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Results for “PULMONARY CIRCULATION”

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At least 73 records · Page 4Linked to original sources
PubMed1989

[Pulmonary circulation in embolic pulmonary edema].

The ultrasonic method was used in acute experiments on cats with open chest under artificial lung ventilation to obtain blood flow in low-lobar pulmonary artery and vein, the blood pressure in pulmonary artery, as well as the left atrial pressure in fat (olive oil) and mechanical (Lycopodium spores) pulmonary embolism. It is shown that pulmonary embolism produces the decrease in the blood flow in pulmonary artery and vein, the increase of the pressure in pulmonary artery and left atria, the increase of lung vessels resistance. The decrease is observed of systemic arterial pressure, bradycardia, and extrasystole. After 5-10 min the restoration of arterial pressure and heart rhythm occur and partial restoration of blood flow in pulmonary artery and vein. In many experiments the blood flow in vein outdoes that in the artery--it allows to suppose the increase of the blood flow in bronchial artery. After 60-90 min there occur sudden decrease of systemic arterial pressure, the decrease of the blood flow in pulmonary artery and vein. The pressure in pulmonary artery and resistance of pulmonary vessels remain high. Pulmonary edema developed in all animals. The death occurs in 60-100 min after the beginning of embolism.

Animals↗
PubMed1982

The fate of circulating amines within the pulmonary circulation.

Pulmonary biogenic amine clearance is a carrier-mediated drug sensitive process associated with uptake into endothelial cells and subsequent metabolism by monoamine oxidase and other enzymes. Its function seems to be maintenance of arterial circulatory homeostasis by biochemically regulating circulating vasoactive hormones. Numerous pulmonary pathologic conditions are associated with alterations in these functions. However, a more precise physiologic role remains to be defined. Areas for further research include: 1. Comparative studies on the ability of endothelium from extrapulmonary and pulmonary vasculatures to extract and metabolize vasoactive amines and other humoral substances. This work must be done both in intact animals and in isolated cultured endothelium derived from organ microvasculatures. 2. Study of factors (e.g. steroids, development, etc) that may regulate pulmonary metabolic functions. 3. Measurements in humans under various clinical conditions. To this end, indicator dilution estimates and transpulmonary gradients have provided intriguing promise of means to assess endothelial metabolic functions in both normal and injured lung.

Animals↗
PubMed2000

Hydrogen peroxide--an intracellular signal in the pulmonary circulation: involvement in hypoxic pulmonary vasoconstriction.

Hypoxic pulmonary vasoconstriction (HPV) is a regulatory feature of the pulmonary circulation that ensures consistent matching of perfusion to ventilation in the normal lung. However, under pathophysiological conditions, HPV contributes to the elevated pulmonary arterial pressure inherent to numerous disease states. Consequently, control of HPV is an avenue of potential therapy for such conditions. This review discusses the role of hydrogen peroxide (H(2)O(2)) as an intracellular signal in the pulmonary circulation, concentrating on the potential involvement of H(2)O(2) in HPV and in the control of pulmonary arterial tone. Sites of hypoxic pulmonary arterial H(2)O(2) production include the mitochondrial electron transport chain, a microsomal electron transport chain containing an NADH oxidoreductase and alternatively, a membrane-bound NADPH oxidase. Each of these sources of H(2)O(2) and the effect of hypoxia on the production of reactive oxygen species are considered. The review also discusses the variance in vascular reactivity of H(2)O(2), which is described to elicit both pulmonary arterial vasoconstriction and dilatation at varying concentrations. The redox capabilities of H(2)O(2) are also considered. The relevance of all of these actions of H(2)O(2) are also assessed as potential pharmacological targets for the future development of therapy for lung diseases that are characterised by some degree of HPV and in the pathogenesis of pulmonary diseases in which reactive oxygen species are implicated.

Humans↗
PubMed1982

Behavior of the pulmonary circulation in chronic obstructive pulmonary disease. Pathogenesis of pulmonary arterial hypertension at an attitude of 2,240 meters.

The hemodynamics of the pulmonary circulation were examined in 28 patients with severe and stable chronic obstructive pulmonary disease (COPD) who were born and raised at high altitude (2,240 meters) (COPD-A). All patients had mean pulmonary pressures (PAP) greater than 16 mmHg. We observed: (1) a low correlation between pulmonary arterial diastolic pressure (PAd) and arterial oxygen saturation (r = 0.38, p less than 0.05); (2) similar PAP in patients with COPD living at sea level (COPD-S) and patients with COPD-A (COPD-S, 32 +/- 7 mmHg; COPD-A, 27.5 +/- 11 mmHg; p = NS), despite more unsaturation in patients with COPD-A (COPD-S, 84.6 +/- 6%; COPD-A, 77.5 +/- 9%; p less than 0.05) and similar arterial pH; (3) lower levels of PAP in COPD-A (COPD-S, 51.7 +/- 10 mmHg; COPD-A, 33.6 +/- 12 mmHg; p less than 0.001) for the same degree of unsaturation (COPD-S, 71 +/- 6%; COPD-A, 71 +/- 8%; p = NS) and a lower arterial pH in COPD-S (COPD-S, 7.34 +/- 0.03; COPD-A, 7.39 +/- 0.04; p less than 0.01). We conclude that pulmonary hypertension caused by chronic alveolar hypoxia is present in COPD-A, but it seems to be decreased when compared with that observed in COPD-S.

Adult↗
PubMed1978

The pulmonary circulation in congenital heart disease. II. Pulmonary hypertension.

In young children with congenital heart disease the pulmonary circulation is exposed to abnormal haemodynamic conditions before it is fully developed. In the newborn infant the persistence or development of pulmonary hypertension rapidly leads to structural change. The speed with which an increase in muscularity can develop has hitherto been underestimated. In most children dying in early infancy with congenital heart disease and pulmonary hypertension the presence of thick walled small arteries is due not to persistence of the high wall thickness of foetal life, but to a rapid postnatal response of the pulmonary circulation to pulmonary hypertension. In older patients with a ventricular septal defect, aged between 3 months and 4 years, the presence of pulmonary hypertension has been shown to interfere with the growth and development of the pulmonary circulation, judging this by reduction in size and multiplication of intra-acinar arteries and an increase in muscularity of both pre and intra-acinar arteries and veins. In these patients elevation of pulmonary vascular resistance was associated with failure of the intra-acinar pulmonary circulation to develop normally and not with obliterative pulmonary vascular disease. Recent studies indicate that growth and development of the peripheral pulmonary circulation can be quantitated in lung biopsies taken from infants and young children with congenital heart disease. It should therefore be possibe to correlate structure and function at a critical period of lung development, before the changes of obliterative pulmonary vascular disease are established.

Aortic Coarctation↗