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At least 145 records · Page 8Linked to original sources
PubMed1986

Effects of adenosine triphosphate on pulmonary circulation in chronic obstructive pulmonary disease. ATP: a pulmonary vasoregulator?

Extracellular adenosine triphosphate (ATP) has potent systemic vasodilator and endothelial-dependent relaxant effects on precontracted vessels. Pulmonary uptake and metabolism of ATP have been described, but experimental effects on pulmonary vessels remain controversial in animals. The effects of an intravenously administered infusion of ATP on pulmonary hemodynamic and gasometric data were assessed in 18 patients with stable chronic obstructive pulmonary disease (COPD). Low doses of ATP (successive rates, 1 and 2 mumol/kg body weight, each for 20 min) were infused in pulmonary hypertensive (H; n = 6) and nonhypertensive (N; n = 6) patients. They were compared with a control group (C; n = 6) that received only solvent, using ANOVA. During ATP infusion, a significant pulmonary vasodilation was demonstrated as simultaneous decreases reached, respectively, -14.2% (Group H; p less than 0.005) and -13.8% (Group N; p less than 0.001) for mean pulmonary artery pressure (Ppa), and -31.7% (H; p less than 0.05) and -20.7% (N; p less than 0.01) for pulmonary vascular resistances (PVR), associated with some worsening of hypoxemia: -6.9% (H; p less than 0.01) and -11.8% (n; p less than 0.005). After ATP withdrawal, significant rebound of these data (above baseline values) reached +10.9% (H; p less than 0.05) and +4.4% (N; p less than 0.05) for Ppa and +24.9% (H; p less than 0.05) and +10.2% (N; p = NS) for PVR. At the low infusion rate used, ATP appeared to be a well-tolerated, short-acting, selective pulmonary vasolidating compound in patients with COPD, but therapeutic use remains premature.

Adenosine Triphosphate↗
PubMed1997

Endothelin in the pulmonary circulation with special reference to hypoxic pulmonary vasoconstriction.

1. The experimental model using periods of ventilation with a gas mixture containing 10% oxygen in the anesthetized pig was found to induce HPV that was reproducible and remained stable for up to two hours. 2. Intrapulmonary infusion of ET-1 during normoxia resulted in a dose-dependent increase in the SVR with a concomitant decrease in CO and rise in PVR. Infusion of ET-3 and S6c evoked similar responses, but of a considerably smaller magnitude. The dose-dependent systemic vasoconstriction evoked by ET-1 infusion was reduced after administration of the combined ETA and ETB receptor antagonist bosentan as well as the selective ETA receptor blockers BMS-182874 and TBC-11251 indicating that this effect is primarily mediated by ETA receptors. ETA receptors are present in porcine pulmonary arteries, since BMS-182874 caused a rightward shift of the concentration-response curve to ET-1 in vitro. 3. Administration of selective ETA- or combined ETA and ETB antagonists but not of a selective ETB antagonist reduced the SVR in normoxic pigs, indicating that ET acting through ETA receptors contributes to systemic vascular tone in the pig. In addition, ETA selective and non-selective ETA and ETB antagonists produced a reduction of PVR, although this effect was less consistent than the influence on SVR. This indicates that ETA receptors may contribute to basal pulmonary vascular tone. The plasma levels of ET-1 increased following the non-selective ET receptor antagonist bosentan but were unaffected by selective ETA receptor antagonism. 4. Intrapulmonary infusion of ET-1 produced in low doses a pulmonary vasodilatation during HPV in the pig. This pulmonary vasodilatory effect was also evident when ET-3 or S6c was infused. The pulmonary vasodilatory effect of ET-1 infusion was abolished following administration of the selective ETB receptor antagonist BQ-788, indicating that the pulmonary vasodilatory effect of ET in HPV in the pig is mediated by ETB receptors. Higher doses of ET-1 infusion during HPV resulted in systemic and pulmonary vasoconstriction. 5. Both combined ETA and ETB blockade using bosentan and selective ETA receptor inhibition using BMS-182874 or TBC-11251 reduced the development of HPV in the pig. In addition, bolus injection of TBC-11251 reversed already established HPV. Selective ETB receptor antagonism had no effect on HPV. These findings suggest that ETA receptor activation contributes to HPV in the pig. 6. The concentration-dependent contraction evoked by ET-1 in human vessels in vitro (LAD, IMA, PA, SV) was reduced after incubation with BQ-123 and bosentan. Inhibition of NO- and prostaglandin-synthesis enhanced the contractions in the LAD and IMA, but not in the PA and SV. These findings are in concord with a predominance of ETA receptors in the investigated vessels. Nitric oxide and prostacyclin seem to be important determinants of the functional response to ET in human LAD and IMA, but of less importance in the PA and SV. 7. In the human vessels investigated, the tissue content of ET-1 was higher than that of ET-3 and resembled the distribution of the perivascular C-fiber peptide CGRP. Tissue content of ET-1 was considerably lower than that of sympathetically stored NPY. In human plasma, the arterial and venous concentration of ET-1 was higher in patients with chronic hypoxemia and borderline hypertension than in the venous samples drawn from healthy subjects. The arterial and venous levels of ET-1 did not differ significantly either at rest or during ET-1 infusion, indicating that the pulmonary circulation does not extract ET-1 in these patients. 8. The study in patients with borderline pulmonary hypertension and chronic hypoxaemia showed no pulmonary vasodilatory effects of intrapulmonary ET-1 infusion but rather systemic vasoconstriction and decreased CO. The AVO2 difference increased markedly during ET-1 infusion. 9. (ABSTRACT TRUNCATED)

Adult↗
PubMed1983

[Hemodynamic relations between systemic and pulmonary circulation in hypertension].

