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 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The surgical techniques described are the result of an evolution over a number of years in the performance of the septation operation and the modified Fontan-Kreutzer repair for patients with double inlet ventricles. Those with associated pulmonary stenosis are best palliated by a classical Blalock-Taussig or Goretex shunt if an operation is required during the first few years of life and later, between two and four years of age, definitive repair by the modified Fontan-Kreutzer operation is advised. Although controversial, we prefer the use of a large nonvalved right atrial-pulmonary artery connection. Ventricular septation remains the best definitive surgical option when pulmonary stenosis is absent or mild. It is contraindicated by severe pulmonary vascular disease and also by less than moderate ventricular enlargement. The need for concomitant AV valve replacement and the use of an extracardiac conduit are associated with increased hospital mortality in our experience. Infants identified during the first year of life who do not have pulmonary stenosis are a difficult subset to manage. If the VSD and subaortic area is large and unobstructed, pulmonary artery banding early in life will control pulmonary vascular resistance and from this standpoint, permit these patients to become ultimately suited to a modified Fontan-Kreutzer repair. Unfortunately, ventricular hypertrophy usually results from pulmonary artery banding and has been associated with higher hospital mortality at the time of definitive repair. When pulmonary artery banding is undertaken for this subset, debanding and definitive repair seems best advised at about two years of age. Pulmonary artery banding is well known to accelerate the development of subaortic stenosis by spontaneous progressive restriction of the VSD. This results in small ventricular cavity size and increased ventricular hypertrophy, which are incremental risk factors for increased hospital mortality by either definitive procedure. When the VSD or subaortic area is narrow and the patient is identified during the first year of life, isolated pulmonary artery banding is inappropriate. The surgical options for these patients include Ebert's two-stage management program consisting of the initial placement of a loose partial septation patch with concomitant pulmonary artery banding, and later debanding and complete septation. Alternatively, a trial of primary complete septation may be warranted, or the use of a procedure consisting of division of the main pulmonary artery with distal closure and anastomosis of the proximal portion to the side of the ascending aorta, coupled with a systemic-pulmonary artery shunt.
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PMID:Surgical treatment of double inlet ventricle ("single ventricle"). 298 Sep 70

A single subcutaneous injection of monocrotaline in rats provokes lung injury, inflammation, and progressive pulmonary hypertension. The specific mediators of the lung injury and inflammation and the relation of these events to the ensuing hypertensive pulmonary vascular disease are not understood. Since the monokine interleukin 1 (IL-1) has been implicated in acute inflammatory reactions, the present study tested the hypotheses that monocrotaline promotes the appearance of IL-1 in the bronchoalveolar spaces of treated rats and that accumulation of the monokine coincides temporally with development of lung injury, inflammation, and/or pulmonary hypertension. As expected, monocrotaline administration was associated with an early phase of pulmonary edema, manifest at Day 7 post-treatment as an increase in the lung wet-to-dry weight ratio, followed at Day 14 post-treatment by development of pulmonary hypertension as evidenced by progressive right ventricular hypertrophy. Lung inflammation also was present at Days 14 and 21 after monocrotaline as indicated by the accumulation of leukocytes in the bronchoalveolar lavage fluid and by an increase in the lung tissue activity of the granulocyte-specific enzyme myeloperoxidase. Interleukin 1, bioassayed in bronchoalveolar lavage fluid using the standard D10 T-cell assay system, was increased slightly at Day 4 postmonocrotaline, returned to baseline at Day 7, and was markedly elevated at Days 14 and 21 after monocrotaline treatment. These observations indicate that increases in the bronchoalveolar lavage fluid content of IL-1 bioactivity are temporally related to the evolution of monocrotaline-induced lung injury, inflammation, and pulmonary hypertension and suggest that the monokine may play a pathogenetic role in these events.
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PMID:Interleukin 1 bioactivity in the lungs of rats with monocrotaline-induced pulmonary hypertension. 312 19

Based on the documented role of polyamines in regulation of cell growth and differentiation, we have proposed that these organic cations are essential for hypertrophic and hyperplastic responses of pulmonary vascular cells which underlie development of hypertensive pulmonary vascular disease. In support of this contention, we have shown in rat models of monocrotaline (MCT)- and chronic hypoxia-induced pulmonary hypertension that whole-lung polyamine contents are elevated and that blockade of polyamine synthesis forestalls development of hypertensive pulmonary vascular remodeling and sustained pulmonary hypertension. To determine if the involvement of polyamines in pulmonary hypertension could be ascribed to events occurring in cells of the vascular wall, as opposed to parenchymal or airways cells, the present study measured polyamine contents as a function of time in macroscopic pulmonary arteries from MCT-treated rats. Rats were given MCT or its vehicle and, at 1,4,7, and 21 days post-treatment, the contents of putrescine, spermidine, and spermine were assessed in whole right lung and in an arterial segment from the left lung consisting of the first and extending to the sixth intrapulmonary branch. Relative to control animals, contents of putrescine and spermidine were elevated in whole lung at 4, 7 and 21 days post MCT while the content of spermine was elevated above control at 21 days. In pulmonary arterial segments, contents of putrescine and spermidine were augmented significantly at 7 and 21 days after MCT treatment. Spermine content in arterial segments was increased at 21 days. Right ventricular hypertrophy indicative of sustained pulmonary hypertension was not evident until 21 days post-treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Polyamine content in pulmonary arteries from rats with monocrotaline-induced pulmonary hypertension. 315 Jul 91

