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

Chronic pulmonary arterial hypertension was produced in six fetal lambs. In four (126 to 139 days' gestation) unilateral fetal renal artery constriction caused systemic arterial mean blood pressure elevations. In another fetus, constriction of the umbilical artery caused a systemic mean blood pressure elevation; in the sixth, partial occlusion of the ductus arteriosus caused isolated pulmonary arterial hypertension. The right lung of each fetus was perfused with fixative at the in vivo mean arterial pressure and the amount of smooth muscle in the fifth generation (resistance) vessels analyzed using the medial width/external diameter ratio. There was a significant increase in the medial width/external diameter ratio in the six experimental animals as compared to that in six normal fetuses. In separate fetuses the increased ratios were due to a decreased external diameter, increased smooth muscle, or both these factors. The total number of resistance vessels was counted in the right lung of each fetus and no significant difference from normal was observed. We postulate that either fetal systemic hypertension or constriction of the ductus arteriosus causes fetal pulmonary hypertension in utero and that this produces increased smooth muscle development in pulmonary arterial resistance vessels; this may be a pathogenic mechanism for the syndrome of persistent pulmonary hypertension of the newborn infant.
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PMID:Fetal hypertension and the development of increased pulmonary vascular smooth muscle: a possible mechanism for persistent pulmonary hypertension of the newborn infant. 2 21

The purpose of this study was to characterize the sequential hemodynamic alterations and pulmonary vascular lesions produced by a single pulmonary artery injection of the vasotoxic pyrrolic alkaloid dehydromonocrotaline in the young beagle. Normotensive pulmonary pressure was replaced by hypertension 21 days after injection. By 28 days, the pulmonary pressure and total pulmonary vascualr resistance of the experimental animals were significantly greater than the controls (p less than 0.01). Right ventricular work increased from a baseline mean of 0.58 to 1.40 kg . m/min. Morphological and morphometrical analyses revealed alveolar edema, increased numbers of alveolar macrophages, cellular hyperplasia in the alveolar septa, and a progressive interstitial fibrosis. The precise mechansims by which dehydromonocrotaline injection initiates and promotes pulmonary hypertension and pulmonary fibrosis still needs clarification; however, our data indicate that the fraction of air space is reduced relative to the fraction of tissue space, and this change occurs with concurrent fibrosis in the alveolar septa and an increased pulmonary arterial pressure although hypoxia was not clinically detectable.
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PMID:Pathophysiology of dehydromonocrotaline-induced pulmonary fibrosis in the beagle. 3 92

Evidence suggests that the initial phase of neurogenic pulmonary oedema results from a centrally mediated, massive, sympathetic discharge. It is postulated that this produces intense, generlised, but transient, vasoconstriction with a resultant shift of blood from the high-resistance systemic circulation to the low-resistance pulmonary circulation. Pronounced increases in pulmonary vascular pressures and blood-volume then produce pulmonary oedema because of the hydrostatic effect of increased pulmonary capillary pressure. In addition, pulmonary hypertension and hypervolaemia injure pulmonary blood-vessels, altering pulmonary capillary permeability and producing lung haemorrhage. After the transient systemic and pulmonary vascular hypertension subside, the patient is left with abnormal pulmonary capillary permeability, so that pulmonary oedema persists in the face of normal haemodynamic and cardiac function.
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PMID:Pathogenesis of neurogenic pulmonary oedema. 5 77

Myocardial involvement in lupus erythematosis takes the form of an interstitial myocarditis with cellular infiltration and fibrinoid necrosis. The most lesions are perivascular, and involve the arterioles. The myocardial fibres are involved secondarily to the vascular lesions, or by grossly, damaging sclerosis. The clinical features are variable:--no clinical features, but haemodynamic evidence of abnormal ventricular function, and perhaps sudden death;--arrhythmias and disorders of atrio-ventricular conduction;--cardiac failure, which may be due to a genuine cardiomyopathy (a part may be played by hypertension, pulmonary hypertension, renal failure, constrictive pericarditis or haemodynamically major valve disorders);--abnormalities of the coronary trunk in a certain number of cases. If anti-nuclear antibodies are present in a cardiomyopathy, the presence of DLE or of a drug-induced lupus syndrome must be suspected. There remain some awkward cases which defy classification, and which systematic use of echocardiography and pericardial and myocardial biopsy may be able to define more accurately.
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PMID:[The myocardiopathies of systemic lupus erythematosus]. 9 56

Neoplastic thrombosis of the pulmonary artery is a rare and little known cause of pulmonary arterial hypertension. The clinical picture is one of acute respiratory failure and progressive right ventricular failure caused by pre-capillary pulmonary hypertension. In the living patient there is no way of distinguishing this condition from that of subacute cor pulmonale due to embolism, especially as the primary tumour is not always found either because it is too small or because it has already regressed by the time it has metastasised. The diagnosis usually rests on histological examination of the lungs, and two pathological types can be distinguished: carcinomatous lymphangitis with secondary invasion and thrombosis of the pulmonary arterioles on the one hand, and the neoplastic arterial emboli of a chorio-epithelioma on the other.
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PMID:[Pulmonary arterial hypertension caused by neoplastic thrombosis of the pulmonary artery]. 10 82

