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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats were treated with beta-adrenergic receptor inhibiting drugs (either propranolol or timolol) from conception until 12 weeks of age to determine if this therapy would alter the development of systemic hypertension or left ventricular hypertrophy. Therapy (propranolol or timolol, 500 mg/liter drinking water) was initiated with breeding parents and continued throughout the pregnancy, nursing, and postweaning periods. Although the heart rates of beta-adrenergic receptor inhibited WKY and SHR rats were consistently reduced with respect to their respective tap-water controls, this therapy did not alter body growth. Hemodynamic studies demonstrated reduced central venous pressure, cardiac index, and maximum acceleration of aortic flow in the beta-adrenergic inhibited rats. In spite of these findings, the arterial pressure of the treated rats and the degree of left ventricular hypertrophy of the SHR were unaltered by treatment. Thus, administration of the beta-adrenergic receptor blocking agents, propranolol or timolol, from conception through the developmental stage of SHR hypertension, failed to alter either the progressive rise in arterial pressure or the development of hypertensive vascular disease and left ventricular hypertrophy.
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PMID:Development of SHR hypertension and cardiac hypertrophy during prolonged beta blockade. 1 18

An African youth who had died from primary pulmonary hypertension was suspected of having ingested a herbal remedy containing the seeds of the local plant Crotalaria laburnoides. Consequently powdered seeds of this plant were fed to 20 Wistar albino rats for 60 dyas to see if this would induce ventricular hypertrophy and associated hypertensive pulmonary vascular disease. At the end of the experimental period right ventricular hypertrophy, medial hypertrophy of the pulmonary trunk and 'muscular pulmonary arteries', and muscularization of the pulmonary arterioles had developed in a proportion of the test animals. These are the morbid anatomical features pathognomonic of a raised pulmonary arterial pressure and show that the seeds of Crotalaria laburnoides contain an agent capable of inducing pulmonary hypertension in rats. This study suggests the value of seeking a history of ingestion of herbal remedies and drugs in cases of unexplained pulmonary hypertension in man.
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PMID:A pulmonary hypertension-producing plant from Tanzania. 12 2

The results of this experiment suggest that the addition of zoxazolamine to the diet may prolong the survival and reduce the incidence of right ventricular hypertrophy and hypertensive pulmonary vascular disease in male rats given a single subcutaneous injection of monocrotaline. Phenobarbitone and cinnarizine were ineffective.
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PMID:Effects of phenobarbitone, cinnarizine, and zoxazolamine on the development of right ventricular hypertrophy and hypertensive pulmonary vascular disease in rats treated with monocrotaline. 13 89

The case is described of a 24-year-old woman who died after suffering from rheumatoid arthritis for eight years. During the last four months of her life there was clinical evidence of pulmonary hypertension. At necropsy the heart showed right ventricular hypertrophy but no congenital defect. Microscopic examination of the lungs disclosed evidence of hypertensive pulmonary vascular disease with medial hypertrophy and intimal fibrosis of muscular pulmonary arteries together with hypertensive changes in the pulmonary arterioles. Some of the muscular pulmonary arteries also showed fibrinoid necrosis of their media and acute arteritis. It was concluded that the fibrinoid necrosis was a minifestation of severe hypertensive pulmonary vascular disease rather than being a primary rheumatoid arteritis of the lung.
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PMID:Unexplained pulmonary hypertension with pulmonary arteritis in rheumatoid disease. 83 68

Ten adult female Wistar albino rats were subjected to a sub-atmospheric pressure of 380 mm Hg for periods up to 35 days. Five control rats were also studied. The rats exposed to chronic hypoxia developed right-ventricular hypertrophy secondary to hypoxic hypertensive pulmonary vascular disease. Electron microscopy of control rats revealed individual smooth muscle cells immediately beneath the endothelium of pulmonary arterioles. On exposure to chronic hypoxia there was a hyperplasia of immature smooth muscle cells to form a distinct media between external and internal elastic laminae. The external lamina is thick and represents the original single lamina of the normal pulmonary arteriole. The inner lamina is thin and is newly formed internal to the smooth muscle cells. In hypoxic hypertensive pulmonary vascular disease there is no form of intimal proliferation so that the associated pulmonary hypertension is reversible.
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PMID:Ultrastructure of hypoxic hypertensive pulmonary vascular disease. 87 35