Alveolar septal fibrosis, the main residual feature in the "healed" stage of bronchopulmonary dysplasia (BPD), was the consistent finding in 28 infants who died at 3 to 40 months of age, all having had moderate to severe BPD in the neonatal period. The cause of death in 68 per cent of the cases was progressive respiratory failure related directly to the residual changes. An additional 18 pe cent of the infants died of pneumonia superimposed on the long-standing healed bronchopulmonary dysplasia. Cardiomegaly was present in 84 per cent of the cases; biventricular hypertrophy was present in 29 per cent of the cases, right ventricular hypertrophy alone in 21 per cent, and left ventricular hypertrophy alone in 21 per cent. Evidence of pulmonary hypertensive vascular disease was found in 68 per cent of the cases. The pulmonary changes of alveolar septal fibrosis are strikingly variable within individual infants, with moderate or severe fibrosis in one area and normally inflated or hyperinflated lung in the adjacent sublobule or lobe. It is postulated that this variability may be related to a protective effect of necrotizing bronchiolitis (a prominent feature of the acute stages of BPD), whereby the occlusion of the bronchioles shields the distal sublobule from the high oxygen tensions and ventilatory pressures used in treating BPD.
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PMID:Pathologic features of long-standing "healed" bronchopulmonary dysplasia: a study of 28 3- to 40-month-old infants. 363 56

Over a 10-year period we encountered 5 infants with a pulmonary artery branch arising from ascending aorta. Surgical re-implantation of this vessel was carried out at ages 2.5, 5, 8, 9, and 19.5 months. Pre-operative cardiac catheterization demonstrated severely raised pulmonary artery pressures in all, equal to systemic in 3, and suprasystemic in 2. Four patients had origin of the right pulmonary artery from ascending aorta with a left aortic arch, and the remaining patient had an anomalous left pulmonary artery associated with a right-sided aortic arch. All patients had substantial reduction in pulmonary artery pressures immediately following surgery. One patient died 18 days post-operatively from extensive lung disease. In all 4 of the survivors, post-operative cardiac catheterization (11 to 85 months after surgery) has shown a drop in pulmonary artery pressures. One patient has been left with mildly elevated systolic values but normal diastolic levels. In 2 of the children, mild stenosis has been found at the site of reimplantation of the pulmonary artery. This anomaly should always be considered as a cause in the setting of a large left to right shunt with tricuspid incompetence and severe right ventricular hypertrophy. Prompt surgical repair, after confirmation of the diagnosis, should prevent death from heart failure or the development of irreversible pulmonary vascular disease.
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PMID:Surgical correction for one pulmonary artery arising from ascending aorta--report of five cases. 365 23

Previous work in our laboratory has shown that the continuous administration of alpha-difluoromethylornithine (DFMO), a highly specific irreversible inhibitor of ornithine decarboxylase (ODC), which is the rate-limiting enzyme in polyamine biosynthesis, prevented the development of pulmonary hypertension and right ventricular hypertrophy induced in rats 21 days after a single injection of monocrotaline (MCT). We now report that DFMO treatment did not influence the proposed first step of MCT pneumotoxicity, that is, the hepatic metabolism of MCT to toxic pyrrolic metabolites. In contrast, DFMO treatment blunted the development of lung perivascular edema at Day 7, inhibited the respective four- and twofold increases in lung putrescine and spermidine contents at Day 21 without significantly altering spermine content, and prevented the arterial medial thickening at Day 21. It thus appears that increased lung polyamine biosynthesis may be essential for the expression of MCT-induced perivascular edema as well as the development of the medial thickening stage of MCT-induced hypertensive pulmonary vascular disease.
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PMID:Suppression of polyamine biosynthesis prevents monocrotaline-induced pulmonary edema and arterial medial thickening. 393

