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Results for “PULMONARY CIRCULATION”

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At least 649 records · Page 36Linked to original sources
PubMed1976

[The relationship between the state of the pulmonary circulation and indices of cerebral gas exchange in patients with acquired heart defects].

The author studied the state of hemeostasis in normals and in patients with acquired heart insufficiency. By means of bloody methods of triple probe samples of the blood inflow and outflow from the brain, and by biochemical methods they also studied 22 normals and 100 patients with acquired heart insufficiency for interrelations between the gas metabolism indices and acid-base equilibrium of the central pulmonary hemodynamics. As a results it was established that the brain blood flux in patients with acquired heart insufficiency in different degrees of pulmonary hypertension is adequate to the metabolic requirement of the brain in oxygen and corresponds to identical indices in normals. There was no relation between the state of pulmonary circulation and brain circulation.

Acid-Base Equilibrium↗
PubMed1977

Acute hemodynamic effects of an alpha- and beta-receptor blocking agent (AH 5158) on the systemic and pulmonary circulation at rest and during exercise in hypertensive patients.

The acute hemodynamic effects of 50 mg. of the alpha- and beta-receptor blocking agent AH 5158, administered intravenously, on the systemic and pulmonary circulation were studied in 13 hypertensive patients at rest in the supine and erect positions, and during exercise, with right heart and brachial artery catheterization. AH 5158 induced a significant fall of systemic blooc pressures under all conditions, whereas the pulmonary systolic and mean pressures were lower at rest and unaltered during exercise. The left ventricular filling pressure largely remained unchanged. Blood pressure was lowered predominantly by a reduction in systemic vascular resistance together with a reduction in cardiac output. These effects were particularly pronounced in the erect position and during exercise. Cardiac output was lowered solely by the reduction of heart rate; stroke volume was unchanged or even increased. The arterial-mixed venous oxygen difference increased in the erect position and during exercise. The pattern of AH 5158-induced hemodynamic adaptation comprising a reduction of both vascular resistance and cardiac output, without evidence of significant negative inotropic action, offers a novel basis for treating hypertension with a single drug. Its pharmacological and hemodynamic profile suggests considerable potential in the treatment of hypertensive patients.

Acid-Base Equilibrium↗
PubMed1996

Combined effects of NO inhalation and intravenous PGF2 alpha on pulmonary circulation and gas exchange in an ovine ARDS model.

OBJECTIVES: Inhalation of nitric oxide (NO) selectively dilates pulmonary vessels in well-ventilated regions. Prostaglandin F2 alpha (PGF2 alpha) is a vasoconstrictor and is reported to enhance hypoxic pulmonary vasoconstriction. The objective of this study was to examine whether the combination of intravenous PGF2 alpha and inhaled NO in ARDS lungs has a beneficial effect on oxygenation. DESIGN: We investigated the effect of intravenous PGF2 alpha infusion (0.05-10.0 micrograms/kg per min) with and without NO inhalation (60 ppm) on the hemodynamics and gas exchange in an ovine ARDS model, examining the pulmonary artery pressure versus the flow plot by varying cardiac output. MEASUREMENTS AND RESULTS: After lung lavage, NO inhalation reduced the mean pulmonary arterial pressure (MPAP) by decreasing the zero-flow pressure intercept from 10.6 +/- 3.8 (mean +/- SD) to 8.5 +/- 3.8 mmHg (p < 0.05) with no significant change in slope. NO inhalation improved PaO2 from 56 +/- 12 to 84 +/- 38 mmHg (p < 0.005) and reduced pulmonary shunt from 65 +/- 5 to 53 +/- 8% (Qs/Qt) (p < 0.001). The dose-dependent effects of PGF2 alpha infusion were: (1) increased MPAP attributed to an increased slope in pulmonary artery pressure-flow plot; (2) decreased cardiac index; (3) decreased Qs/Qt with unchanged PaO2. The dose-dependent decrease in Qs/Qt after PGF2 alpha infusion was attributed to the decreased cardiac output. CONCLUSIONS: It is suggested that inhalation of NO reduced the critical vascular pressure near alveoli without affecting upstream vessels, while infused PGF2 alpha constricted the larger upstream pulmonary artery vessels without appreciably affecting the critical pressure. Inhalation of NO into well-ventilated lung areas shifted perfusion to well-oxygenated areas, and there was no supplemental shift in blood flow by adding an infusion of PGF2 alpha.

Administration, Inhalation↗
PubMed1989

Cyclooxygenase inhibition and effects of hypoxia on pulmonary circulation and gas exchange in anesthetized dogs.