Central and pulmonary circulation was studied in 111 patients with essential hypertension, stages I, IIa, IIb, using radio- and polycardiographic techniques. Pulmonary circulation changes associated with output hypertension were manifested in increased systolic pressure in the pulmonary artery and vascular volume of the lungs with increased venous return, and high blood flow rate combined with relatively normal pulmonary vascular resistance (total pulmonary resistance). Decreased cardiac output in vasoconstrictive pressor mechanism results from high total pulmonary resistance and reduced venous return, in addition to high peripheral resistance. Pulmonary hemodynamic changes were particularly pronounced in patients with normokinetic circulation. A quantitative assessment of relationships between major parameters of systemic and pulmonary circulation brought out close functional bonds within one circulatory variant. The findings obtained revealed similar patterns in the mechanisms of systemic and regional pressure formation in essential hypertension.

Adolescent↗
PubMed1992

Circulating endothelin is not extracted by the pulmonary circulation in man.

To determine whether endothelin is extracted from plasma during passage through the pulmonary circulation, we measured its concentration at several points, including the pulmonary artery and the left superior pulmonary vein in seven patients undergoing cardiac surgery. Endothelin concentrations were very similar at all sites sampled. In patients undergoing coronary artery bypass grafting, there is no net pulmonary clearance of endothelin.

Adult↗
PubMed1997

Pulmonary circulation after biventricular repair in patients with major systemic-to-pulmonary collateral arteries.

OBJECTIVE: To determine factors affecting postoperative pulmonary circulation in patients with major systemic-to-pulmonary collateral arteries. METHODS: A total of 48 patients underwent biventricular repair subsequent to unifocalization at ages in the range 1-34 years. The preparative procedures consisted of ligation of the collateral arteries in 6, plasty to the pulmonary arteries using no artificial materials in 12 and extensive reconstruction using heterologous pericardial tubes in 30. The number of the pulmonary vascular segments unifocalized was 9-18 (16 +/- 3). The amount of flow draining via residual minute systemic-to-pulmonary collaterals measured at the time of repair was 4-58% (24 +/- 16%) of the total perfusion by the cardiopulmonary bypass machine. RESULTS: This value was 40 +/- 16% in 5 patients dying in the short term after repair. The number of segments was nine or ten after unifocalization in 2 of these. Another 4 patients died in the longer term, 3 of these with CATCH 22 syndrome dying because of pulmonary hypertension. Postoperative catheterization demonstrated mean pulmonary arterial pressures in the range 8-40 (21 +/- 9) mmHg and pulmonary resistance in the range 1.7-10 (5.0 +/- 2.1) units/m2. Pulmonary resistance was correlated statistically to age at repair (r = 0.77), the number of pulmonary vascular segments (r = -0.41) and to percent collateral flow (r = 0.48). The use of a heterologous pericardial tube for unifocalization was also related probably to higher pulmonary resistance. CONCLUSION: It is essential to accomplish effective unifocalizations followed by earlier definitive repair so as to establish better pulmonary circulation.

Aorta↗
PubMed1991

Tone-dependent responses to endothelin in the isolated perfused fetal sheep pulmonary circulation in situ.

Pulmonary vascular responses to endothelin (ET-1), a peptide derived from endothelial cells in culture, were investigated in the ovine fetus delivered by cesarean section from chloralose-anesthetized ewes with intact umbilical circulation. Circulation to the lower left lobe of the fetal lung was isolated in situ and perfused at constant flow with blood withdrawn from the inferior vena cava. Injection of graded doses of ET-1 into the left pulmonary artery decreased pulmonary arterial perfusion pressure in a dose-related manner. At doses of 100, 300, and 1,000 ng, pulmonary vascular resistance per kilogram body weight (PVR/kg) was decreased 30, 40, and 42%, respectively. However, when fetuses were ventilated with 100% oxygen, 100- and 300-ng doses of ET-1 decreased PVR/kg by 5 and 9%, respectively. In contrast, injection of 1,000 ng of ET-1 resulted in a reversal of the response, and PVR/kg was increased by 70%. Ventilation of the right lung alone resulted in a similar reversal of the vasodilator response to 1,000 ng of ET-1, and a 138% increase in PVR/kg was recorded. These studies demonstrate for the first time that ET-1 has vasodilator activity in the normally high-tone ovine fetal pulmonary circulation. In addition, these results show that ET-1 has vasoconstrictor activity in the newly ventilated low-tone pulmonary vasculature. The present data indicate the pulmonary vascular responses to ET-1 are tone dependent in the ovine fetal pulmonary circulation.