Evaluation was made of 17 patients who underwent conduit reconstruction of the right ventricular outflow tract (for anomalies other than truncus arteriosus) at the Texas Heart Institute between December, 1965, and June, 1974. Fifteen patients survived the operation and have shown substantial clinical improvement. Several different conduits were used, principally an allograft aorta with the aortic valve and mitral leaflet attached, a woven Dacron prosthesis containing a xenograft (porcine) valve, and a valveless Dacron tube graft. Allograft conduits are sometimes difficult to procure and keep and tend to calcify with passage of time. Woven Dacron prostheses are favored because they are readily available in a wide range of sizes. We believe it is not necessary for the conduit to contain a valve unless the patient has pulmonary hypertension, in which case we use a xenograft (porcine) valve because this valve does not require the long-term use of anticoagulants, a difficult regimen to manage in children. The largest possible prosthesis must be used; otherwise right ventricular hypertension will persist. Indications for conduit reconstruction include anomalous coronary arteries crossing the right ventricular outflow tract, discontinuity of the pulmonary arteries, and pulmonary atresia with a ventricular septal defect. Our current method of managing pulmonary atresia with ventricular septal defect (pseudotruncus arteriosus) includes palliative shunting to relieve hypoxemia during infancy and to permit full development of the pulmonary arteries for eventual total correction at a more optimal age when a larger conduit may be used.
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PMID:Conduit reconstruction of right ventricular outflow tract. Experience with 17 patients. 12 41

Definitive, if not curative surgery is available for the eight most common congenital cardiac defects-ductus arteriosus, ASD, coarctation, pulmonary valve stenosis, aortic valve stenosis, tetralogy of Fallot, and transposition. The results of surgery for uncomplicated cases of DA, ASD, VSD, and coarctation usually can be determined by clinical means (including chest radiogram and ECG). Postoperative heart catheterization is recommended for evaluation of the patient who has had surgery for pulmonary valve stenosis or artic stenosis and is necessary after tetralogy of Falot or transposition of the great arteries repair to identify the important postoperrative residua and sequelae. The term "curative" surgery probably shoud be reserved for operation for divion of ductus arteriosus unassociated with pulmonary hypertension and performed in childhood. After closure of ASD, patients should continue to be observed for late development of arrhythmias and persistent cardiac enlargement, although the incidence of these problems is low. After VSD closure the patient is still followed at intervals for possible ill effects of the ventriculotomy scar, manifest as arrhythmias, ventricular aneurysm or myocardial insufficiency. The patient with coarctation repair must be observed for a possible late complication from one of the several clinically silent cardiovascular or cerebrovascular anomalies as well as for the change of restenosis or unrelieved hypertension...
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PMID:Residuae, sequelae, and complications of surgery for congenital heart disease. 12 37

Changes in the density and distribution of pulmonary mast cells were determined in six mammalian species exposed to hypobaric hypoxia (PB = 435 Torr) for 19-48 days. Control animals were studied at 1,600 m (PB = 635 Torr). Total lung mast cell hyperplasia was observed only in calves exposed to high altitude. Pigs, rats, and sheep exhibited small, but insignificant, increases in mast cell density. Perivascular mast cell proliferation adjacent to vessels of 30-500 mum in diameter was seen in both calves and pigs. Bronchial, alveolar septal, and systemic tissue (tongue) mast cell hyperplasia was not observed in any of the species. Three indices of pulmonary hypertension (right ventricular hypertrophy, medial thickness of pulmonary arteries, and pulmonary arterial pressure) correlated with perivascular mast cell density. The findings indicate that perivascular mast cell proliferation may relate more to the morphological pulmonary vascular changes and to pulmonary hypertension than to hypoxia, leading to the speculation that mast cells increase in number in response to the hypertension, rather than to mediate and maintain the hypertension.
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PMID:Lung mast cell density and distribution in chronically hypoxic animals. 13 66

We examined the pulmonary vascular reactivity of normotensive rats (NR) and spontaneously hypertensive rats (SHR) to acute and chronic pressor stimuli. In rats kept at low altitude (1,520 m), SHR had a slight degree of right ventricular hypertrophy, but there was no difference between SHR and NR in either right ventricular systolic pressure or pulmonary artery wall thickness. When compared to blood-perfused lungs from low altitude NR, lungs from low altitude SHR were normoresponsive to acute airway hypoxia, hyporesponsive to intra-arterial angiotensin II, and hyperresponsive to intra-arterial prostaglandin F2alpha. After exposing rats to simulated high altitude (4--6 weeks at 4,270 m) to induce hypoxic pulmonary hypertension, SHR had a higher right ventricular systolic pressure, a greater degree of right ventricular hypertrophy, and more pulmonary artery medial thickening than did NR. The results indicate that although the pulmonary vasculature of SHR does not become hypertensive spontaneously, it might have an increased tendency to develop hypertension when exposed to an appropriate stimulus, i.e., chronic airway hypoxia.
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PMID:Pulmonary vascular reactivity in the spontaneously hypertensive rat. 15 32

Evidence suggests the following pathogenesis for neurogenic pulmonary edema. The initial phase results from a centrally mediated, massive, sympathetic discharge. This produces intense, generalized, but transient, vasoconstriction with a resultant shift of blood from the high-resistance systemic circulation to the lowresistance pulmonary circulation. Marked increases in pulmonary vascular pressures and marked increases in pulmonary blood volume then produce pulmonary edema because of the hydrostatic effect of increased pulmonary capillary pressure. In addition, pulmonary hypertension and hypervolemia injure pulmonary blood vessels, altering pulmonary capillary permeability and producing lung hemorrhage. After the transient systemic and pulmonary vascular hypertension subside, the patient is left with abnormal pulmonary capillary permeability, so that pulmonary edema persists in the face of normal hemodynamics and normal cardia function.
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PMID:Speculations on neurogenic pulmonary edema (NPE). 17 54


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