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

Left ventricular hypertrophy (LVH) is both a target organ response to hypertensive vascular disease and a factor that might be responsible for other cardiovascular events. Therefore we studied by means of echocardiography 41 patients with untreated hypertension classified into 4 groups according to electrocardiographic and chest X-ray LVH criteria. The patients in group IV had in addition a history of coronary disease. Thirty-seven patients (92%) presented concentric LVH and 4 patients combined LVH and dilatation. Five patients from group IV presented impairment of interventricular septum or posterior wall motion. Thirty-seven patients (92%) had increased left ventricular mass (p less than 0.01). Ejection fraction was normal in groups I, II and III but significantly decreased (p less than 0.001) in group IV. We conclude that LVH is part of the natural evolution of hypertensive vascular disease. Echocardiography proved to be the most indicated method for the assessment of cardiac dimensions and function in hypertensive heart disease.
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PMID:M-mode echocardiography in hypertensive heart disease. 624 Jan 11

We have investigated the role of angiotensin converting enzyme (ACE) in the development of pulmonary hypertension, right ventricular hypertrophy, and pulmonary vascular disease in rats given a single subcutaneous injection of the pyrrolizidine alkaloid monocrotaline. Thirty-six young female Wistar rats were divided into a test group of 27 animals and a control group of nine animals. Each test rat was given a single subcutaneous injection of monocrotaline (60 mg/kg body weight). On the first, third, fifth, seventh, tenth, twelfth, fourteenth, seventeenth, and twenty-second days after the injection of monocrotaline the mean right ventricular systolic blood pressure was measured in one control and three test rats. The animals were then killed and we measured the specific activity of ACE in serum and lung homogenate. We also evaluated muscularisation of pulmonary arterioles, medial hypertrophy of muscular pulmonary arteries, and right ventricular hypertrophy. The sequence of changes was as follows: muscularisation of pulmonary arterioles and medial hypertrophy of muscular pulmonary arteries were apparent seven days after administration of monocrotaline; pulmonary hypertension and reduced lung ACE activity occurred after 10 days; right ventricular hypertrophy was detected after 12 days. Serum ACE activity was unchanged. It is concluded that the reduction in lung ACE activity is a result rather than a cause of the pulmonary hypertension. This reduction in lung ACE activity may be a protective mechanism designed to limit the elevation of the pulmonary arterial pressure.
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PMID:Angiotensin converting enzyme activity and evolution of pulmonary vascular disease in rats with monocrotaline pulmonary hypertension. 628 33

Previous work in our laboratory has shown that the development of monocrotaline-induced pulmonary vascular disease in rats is preceded by a prolonged activation of lung ornithine decarboxylase (ODC). We now report that significant increases in rat lung adenosylmethionine decarboxylase activity and levels of the diamine putrescine and the polyamines, spermidine and spermine, are produced by a single dose of monocrotaline (MCT). Lung putrescine levels were increased from days 7 through 21, and both spermidine and spermine were first elevated at day 10 following MCT administration. This sustained elevation of lung polyamine levels substantially preceded the development of right ventricular hypertrophy and pulmonary hypertension, which were first evident at days 14 and 16, respectively. Continuous treatment with alpha-difluoromethylornithine, a highly specific enzyme-activated, irreversible inhibitor of ODC activity, prevented the development of MCT-induced pulmonary toxicity. It thus appears that ODC and the polyamines may be important mediators of hypertensive pulmonary vascular disease that develops in response to monocrotaline administration.
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PMID:Polyamines and the development of monocrotaline-induced pulmonary hypertension. 643 45

Left ventricular hypertrophy is an adaptive response to increased intraventricular pressure, and is consistently encountered in patients with hypertension or aortic stenosis. While it has long been appreciated that the extent of hypertrophy correlates positively with the level of pressure, the age of the individual, and with indices of body size, recent evidence suggests that left ventricular structure and function also varies with gender. Elderly women with aortic stenosis, in several recent studies, have been shown to develop more marked concentric hypertrophy, lower levels of wall stress, and higher indices of systolic function. Similarly, in recent studies of extreme hypertensive hypertrophy, there is a strong female preponderance. The explanation for these findings is not clear at present, though it is possible that men with extensive hypertrophy have succumbed to complications of vascular disease at an earlier age. The syndrome of extreme hypertrophy complicating hypertension and aortic stenosis, more commonly seen in women, requires a carefully tailored clinical approach.
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PMID:Gender differences in older patients with pressure-overload hypertrophy of the left ventricle. 755 6

