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Results for “PULMONARY HEART DISEASE”

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At least 739 records · Page 41Linked to original sources
PubMed2000

[A study on the changes of blood levels of type III procollagen and type IV collagen in relation to artery blood gas and lung function in patients with cor pulmonale].

This study was conducted to explore the changes of PC III (type III procollagen) and C IV (type IV collagen) in the serum in patients with chronic pulmonary heart diseases. The blood levels of PC III and C IV in 25 patients with chronic pulmonary heart diseases and 20 normal subjects were measured by radioimmunoassay and were analysed in relation with the artery blood gas and pulmonary function parameters. The results revealed that the blood levels of PC III and C IV in the patients were significantly higher than those in normal subjects, and were negatively correlated with PaO2, FEV1%, MBC and MMEF (P < 0.05, P < 0.01). The results suggest that the blood levels of PC III and C IV of patients with chronic pulmonary heart diseases are significantly increased and significantly correlated with pulmonary function damage and hypoxia.

Aged↗
PubMed1993

Measurement of platelet-activating factor in human blood by high performance thin layer chromatography and its clinical application.

Platelet-activating factor (PAF) present in the blood of the patients with chronic pulmonary heart disease and asthma has been detected by high performance thin layer chromatography (HPTLC). The patients with chronic pulmonary heart disease accompanied by carbon dioxide retention (PaCO2 > 6.67 kPa) have a higher level of PAF in blood (0.75 +/- 0.27 microgram/ml) than those who have no carbon dioxide retention (PaCO2 < 6.67 kPa, PAF 0.41 +/- 0.25 microgram/ml) and those in the normal control group (0.45 +/- 0.20 microgram/ml), with P < 0.05 in all. The patients with asthma have a higher PAF in blood (0.83 +/- 0.05 microgram/ml) than those in the control group (P < 0.005). These findings suggest that PAF plays an important role in episodes of chronic pulmonary heart disease and asthma.

Asthma↗
PubMed1983

Congenital heart disease and pulmonary artery hypertension. I. Pulmonary vasoreactivity to 15% oxygen before and after surgery.

Pulmonary vasoreactivity at sea level was studied in 22 children before and in 15 children after corrective cardiac surgery for congenital heart disease and pulmonary artery hypertension; 8 children were studied both before and after cardiac surgery. During cardiac catheterization in 28 children, pulmonary and systemic hemodynamics were determined in room air and during breathing of 15% oxygen, which corresponds to a maximal hypoxic level commonly encountered during airplane travel. Before surgery, 19 of 22 children tolerated 15% oxygen (O2), which caused the following hemodynamic changes from room air status: the ratio of pulmonary to systemic arterial pressure increased from 0.70 to 0.78 (p less than 0.05), the ratio of pulmonary to systemic flow decreased from 2.2 to 2.0 (p greater than 0.05) and the ratio of pulmonary to systemic vascular resistance increased from 0.33 to 0.40 (p less than 0.02). In two children, severe pulmonary vasoconstriction developed within 5 minutes of 15% oxygen administration, requiring immediate discontinuation of hypoxia; neither patient had lasting deleterious effects. There was no evidence of increased pulmonary vasoreactivity in children with Down's syndrome compared with genetically normal children. After corrective surgery in 15 children (including both of the hyperreactors), no significant pulmonary vascular response to 15% oxygen was found. It is concluded that, in a small number of children with unrepaired congenital heart disease and pulmonary artery hypertension, pulmonary vascular hyperreactivity can be induced by breathing 15% oxygen; this reaction is life-threatening but reversible with the administration of 100% oxygen.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2001

Plasma levels of asymmetrical dimethyl-L-arginine in patients with congenital heart disease and pulmonary hypertension.

