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Results for “PULMONARY CIRCULATION”

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At least 955 records · Page 53Linked to original sources
PubMed1992

ANP decreases arterial oxygen partial pressure by increasing shunt flow in pulmonary circulation.

This study was designed to clarify the decreased arterial oxygen partial pressure (PaO2) mechanism induced by atrial natriuretic peptide (ANP) infusion. In order to examine the effects of ANP on gas exchange across the normal lungs, ANP was infused to eight anesthetized dogs, ventilated with mixed gases of oxygen and nitrogen. PaO2 and venous oxygen partial pressure (PvO2), ventilation-perfusion ratio (VA/Q), shunt-total blood flow ratio (QS/QT) were measured before and during ANP infusion under ventilation with 10, 20, 30% oxygen. In this study ANP decreased PaO2 from 89.0 +/- 4.2 to 85.4 +/- 5.4 mmHg during 20% oxygen ventilation, and from 138.1 +/- 3.6 to 132.5 +/- 4.1 mmHg during 30% oxygen ventilation. ANP increased VA/Q and QS/QT. We conclude that the decrease in PaO2 caused by ANP infusion was mainly due to the increased venous admixture.

Animals↗
PubMed2003

Characterization of the pulmonary circulation according to hemodynamic changes by computed tomography.

Increased or decreased pulmonary blood flow (PBF) and an increased pulmonary vascular resistance (PVR), represent common and important change in pulmonary hemodynamics. In this study, we constructed 3 hemodynamic models in 5 dogs, that is, an increased and a decreased PBF model, and an increased PVR model. A CT perfusion scan was performed in each hemodynamic model. Perfusion parameters including blood flow (BF), blood volume (BV), mean transit time (MTT), and maximal slope (MS) were calculated automatically by specialized software and analyzed for changes according to hemodynamic status. In terms of the normal state, blood flow was affected by gravity and dependent area showed higher BF and BV and lower MS and MTT than the non-dependent area. The decreased PBF model showed a significant increase in BF and MS (p=0.046, 0.005) but no significant change in BV (p > 0.05), and a slight elongation of MTT (p > 0.05) versus the normal state. The increased PBF model showed a slightly increased BV and a slightly decreased MTT (p > 0.05). The increased PVR model showed significant reduction in BF, BV, and MS (p < 0.000, 0.007, 0.000) and a slight increase in MTT, but without statistical significance (p > 0.05). However, it was noticeable that the distribution of MTT with respect to gravity in the normal lung was completely reversed in the increased PVR model. In conclusion, based on our understanding of perfusion characteristic in normal state, abnormal regional hemodynamic changes in the lung can be detected and evaluated. Predicting changes in pulmonary vascular resistance should be possible by a thorough analysis of CT perfusion parameters.

Animals↗
PubMed1985

[The autonomous nervous system and pulmonary circulation. Stimulation of chemoreceptors and ventilation/perfusion ratios].

The existence of neurogenic pulmonary vasomotrocity and of vasomotor reflexes elicited by stimulation of peripheral chemoreceptors has been demonstrated in different animal species. There are efferent noradrenergic and cholinergic nerve endings in the walls of musculo-pulmonary arteries. Stimulation of sympathetic efferents and exogenous noradrenaline cause vasoconstriction of pulmonary arteries when initial vasomotor tone is normal. There are also beta-adrenergic and cholinergic vasodilation pathways whose effects oppose the above mentioned vasoconstrictor ones, are blocked by the corresponding inhibitors, and can be demonstrated when initial vasomotor tone is high. The role of pulmonary vasomotor tone in the distribution of ventilation perfusion ratios is unknown. The stimulation of peripheral chemoreceptors causes a rise in pulmonary vascular resistance. Inversely, the stimulation of peripheral chemoreceptors by hypoxia prevents the local vasoconstrictor effect of localised alveolar hypoxia in sheep. There are thus theoretical reasons to think that the effect on regional pulmonary resistance of nervous stimulation may differ in cases of inhomogeneous lung disease, according to the local state of the pulmonary vessels. Consequently, it is not possible to anticipate the effect of stimulating chemoreceptors on the distribution of ventilation/perfusion ratios.

Animals↗
PubMed1996

Developmental regulation of angiotensin converting enzyme and angiotensin type 1 receptor in the rat pulmonary circulation.

Factors that influence the development of the normal pulmonary vasculature are poorly understood. Since increased local production of angiotensin II (AII) by angiotensin converting enzyme (ACE) has been implicated in the medial hypertrophy of systemic and pulmonary hypertension, we questioned whether ACE and angiotensin receptor expression may influence the muscularization of the normal pulmonary vasculature during development. The approach employed measurement of lung ACE activity, assessment of local ACE expression by immunohistochemistry, and angiotensin type 1 receptor (AT1) expression by in situ hybridization in rat lungs ranging from 15 days of intrauterine life (term = 21 d) to adulthood. The temporal and spatial pattern of ACE expression was compared with that of the endothelial marker, von Willebrand factor (vWF), and the smooth muscle cell markers, alpha smooth muscle actin and smooth muscle myosin. ACE activity was first detected in lung homogenates on day 17 of gestation (1 +/- 0.2 mU/mg) and increased progressively to term (27.7 +/- 3.2 mU/mg). However, the greatest increase in lung ACE activity to adult levels (379 +/- 25.2 mU/mg) occurred between 2 and 4 wk of postnatal life. Immunohistochemistry demonstrated vWF expression by vascular endothelium throughout the lung as early as day 15 of gestation. In contrast, ACE expression was observed in the endothelium of only hilar pulmonary arteries on day 15 of gestation, and thereafter was noted to be expressed in endothelial cells of progressively more distal arteries, such that by term, endothelial cells of all muscularized arteries expressed ACE. Alveolar capillary ACE expression was not detected until day 20 of gestation, and increased dramatically after birth. Smooth muscle actin expression in lung arteries closely paralleled the expression of endothelial ACE. AT1 receptor mRNA was first expressed in the peripheral lung on day 17 of gestation by non-epithelial undifferentiated mesenchyme. In contrast, AT1 mRNA signal was much reduced in differentiated smooth muscle. We speculate that ACE expression in the fetal lung circulation may influence the muscularization of fetal pulmonary arteries by the interaction of locally produced angiotensin II with the AT1 receptor.

Animals↗