NG-nitro-L-arginine methyl ester (L-NAME) and 11-desoxycorticosterone plus salt intake (DOCA-salt) hypertensive rat models were compared to study the possible involvement of model-specific factors in the development of renal angiopathy and left ventricular hypertrophy (LVH). Blood pressure was measured in L-NAME, DOCA-salt hypertensive, and control Wistar rats, and the lesions of nephroangiosclerosis and left ventricular hypertrophy were evaluated after 7 weeks. Arterial wall cyclic guanosine monophosphate, plasma renin activity (PRA), and renal renin storage were assessed in parallel. For the same level of hypertension in the two models, the renal arterial fibrinoid necrotic lesions were significantly more frequent in L-NAME than in DOCA-salt hypertensive rats. In DOCA-salt hypertensive rats, PRA was decreased and arterial cGMP increased compared to controls. In the L-NAME model, arterial cGMP decreased and PRA showed a bimodal distribution in this intermediate stage of hypertensive disease. LVH was observed in DOCA-salt rats and only in the L-NAME rats with a high level of PRA. There was a close correlation between the lesions of nephroangiosclerosis, left ventricular index, and plasma renin activity in L-NAME rats. We therefore suggest that the activation of the renin-angiotensin system participates specifically in the development of the second stage of hypertension during chronic blockade of NO synthase involving nephroangiosclerosis and LVH.
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PMID:Renal hypertensive angiopathy. Comparison between chronic NO suppression and DOCA-salt intoxication. 775 45

Increased blood pressure can be observed in about 15-20% of the Swiss population. Hypertension causes few or no symptoms, but is an important risk factor for myocardial infarction, stroke, renal failure and peripheral vascular disease. All these clinical complications of hypertension are preceded by functional changes of blood vessels and the myocardium (left ventricular hypertrophy). In conduit arteries, hypertension is associated with atherosclerotic changes, while in resistance arteries only increased medial thickness can be observed. In atherosclerosis, functional changes of the endothelium, vascular smooth muscle, platelets and monocytes occur. These changes lead to hypercontractility, increased interaction of circulating blood cells with the blood vessel wall, and to proliferation and migration of vascular smooth muscle cells. These events impair local blood flow and eventually may cause vascular occlusion. The endothelium plays a particularly important role as a regulator of these mechanisms. Accordingly, it is likely that an endothelial dysfunction occurs at the very beginning of the atherosclerotic process. In resistance arteries, remodeling of vascular smooth muscle cells leads to thickening of the media with encroachment on the lumen due to an increased media lumen ratio. These hypertension-induced vascular changes are in part reversible by antihypertensive drugs. Hypertension-induced vascular disease is preceded by numerous alterations in the expression, secretion and action of mediators and receptors of endothelial cells, vascular smooth muscle, platelets and monocytes. It is hoped that increased understanding of the cellular/molecular mechanisms of hypertensive vascular disease will allow more effective therapy (and in the future also gene therapy) as well as better prevention of coronary artery disease in hypertensive patients.
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PMID:[Hypertension and vascular diseases: molecular and cellular mechanisms]. 787 5

The pathogenic mechanisms by which increased pressure and flow lead to pulmonary vascular disease are poorly understood, especially in newborns. To study the pathophysiological correlations and timing of the development of structural changes in response to high flow in nonhypoxic neonates, a model of high pulmonary flow was developed in newborn calves by anastomosis of the isolated left pulmonary artery (LPA) to the aorta. LPA pressure and flow increased acutely. LPA pressure reached near-systemic levels by 10 wk, whereas LPA flow was maximally increased at 1 mo before decreasing in several calves. Right pulmonary arterial pressure remained normal, and ventricular hypertrophy did not develop. Morphometric evaluation of the left lung demonstrated decreased arteriolar diameter, increased medial thickness, muscularization of arterioles at the bronchoalveolar junction, luminal obliteration of small arteries, and dilation lesions. The LPA pressure and vascular changes were greater and developed over a shorter time period than did prior models of nonhypoxic flow-induced pulmonary vascular changes. Lesser degrees of decreased arteriolar diameter and muscularization of small vessels were seen in the right lung, indicating a difference in the vascular response to moderately increased flow vs. increased pressure and flow. Thus, calves with an isolated LPA-to-aortic anastomosis simulate the hemodynamic and pulmonary vascular changes seen in newborns with congenital heart defects. Such calves may serve as models to assess effects of mechanical stresses on a newborn's vasculature.
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PMID:Pulmonary hypertension and arterial changes in calves with a systemic-to-left pulmonary artery connection. 800 41

