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Results for “PULMONARY CIRCULATION”

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PubMed2000

Osteocalcin metabolism in the pulmonary circulation.

The aim of this study was to evaluate the role of the pulmonary vessel endothelium in the removal of circulating osteocalcin, by measuring the osteocalcin levels in serum from pulmonary and radial artery blood from 39 patients undergoing aorto-coronary bypass. Because of the discrepancies between methods of measurement, two methods were used. Significant differences were observed in group A (n = 18), tested with heterologous radioimmunoassay (2.85 +/- 0.67 microg l-1 in the pulmonary versus 2.69 +/- 0.67 microg l-1 in the radial artery serum, P<0.001) and in group B (n = 21), tested with a two-site immunoradiometric assay (5.22 +/- 1.46 versus 4.93 +/- 1.36 microg l-1, P<0.01). The percentage differences were -5.54 +/- 4.76% (P<0.001) in group A and -4.99 +/- 8.13% (P<0.01) in group B; the comparison between the percentage differences was not significant. These different osteocalcin concentrations between the two vascular compartments were considered a marker of osteocalcin degradation. Therefore, the study seems to demonstrate that, as well as kidney, liver and bone, the lung is a relevant site of osteocalcin catabolism. The proteolytic activity of pulmonary vessel endothelium seems to involve about 5% of the circulating peptide.

Aged↗
PubMed1985

Autonomic regulation of the pulmonary circulation.

Responses to vagal stimulation, acetylcholine, catecholamines, and sympathetic nerve stimulation were investigated in the feline pulmonary vascular bed under conditions of controlled pulmonary blood flow and constant left atrial pressure. Results of these studies suggest that, in the cat, the vagus is composed of efferent fibers from both the sympathetic and parasympathetic systems. The data also suggest that the feline pulmonary vascular bed is functionally innervated by cholinergic nerves, and that vagal stimulation dilates the pulmonary vascular bed by releasing acetylcholine, which acts on muscarinic receptors in pulmonary vessels. alpha and beta 2-adrenoceptors appear to be present in the feline pulmonary vascular bed, and both types of adrenergic receptors are innervated by the sympathetic nervous system. Selective alpha 1- and alpha 2-receptor agonists produce pulmonary vasoconstrictor responses, suggesting the presence of both alpha 1- and alpha 2-receptor subtypes in the feline pulmonary vascular bed. The pulmonary vascular response to norepinephrine, dopamine, and dobutamine is the algebraic summation of activation of alpha- and beta-adrenoceptors. Dopamine possesses greater alpha-(vasoconstrictor) activity when compared to dobutamine, whereas dobutamine has greater beta-(vasodilator) activity.

Acetylcholine↗
PubMed1987

Comparative effects of leukotrienes on porcine pulmonary circulation in vitro and in vivo.

The present study examined the effect of leukotrienes on porcine pulmonary vasculature both in vivo and in vitro. In vitro studies using isolated vascular strips demonstrated that pulmonary arterial smooth muscle contracted to leukotriene C4 (LTC4), whereas pulmonary vein smooth muscle did not. Pulmonary arterial contraction was due to both the direct action of LTC4 and secondarily generated thromboxane A2 (TxA2). In vivo, LTC4 injection caused a pronounced but transient increase in pulmonary arterial pressure and pulmonary arterial wedge pressure (Ppw), with a smaller effect on left ventricular end-diastolic pressure. Effects of LTD4 were smaller with comparable pressure changes at all three sites, suggesting a primary cardiac effect. Like LTC4, histamine caused a disproportionate increase in Ppw vs. left ventricular end-diastolic pressure. These observations suggest that LTC4 causes pulmonary venoconstriction in vivo despite its lack of effect on pulmonary vein smooth muscle in vitro. This discrepancy may be due to venoconstrictor effects of TxA2 generated from upstream pulmonary arterial vessels.

Animals↗
PubMed1985

Effects of exogeneous leukotrienes on the pulmonary circulation.

This review illustrates the diverse effects of LTB4 and the peptidoleukotrienes (LTC4 and LTD4) on pulmonary hemodynamics and lung fluid balance. LTB4 had a lesser effect on pulmonary hemodynamics compared to the peptidoleukotrienes. The small increases in pulmonary artery pressure and pulmonary vascular resistance were the result of precapillary constriction associated with increases in effluent thromboxane concentration. On the other hand, peptidoleukotrienes resulted in marked increases in thromboxane concentrations, pulmonary artery pressure, pulmonary capillary pressure, and pulmonary vascular resistance. Increased thromboxane generation probably contributes to the noted hemodynamic alterations following peptidoleukotriene administration. Moreover, in the isolated perfused guinea pig lung, there was also a direct effect of LTD4 on pulmonary hemodynamics which was not blocked by cyclooxygenase inhibition. This latter, resistant vasoconstrictor response is analogous to the LTD4-mediated pulmonary vasoconstriction in some species which is not dependent on cyclooxygenase (Kadowitz et al., 1984). The primary site of vasoconstriction with LTD4 was in the postcapillary vessels in contrast to the LTB4 response. LTB4 increased lung vascular permeability directly (perhaps by a direct endothelial contracture) and may also contribute to increase in permeability via neutrophil activation. However, the neutrophil dependent permeability-increasing response could not be demonstrated in the isolated perfused guinea pig lung; thus, this response requires further study. In contrast, LTC4 and LTD4 had no effect on lung vascular permeability in the awake sheep, isolated perfused guinea pig lung, and the cultured bovine pulmonary endothelial monolayer system.

Animals↗