Prolonged administration of the anorexigen chlorphentermine hydrochloride to young male Wistar albino rats for up to one year failed to induce in them either right ventricular hypertrophy or hypertensive pulmonary vascular disease. There was, however, the development of a pronounced pulmonary histiocytosis. Studies by light and electron microscopy showed that these histiocytes disintegrated to liberate their lamellar inclusions into the alveolar spaces, producing a picture reminiscent of alveolar proteinosis. Fibrosing alveolitis occurred in only one animal and was thought to be related to inflammatory changes rather than as a development of the pulmonary histiocytosis. Attention is drawn to the fact that thick-walled large pulmonary arteries are entirely normal in rats and should not be misinterpreted as evidence of hypertensive pulmonary vascular disease in test animals.
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PMID:Effects of prolonged administration of chlorphentermine on the rat lung. 445 81

When acute myocardial infarction occurs in patients with hypertension and left ventricular hypertrophy (LVH), the incidence of sudden cardiac death increases markedly. Possible explanations include increased size of the occluded vascular bed secondary to more extensive atherosclerotic coronary vascular disease in the presence of hypertension, decreased coronary reserve secondary to LVH, and intrinsic electrophysiologic abnormalities in hypertrophied cardiac muscle. To explore these possibilities, we produced acute circumflex coronary occlusion during the resting, conscious state in 32 control dogs and in 28 dogs with hypertensive LVH. Before coronary occlusion, mean arterial pressure was 96 +/- 0.1 mm Hg in control dogs and 125 +/- 5 mm Hg in dogs with hypertensive LVH (p less than 0.01). The control left ventricular/body weight ratio was 4.5 +/- 0.1 g/kg, compared with 6.1 +/- 0.1 g/kg in hypertensive LVH (p less than 0.01). Cumulative mortality at 6, 24 and 48 hours was 9%, 13% and 16% in control dogs and 32%, 43% and 54%, respectively, in dogs with hypertensive LVH (all p less than 0.01 vs control). The perfusion fields of the occluded vessel defined by postmortem coronary angiography were similar in the two groups (31 +/- 2% of left ventricular mass for control vs 29 +/- 2% for hypertensive LVH). Thus, the increased incidence of sudden cardiac death after coronary artery occlusion in hypertensive LVH dogs cannot be explained by increased size of the occluded vascular bed and is probably related to the decreased coronary reserve or intrinsic electrophysiologic abnormalities that characterize pressure-induced hypertrophied cardiac muscle.
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PMID:Effects of chronic hypertension and left ventricular hypertrophy on the incidence of sudden cardiac death after coronary artery occlusion in conscious dogs. 621 Apr 60

Atherosclerosis of the pulmonary arteries is a common autopsy finding and is associated with a variety of clinical conditions. To delineate the morphologic changes associated with pulmonary artery atherosclerosis, autopsies of 337 consecutive adults (greater than 15 years of age) were studied. For each, 35 features were studied, including age, coronary vascular disease, cardiac chamber hypertrophy and dilation, pulmonary artery and aortic atherosclerosis, and pulmonary thromboemboli and emphysema. These were compared using correlation coefficients and forward and backward stepwise regression procedures for selected variables. Pulmonary artery atherosclerosis correlated significantly with age, right ventricular dilation and hypertrophy, pulmonary emphysema, and aortic atherosclerosis. Regional evaluations of systemic and pulmonary atherosclerosis showed highly significant internal correlations. In the ligamentum arteriosum, the intensity of atherosclerosis over the aortic insertion correlated with the severity of a similar atheroma at the pulmonary artery insertion. With the multiple-regression procedure, pulmonary artery atherosclerosis was a significant predictor of aortic atherosclerosis, right ventricular hypertrophy, and pulmonary embolization. Our study shows that pulmonary embolization. Our study shows that pulmonary embolization. Our study shows that pulmonary artery atherosclerosis is accelerated in patients with atherosclerosis of the systemic arteries and the pathologic lesions associated with hypertensive pulmonary vascular disease.
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PMID:Pulmonary artery atherosclerosis: correlation with systemic atherosclerosis and hypertensive pulmonary vascular disease. 621 13

Left ventricular hypertrophy is both a target organ response to hypertensive vascular disease as well as a factor that might be responsible for other cardiovascular events. Recent work confirms that the increased cardiac mass associated with hypertension results as a structural adaptation to the increased afterload imposed on the heart. Initially there is a transient period of hyperfunction that is followed by the sustained structural adaptative period of stable hyperfunction. Even before left ventricular failure supervenes, the ventricular mass demonstrates impaired contraction. This article reviews the hemodynamic evidence in favor of this sequence of events but, in addition, points to the pathophysiological and clinical factors that may be responsible for the increased cardiac mass in addition to the pressure overload. These include: the pressor mechanisms per se; the age, sex, and race of the patient; and coexisting diseases. Some of these factors may account in part for the regression of cardiac mass with antihypertensive therapy. However, until we understand more clearly those factors that transduce the physical stimulus for hypertrophy into biochemical events, we shall neither understand completely the development of this structural adaptation of the heart nor its regression with treatment.
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PMID:Physiologic considerations in left ventricular hypertrophy. 622 89


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