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At least 55 records · Page 3Linked to original sources
PubMed1980

[Hemodynamics of pulmonary circulation during pulmonary resection (author's transl)].

In 22 patients continuous measurement of the pulmonary artery pressure was performed during pulmonary resection. A remarkable elevation of the pulmonary artery pressure was observed: a) at the introduction of anesthesia, b) when the lung was compressed during the preparation of the hilus-vessels, c) when the pulmonary artery was ligated, d) at probatory inflation of the lungs. The factors causing the elevation of the pulmonary artery pressure during pulmonary resection are discussed.

Aged↗
PubMed1979

[Role of changes in the hemodynamics of the pulmonary circulation in pulmonary gas exchange].

High pressure in the lung artery was maintained with the aid of i. v. serotonin administration (0.5 mg/ml) in dogs during 10 min. The simultaneous increase of the intravascular pressure in minor circulation and of the lung volume circulation was followed by an increasing blood volume in lungs, diffusion capacity of lungs, oxygen tension in the arterial blood, and satiation of the latter with oxygen. The combined action of the above two hemodynamic factors aids to opening of latent vascular areas, to a more regular distribution of perfusion over the lung areas according to the ventilation level. This mechanism seems to be one of the first compensatory responses to disturbances in the lung gas exchange.

Animals↗
PubMed1976

[Reproductibility of the true measurement of blood volume, cardiac output, mean pulmonary circulation time and pulmonary blood volume by radiocardiography].

Radiocardiography provides a simple method of measurement of blood volume, cardiac output, mean pulmonary circulation time, and pulmonary blood volume. The use of a computer allows the results to produced immediately provided that the circulating blood volume is measured during the test anpd that the radiocardiographic tracing is analysed by an entirely automatic method. The reproducibity of the results given by this automatic method has been studied in 35 patients, two measurements being made at 20 minute intervals. The standard deviation of the percentage difference between consecutive measurements was 5.8% for the blood volume, 10.4% for the cardiac output, 8.8% for the mean pulmonary circulation time, and 9.7% for the pulmonary blood volume.

Adolescent↗
PubMed1990

[Pulmonary circulation in experimental pulmonary edema during diverse artificial respiration regimes].

In acute experiments on cats with closed chest by ultrasonic method the authors studied the blood flow in low-lobar pulmonary artery and the vein, the blood pressure in pulmonary artery, lung vessels resistance in experimental pulmonary edema caused by intravenous infusion of mixture fatty acids at artificial ventilation of increased frequencies or volumes, at was shown, that artificial ventilation of increased frequencies in pulmonary edema reduces the pressure increase in pulmonary artery, lung vessels resistance and increases the blood flow in pulmonary artery and vein. Artificial ventilation of increased volumes produces more intense pressure increase in pulmonary artery and lung vessels resistance than in initial ventilation but the blood flow was slightly changed. The authors assume that artificial ventilation of increased frequencies or volumes in pulmonary edema due to pulmonary circulation change reduces the pulmonary edema intensity at the beginning.

Animals↗
PubMed2005

Current perspectives modern hemodynamic evaluation of the pulmonary circulation. Application to pulmonary arterial hypertension and embolic pulmonary hypertension.

The hemodynamic evaluation of the pulmonary circulation normally includes the measurements of mean pulmonary artery pressure and a calculation of pulmonary vascular resistance (PVR). The definition of PVR can be improved by the measurements of pulmonary vascular pressures at several levels of flow to derive a pressure-flow line, and the site of PVR can be identified by the analysis of pulmonary artery pressure decay curves after balloon occlusion. An analysis of the morphology of pulmonary artery pressure and flow waves informs about right ventricular (RV) hydraulic load. As pulmonary hypertension is clinically a right heart failure syndrome, it is important to measure the coupling of RV to pulmonary arterial function. This can be done using a single beat method with sampling and synchronization of instantaneous pulmonary artery flow and RV pressure to calculate a ratio of end-systolic to arterial elastances. The optimal value of this ratio is depressed in minimally symptomatic pulmonary arterial hypertension patients, indicating pending right heart failure.

Blood Flow Velocity↗
PubMed1989

Effects of beta-agonist and antagonist on the pulmonary circulation and the pulmonary pressor response to 5-HT.

We investigated the effects of beta-agonist and antagonist (isoproterenol, propranolol) on the pulmonary circulation and on the pulmonary pressor response to 5-HT in an isolated canine lung lobe. The pulmonary vessels were dilated by isoproterenol at doses up to 200 micrograms, but were constricted by alpha-adrenoceptor stimulation at relatively high doses. The mechanism by which isoproterenol inhibited the 5-HT response is probably related to the stimulation of beta-adrenoceptors at the lower doses and to the stimulation of alpha-adrenoceptors at the higher doses. Propranolol alone had no effect on pulmonary vascular tone, but inhibited the 5-HT response markedly at doses high, possibly by directly blocking the 5-HT receptors.

Adrenergic beta-Agonists↗
PubMed1993

New perspectives in the pulmonary circulation and hypoxic pulmonary vasoconstriction.

In the past few years there has been a reawakening of interest in the systems that underly pulmonary vascular control and an increased awareness of the clinical potential of pharmacological manipulation of the pulmonary circulation. Nevertheless, although so much has been learned about the physiological role of the endothelium, vasoactive substances, and neural modulation of the pulmonary vasculature; how these disparate influences interact to control the matching of ventilation to perfusion remains uncertain. Consequently, even less is known of the way in which lung injury influences these regulatory processes. It is likely that the response to hypoxia may involve a system with many pathways and much redundancy, such that blockade of the production of a single agent has only a minor effect on HPV. We speculate that the products of arachidonic acid metabolism, PAF, adenosine and EDRF, may act in concert with neural pathways in a 'microenvironment' bounded by the alveolus and endothelium to modify pulmonary vascular tone during both normoxic and hypoxic conditions.

Animals↗