The appearance of the right ventricular myocardium on thallium 201 myocardial perfusion images was evaluated in patients with chronic pulmonary hypertension and compared to patients without pulmonary hypertension. Four groups of patients were studied: 1) eight normals, 2) five patients with angiographically documented coronary artery disease and normal pulmonary artery pressures, 3) ten patients with moderate to severe pulmonary parenchymal or vascular disease and documented pulmonary hypertension and 4) eight patients with chronic left ventricular dysfunction and pulmonary hypertension discovered during cardiac catheterization. The right ventricular free wall was visualized on the thallium 201 myocardial perfusion image in only one of eight normals (group 1) and in only one of the five patients with coronary artery disease (group 2) and measured 0.5 cm and 0.9 cm in thickness, respectively. In patients with documented pulmonary hypertension the right ventricle was visualized on low contrast thallium 201 myocardial perfusion image in all patients. The apparent right ventricular free wall thickness measured from the ungated thallium 201 myocardial perfusion images was 1.7 +/- 0.3 cm in group 3 and 1.5 +/- 0.2 cm in group 4. Right ventricular hypertrophy was detected by electrocardiography in only five of ten patients in group 3 and only one of eight patients in group 4. Thallium 201 myocardial perfusion imaging appears to be a useful technique for assessing the effects of chronic pulmonary hypertension on the right ventricular myocardium.
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PMID:Thallium 201 myocardial imaging in patients with pulmonary hypertension. 97 75

Administration of the pyrrolizidine alkaloid monocrotaline (MCT) to rats results in hypertensive pulmonary vascular disease characterized by a structurally based increase in pulmonary vascular resistance and right ventricular hypertrophy. Alterations in lung angiotensin converting enzyme activity in MCT-treated rats have suggested a role for angiotensin II (AII) in the pathogenesis of this model of hypertensive pulmonary vascular disease. To determine if increases in AII contribute to the development of pulmonary hypertension in MCT-treated rats, we examined the effect of chronic administration of the nonpeptide AII receptor antagonist Losartan on indices of pulmonary hypertension, Losartan (DuP 753; 10 mg/kg s.c.) administration for 21 days did not prevent the development of hypertensive pulmonary vascular disease in MCT-treated rats. However, 18 hr after the last dose of Losartan, AII (0.1 micrograms/kg i.v.)-induced pressor responses were inhibited by 63% in Losartan-treated rats. Losartan administration in MCT-treated rats did not prevent increases in pulmonary artery pressure or development of right ventricular hypertrophy. Additionally, increases in medial arterial thickness in pulmonary artery vessels (less than 50 microns and 50-100 microns external diameter) from MCT-treated rats were still evident in Losartan-treated rats. However, Losartan administration decreased medial pulmonary artery thickness of 50 to 100 microns external diameter vessels in control rats. These results demonstrate that AII. acting at the AT1 receptor subtype, does not contribute to pulmonary hypertension in this animal model.
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PMID:Angiotensin II and monocrotaline-induced pulmonary hypertension: effect of losartan (DuP 753), a nonpeptide angiotensin type 1 receptor antagonist. 152 21

The relation of variables obtained from a baseline examination to death from ischemic heart disease (IHD), cerebro-vascular disease (CVD) and sudden death (SUD) was analyzed in a case-control study. From questionnaire survey of approximately 180,000 subjects who underwent baseline health examinations in 1971-1986 at Aichi prefectural center of health care, 148 deaths were selected for this study. The number of cases on IHD, CVD and SUD was 36, 60, and 52, respectively. Mean age of cases was 54.8 years old and the mean follow up interval between baseline examination and death was 3.7 years. Four controls matched according to year of baseline examination, age and sex were chosen arbitrarily for each case, and odds ratios for the three diseases were estimated. In some of the matched sets, odds ratios at a follow up examination were compared with that at the first examination. The results were as follows: 1) Variables showing positive relationships to death from each of the three diseases were hypertension, high fasting blood sugar, abnormality of cardio-thoracic ratio, ST-T abnormality in ECG, left ventricular hypertrophy in ECG. The odds ratio for ST-T abnormality in ECG was significant for all three causes of death. 2) High total cholesterol showed a significant positive relation only to death from IHD. As to death from CVD and SUD, albuminuria and sclerotic changes in fundus oculi were positively and significantly related. Risk factors differed for deaths from the three diseases. 3) In death from IHD and CVD, odds ratio at the second examination was apt to be higher than that at baseline examination. In death from SUD, however, odds ratios at the first and the second examination showed no significant difference.
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PMID:[Relation of baseline examination results to death from ischemic heart disease, cerebro-vascular disease and sudden death]. 177 65