A 26-year-old woman with systemic lupus erythematosus (SLE) developed dyspnea and hypoxemia on exertion. She died from rapidly progressive respiratory failure. Autopsy revealed right ventricular hypertrophy and occlusion of the pulmonary veins compatible with pulmonary venoocclusive disease (PVOD). Although PVOD has been reported in patients with suspected collagen vascular disease, this appears to be the first reported case of PVOD occurring in a patient with SLE.
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PMID:Pulmonary venoocclusive disease in a patient with systemic lupus erythematosus. 801 50

Rapidly accumulating evidence suggests that a proportion of patients with acquired immunodeficiency syndrome (AIDS) develop hypertensive pulmonary vascular disease reminiscent of primary pulmonary hypertension. As an initial step to explore the link between AIDS and hypertensive pulmonary vascular disease, the present study determined whether pulmonary hypertension is present in a well-characterized murine model of retrovirus-induced immunodeficiency. In agreement with previous reports, mice infected with the LP-BM5 murine leukemia virus developed polyclonal B and T cell activation followed by progressive and severe B and T cell immunodeficiency. At 12 wk postinfection, when persistent immunodeficiency was established, mice were anesthetized, and right ventricular systolic pressure was determined in open-chest, mechanically ventilated animals. Mean right ventricular systolic pressure was 14.7 +/- 1.3 mm Hg in control animals and was increased significantly to 22.5 +/- 3.2 mm Hg in virus-infected mice. Right ventricular hypertrophy was also present in infected mice as evidenced by a 27% increase in the ratio of right to left ventricular weights; there were no group-dependent differences in the left ventricular to total-body weight ratio. Morphometric evaluation indicated that medial thickness in muscularized pulmonary arteries, expressed as a percentage of the external diameter, was 9.6 +/- 0.4% in control lungs and increased to 14.4 +/- 0.5% in lungs from infected animals. Qualitative histopathologic analysis suggested increased perivascular collagen deposition in lungs from infected animals relative to control animals. Unlike AIDS patients with pulmonary hypertension, infected mice did not exhibit plexiform lesions or intimal fibrosis of the pulmonary arteries.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulmonary hypertension in a murine model of the acquired immunodeficiency syndrome. 802 49

The chemical signaling pathways which orchestrate lung cell responses in hypertensive pulmonary vascular disease are poorly understood. The present study examined temporal alterations in lung basic Fibroblast Growth Factor (bFGF) in a well characterized rat model of monocrotaline (MCT)-induced pulmonary hypertension. By immunohistochemical analysis, there were progressive increases in bFGF in airway, vascular and gas exchange regions of MCT-treated rat lungs. Increases in bFGF preceded the onset of right ventricular hypertrophy at day 21 after MCT administration. Enhanced bFGF immunostaining was observed as early as day 4 in focal areas of the parenchyma, and by day 14 there was enhanced bFGF staining in alveolar macrophages, neutrophils and alveolar septa, which persisted through day 21. In conducting airways, there was elevated bFGF immunostaining in the smooth muscle cell (SMC) layer by days 4 and 7 and in the ciliated epithelium and its basement membrane at days 14 and 21. Cells morphologically similar to Clara cells in the luminal surfaces of bronchioles stained intensely on days 14 and 21. In the nucleus and cytoplasm of medial SMCs within pulmonary arteries, there was a progressive increase in bFGF staining starting at day 4. Lung bFGF mRNA was increased slightly at days 1, 4 and 7, while lung bFGF protein, as judged by western blot analysis, was increased at days 14 and 21 compared to controls. The present results, considered in teh light of teh documented roles of bFGF in vascular cell migration, growth and synthesis of extracellular matrix components, suggest that bFGF may contribute to the structural remodeling processes underlying the development of chronic pulmonary hypertension in MCT-treated rats.
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PMID:Basic fibroblast growth factor alterations during development of monocrotaline-induced pulmonary hypertension in rats. 867 46


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