among persons before the onset of cerebral infarction is presented.
Stroke
PMID:Changing pattern of cerebral infarction: 1945--1974. 52 5

1 Fifteen patients with suspected acute myocardial infarction and systemic BP of greater than 160/110 mmHg were treated with an incremental infusion of labetalol. 2 Systemic BPs were safely and effectively lowered to less than 130 mm Hg systolic or 90 mmHg diastolic in all pateints. 3 Heart rate, mean pulmonary artery wedge pressure cardiac index and stroke work index were significantly reduced. 4 The dose of labetalol varied from 30 mg--440 mg and was significantly higher (mean 295 mg) in those patients with pre-existing systemic hypertension compared with others (mean 133 mg). 5 No side-effects occurred and all patients survived to leave hospital.
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PMID:Labetalol infusion in acute myocardial infarction with systemic hypertension. 52 7


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