To investigate whether endogenously produced prostanoids are involved in hypoxic pulmonary vasoconstriction, pulmonary hemodynamic and gas exchange parameters and eicosanoid metabolites were measured in 5 anesthetized, artificially ventilated dogs (mean body weight 27 kg). Hypoxia elicited pulmonary vasoconstriction, but blood plasma levels of thromboxane B2 (TXB2) and 6-keto-prostaglandin F 1 alpha (6kPGF1 alpha) (stable metabolites of TXA2 and prostaglandin I2, respectively) remained unchanged. Administration of the cyclooxygenase inhibitor indomethacin blocked the synthesis of prostanoids, so that 6kPGF1 alpha and TXB2 levels decreased to values below the detection level (10 pg.ml-1) both during normoxia or hypoxia, but did not affect pulmonary vascular resistance or the alveolar-arterial PO2 difference (PAi-Pa)O2. The pulmonary vascular bed remained, however, responsive to TXA2 as evidenced by infusion of the TXA2 mimetic, U 46619, which significantly increased the pulmonary vascular resistance and (PAi-Pa)O2. Our data suggest that prostanoids are not involved in eliciting the effects of hypoxia on pulmonary hemodynamics and gas exchange efficiency.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Response of pulmonary circulation to oral pirbuterol in chronic airflow obstruction.

The effects of the oral beta agonist pirbuterol on pulmonary haemodynamics and gas exchange were studied in nine patients with severe irreversible airflow obstruction and moderate arterial hypoxaemia. After administration of 15 mg pirbuterol pulmonary vascular resistance fell by 19% but cardiac output rose by 24%, so that pulmonary arterial pressure showed no significant change. Systemic arterial oxygen pressure fell by 7%, limiting the rise in oxygen delivery to 21%. All changes were significant at the 2% level. These results show that pirbuterol dilates the pulmonary bed at the cost of a slight worsening of gas exchange, which is compensated by an independent rise in blood flow.

Adrenergic beta-Agonists↗
PubMed2003

[Pulmonary circulation in the history of medicine].

The history of medicine is frequently equivocal, fanciful and contradictory because of the interlacing with philosophy, theology and astronomy. However, old achievements, that were completely forgotten, are frequently rediscovered and hailed as new. Although widely dispersed in the centuries, we believe that a continual progress in the knowledge of pulmonary circulation is present in the works of the ancient scientists. For instance, Galen's statements that heart and lung act together and that they contribute to the preservation of body heat may anticipate the modern ideas of the metabolism and of heart-lung unit.

Cardiology↗
PubMed1996

Cell-extracellular matrix interactions in the ductus arteriosus and perinatal pulmonary circulation.

Our studies and those of others have shown that changes in the extracellular matrix have profound effects on vascular remodeling. In the ductus, increased production of endothelial hyaluronan and smooth muscle cell chondroitin sulfate and fibronectin and impaired elastin fiber assembly are features critical to smooth muscle cell migration into the subendothelium and intimal cushion formation. There is a developmentally orchestrated process that involves post-transcriptional mechanisms of gene regulation. Closure of the ductus arteriosus is associated with further changes in matrix expression and programmed cell death. The changes in the extracellular matrix that induce neointimal formation are also observed in pathological conditions in pulmonary and coronary arteries. Plasticity of the pulmonary circulation in the perinatal period also involves matrix regulation, and processes that prevent the normal decrease in pulmonary vascular resistance will result in impaired matrix regulation, and in the development of structural changes in the pulmonary arteries, including abnormal smooth muscle cell differentiation, hypertrophy and proliferation, which sustain the elevation in pulmonary artery pressure.

Animals↗
PubMed1985

[Pulmonary circulation hemodynamics in patients with post-infarct left ventricular aneurysm].

The catheterization of right and left compartments of the heart and cinecoronaroventriculography were carried out in 92 patients with chronic post-infarction left-ventricular aneurysm. Fifty-four patients (group 1) showed no clinical signs of heart failure or just a first-stage failure, and 38 patients (group 2) had heart failure at stages IIA and IIB. Highly significant intergroup differences were demonstrated between pressure values in the pulmonary artery (28.7 +/- 1.3 and 48.0 +/- 3.6 mm Hg in groups 1 and 2, respectively), pulmonary capillaries (13.5 +/- 0.7 and 21.4 +/- 2.0 mm Hg), the right atrium (7.1 +/- 0.4 and 9.7 +/- 0.7 mm Hg) as well as right-ventricular end diastolic pressure (6.6 +/- 0.5 and 10.6 +/- 1.0 mm Hg). It is suggested that pulmonary circulation adequately reflects the clinical stage of chronic heart failure in patients with post-infarction left-ventricular aneurysm. Impaired blood outflow from pulmonary veins due to reduced ventricular pump function and inadequate elasticity of the ventricular wall is the primary link in the pathogeny of pulmonary hypertension in patients with left-ventricular aneurysm.

Adult↗