The heart is one of the major target organs that becomes secondarily involved with the unrelenting and progressive vascular disease of essential hypertension. As a result of this increasing afterload that is imposed upon the left ventricle, the ventricular chamber adapts structurally and functionally. Structural changes involve an increase in muscle mass that is achieved through left ventricular hypertrophy (in a manner similar to the arteriolar changes demonstrated by increased thickening). Unless antihypertensive therapy is interdicted in this disease process, left ventricular failure will ensue as the major cardiac hemodynamic consequence. Left ventricular hypertrophy is also associated with a risk that is independent of the pressure overload and hemodynamic risk. Although antihypertensive therapy will reduce from the hemodynamic alterations, only recently have epidemiological findings suggested that the independent risk of LVH may be reduced with pharmacological therapy. There are no data available to indicate just which agents may reduce the risk from LVH; but relatively recent studies seem to indicate that while all agents may reduce LVH with prolonged therapy only certain classes of agents will do so independent of their hemodynamic factors. Some of these agents, however, may impair cardiac function if arterial pressure is increased abruptly following therapeutic reduction of cardiac mass. Other agents may preserve normal function--or even may improve function. Among those classes of antihypertensive agents that reduce cardiac mass at least in part due to nonhemodynamic factors, are the angiotensin converting enzyme inhibitors, the calcium antagonists, and most adrenergic inhibitors. Evidence will be presented demonstrating the hemodynamic/structural dissociation of those pharmacological agents that reduce cardiac mass with short-term treatment in spontaneously hypertensive rats with left ventricular hypertrophy. Although centrally active adrenolytic, angiotensin converting enzyme (ACE) inhibitors, and calcium antagonists all reduce cardiac mass, their structural and cardiac functional effects differ greatly. Even within the ACE inhibitor group their effects vary--improving, impairing, or not changing the Frank-Starling relationships following reduction in left ventricular mass. We postulate great variability of cardiac intramyocytic penetrance of the pharmacological agents and their local intracellular effects on mitogenesis of the ventricular myocyte. The implications on cardiac function and therapy have vast potential. Therefore, current investigative areas involving new concepts of molecular biology of the cardiac myocyte may provide great promise to the quest of unraveling some of the newly postulated questions: What is the role of ionized intracellular calcium? Do the local renin-angiotensin systems in the cardiac and vascular myocyte participate in the development and regression of hypertrophy?(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Left ventricular hypertrophy: dissociation of structural and functional effects by therapy. 183 47

Rats with established monocrotaline (MCT)-induced pulmonary hypertension also exhibit a profound increase in lung resistance (RL) and a decrease in lung compliance. Because airway/lung dysfunction could precede and influence the evolution of MCT-induced pulmonary vascular disease, it is important to establish the temporal relationship between development of pulmonary hypertension and altered ventilatory function in MCT-treated rats. To resolve this issue, we segregated 47 young Sprague-Dawley rats into four groups: control (n = 13), MCT1 (n = 9), MCT2 (n = 11), and MCT3 (n = 14). Each MCT rat received a single subcutaneous injection of MCT (60 mg/kg) 1 MCT1), 2 (MCT2), or 3 (MCT3) wk before the functional study. At 1 wk after MCT, significant increases in RL and alveolar wall thickness were observed, as was a significant decrease in carbon monoxide diffusing capacity (DLCO). Medial thickness of pulmonary arteries (50-100 microns OD) and right ventricular hypertrophy were not observed until 2 and 3 wk post-MCT, respectively. Coincident with the right ventricular hypertrophy at 3 wk post-MCT were decreased DLCO and increased alveolar wall thickness and lung dry weight. Pressure-volume curves of air-filled and saline-filled lungs showed marked rightward shifts during the 1st and 2nd wk after MCT administration and then decreased at the 3rd wk. These data suggest that MCT-induced alterations in airway/lung function preceded those of pulmonary vasculature and, therefore, implicate airway/lung dysfunctions as potentially contributing to the later development of pulmonary vascular abnormalities.
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PMID:Ventilatory dysfunction precedes pulmonary vascular changes in monocrotaline-treated rats. 190 54


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