Asymmetrical dimethyl-L-arginine (ADMA) is an endogenous inhibitor of nitric oxide synthase. We hypothesized that plasma levels of ADMA could be increased in patients with congenital heart disease and pulmonary hypertension. Cardiac catheterization was performed in 20 children and young adults with congenital heart disease with a median age of 10 years (range, 4 months to 33 years). The patients were assigned to group I (high flow, low pressure; n = 14) when Qp/Qs was 1.5 or greater and the mean PAP was less than 25 mm Hg or to group II (high pressure, high resistance; n = 6) when the mean PAP was greater than 25 mm Hg and Rp/Rs was greater than 0.3. Blood samples were taken from pulmonary vein or left ventricle. ADMA was measured by high-performance liquid chromatography. In addition, levels of ADMA were measured in peripheral venous blood obtained from eight control patients. Levels of ADMA in control patients (median, 0.21 microM/l; range, 0.08-0.27 microM/l) did not differ from levels obtained in group I (median, 0.30 microM/l; range, 0.06-0.49) microM/l). Patients in group II showed increased plasma levels of ADMA (median, 0.55; range, 0.25-0.79) (p < 0.01). Inhibition of nitric oxide synthase by increased levels of ADMA might contribute to pulmonary hypertension in patients with congenital heart disease.

Adolescent↗
PubMed1992

Pathophysiological and metabolic manifestations of pulmonary vascular disease in children.

In children with congenital heart disease pulmonary vascular disease can be fatal for a variety of reasons. Even before the classical changes of advanced pulmonary vascular obstructive disease have developed, a marked increase in pulmonary vascular smooth muscle can be fatal due to pulmonary hypertensive crises. After the Fontan procedure, a modest increase in muscularity can jeopardise the outcome since there is no subpulmonary ventricle to support the pulmonary circulation. Following heart transplantation, a slight increase in muscularity can cause failure of the donor right ventricle unless that heart is already hypertrophied as in the domino procedure. In all children with pulmonary hypertension, either persistent pulmonary hypertension of the newborn or secondary to congenital heart disease the pulmonary vasculature fails to remodel normally after birth. Newborn vessels are characterized by the immaturity of the smooth muscle cells and the paucity of connective tissue. In the hypertensive lung smooth muscle differentiation and connective tissue deposition is accelerated. In children with congenital heart disease intimal changes follow. In these children the potential reversibility of disease following intracardiac repair is determined by the type of pathological change present at the time of repair. However, pulmonary hypertensive crises can occur in young children with potentially reversible disease. Operability is not synonymous with the potential reversibility of pathological lesions. Correlations between structural findings at lung biopsy and haemodynamic findings at cardiac catheterization have improved the accuracy with which the natural and unnatural history of pulmonary vascular disease can be predicted, but is still inadequate because we do not understand the functional implications of the changes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

Oral hydralazine in patients with pulmonary vascular disease secondary to congenital heart disease.

Two patients with pulmonary vascular obstructive disease secondary to congenital heart disease were evaluated hemodynamically before and during oral hydralazine therapy. Both patients were assessed postoperatively and had no significant residual shunts. Pulmonary vascular resistance failed to decrease, and an increase in pulmonary arterial pressure occurred because of increased cardiac output secondary to systemic arteriolar dilatation. These responses were sufficiently consistent to warrant a warning against the use of oral hydralazine except under controlled conditions in patients with secondary pulmonary vascular obstructive disease.

Administration, Oral↗
PubMed1992

[Changes in acetylcholine and acetylcholinesterase in blood during pulmonary hypertension].

Two models of pulmonary hypertension in rats have been made with either monocrotaline or passive smoking (with or without infection). The decrease of RBC acetylcholinesterase activity and the increase of acetylcholine content in blood were detected in both rat models, but did not in rats which were only once infected by E. Coli, and the pulmonary pressure of the latter did not raise either. Comparing 30 cases of acute attack period of chronic pulmonary heart disease with 30 cases of normal persons, RBC acetylcholinesterase decreased significantly, indicating that hyperfunction of cholinergic nerve existed in pulmonary hypertension and pulmonary heart disease.

Acetylcholine↗
PubMed1981

Structural congenital heart disease in the newborn. Its differentiation from nonstructural cardiac or pulmonary disease.

This article discusses structural congenital heart disease in the newborn. Emphasis is given to the clinical and laboratory diagnosis including the indication for cardiac catheterization and angiography. The discussion includes the group of cyanotic, noncyanotic and other structural congenital heart diseases, as well as the group of neonatal cardiopulmonary distress without structural heart disease. An outline of the general management of these entities is included in the presentation.

Angiocardiography↗