Animals↗
PubMed1999

[Vasomotor control of the pulmonary circulation].

It was demonstrated that pulmonary vessels, in contrast to systemic vessels, 1) have a low basal vascular tone, 2) constrict in response to hypoxia and 3) do not display significantly prominent vasomotion during autonomic nerve stimulation. However, details about these characteristics have not been clarified sufficiently by conventional methods; namely, measuring pressure-flow relationships and vascular tension of isolated larger conduit pulmonary vessels. Recent technological advances in studying pulmonary circulation now permit us to reveal that vasomotor responses to respiratory gases and neurohumoral factors differ not only quantitatively but also qualitatively between the central conduit and peripheral resistance vessels (approximately 100- to 500-micron diam.). They also reveal that an increase in pulmonary sympathetic nerve activity can cause pulmonary vasodilation as well as vasoconstriction. The former has been partly explained by the most recent findings regarding the distribution differences of NO synthases and K+ channels between the resistance and conduit vessels. Concerning the latter, initial vascular tone appears to play an important role. The increased pulmonary sympathetic nerve activity has a beta-receptor-mediated pulmonary vasodilator effect under low pulmonary vascular tone conditions but an alpha-receptor-mediated constrictor effect under enhanced vascular tone conditions. This may serve to maintain homeostasis of the pulmonary circulation and a good balance between the right and left ventricle outputs. Here, I have reviewed new developments related to the mechanisms for controlling pulmonary vascular tone under different states: normal, acute and chronic hypoxia, and hemorrhagic hypotension. I have also described the effects of inhaled NO and PGI2 as selective pulmonary vasodilators used for pulmonary hypertension.

Administration, Inhalation↗
PubMed1976

Pressure-flow-volume relationships in pulmonary circulation of normal highlanders.

Pulmonary vascular pressures and blood flow were measured with and without unilateral pulmonary arterial occlusion (UPAO) at rest and during exercise in 10 normal highlanders at La Paz, Bolivia (altitude, 3,750 m). In 6 other highlanders at rest and during exercise, pulmonary pressures, flow, and blood volume were measured during air breathing (PIO2 congruent to 100 Torr) and 29-30% oxygen (PIO2 congruent to 150 Torr). During air breathing, pulmonary vascular resistance was elevated at rest and did not change with exercise. Pulmonary arterial pressure rose less at rest with UPAO than during exercise without UPAO, and pulmonary vascular resistance was less in the former. Raising PaO2 to normal sea-level values had no effects on the pulmonary circulation at rest but prevented to a large extent the rise in pulmonary arterial pressure during exercise. Hence pulmonary vascular resistance during exercise was lower with oxygen than without. Thus, hypoxic vasoconstriction contributed to the pulmonary hypertension during exercise in normal highlanders. Circumstantial evidence suggests that this is related to the profound mixed venous hypoxemia caused by exercise in a hypoxic environment.

Adolescent↗
PubMedDate not supplied

Massive pulmonary hemorrhage from dual circulation pulmonary arteriovenous malformations in hereditary hemorrhagic telangiectasia.

Pulmonary arteriovenous malformations (AVMs) are commonly supplied by the pulmonary arterial system and rarely by the systemic bronchial circulation. The authors outline the case of a young woman with pulmonary AVMs as part of hereditary hemorrhagic telangiectasia with the uncommon presentation of massive hemoptysis. Management of her recurrent, life-threatening pulmonary hemorrhage was complicated by pulmonary AVMs that were supplied by both the pulmonary and systemic bronchial arterial circulatory systems. Transcatheter embolotherapy of the higher pressure bronchial systemic circuit was necessary for acute hemostasis.

Adult↗
PubMed1986

Adrenoceptor function in the bovine pulmonary circulation.

The bovine pulmonary vascular response to alpha- and beta-agonists was studied using an awake intact calf model. Pulmonary arterial pressure, pulmonary arterial wedge pressure, left atrial pressure, systemic arterial pressure, and cardiac output were measured in response to 3 min infusions of isoproterenol (beta-agonist; 0.12, 0.24, 0.48, 0.9, and 1.8 micrograms X kg-1 X min-1) and phenylephrine (alpha-agonist, 0.15, 0.30, 0.60, 1.15, and 2.30 micrograms X kg-1 X min-1). Phenylephrine caused an increase in vascular resistance in the pulmonary arterial and venous compartments. The slope of the resistance in response to phenylephrine was greater in the pulmonary arterial than pulmonary venous circulation. Isoproterenol resulted in a dose-dependent decrease in vascular resistance in the pulmonary arteries and veins. The vascular resistance was decreased to the same level in the pulmonary arteries and veins although the arteries showed a greater percent change. In addition, isoproterenol infusion resulted in a transient decrease in arterial pH and increase in values for packed cell volume and haemoglobin.

Adrenergic beta-Agonists↗