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At least 271 records · Page 15Linked to original sources
PubMed1989

Severity of cardiac failure from the standpoint of pulmonary circulation: studies centered on distribution of pulmonary perfusion.

In a normal man sitting upright, pulmonary perfusion is several times greater in the lower lung zone than in the upper zone. This pattern may sometimes be reversed in patients with cardiac disease. Tc99m-macro-aggregated albumin pulmonary perfusion images were computerized to isocounts area images (digital perfusion images; DPI). DPI were applied to various types of cardiac disease and patterns of DPI were divided into 4 classes according to amount of nonperfused pulmonary vascular bed. C-0; normal perfusion. C-1; decrease of nonperfused pulmonary vascular bed. C-2; disappearance of nonperfused pulmonary vascular bed. C-3; decrease of pulmonary vascular bed. In 71 patients with mitral stenosis relationships between pulmonary hemodynamics during exercise and distribution of pulmonary perfusion were studied, i.e. at rest (n = 71, mean pulmonary arterial pressure; 23 mmHg-cardiac index; 2.4 L/m) and during exercise C-0 (n = 13, 41 mmHg-5.4 L/m), C-1 (n = 17, 52 mmHg-5.2 L/m), C-2 (n = 27, 52 mmHg-4.5 L/m) and C-3 (n = 14, 65 mmHg-3.6 L/m) respectively. In patients with congestive heart failure cardiac status was classified to 4 classes according to ejection fraction and DPI. Patients with EF less than 30% and DPI more than C-2 showed high morbidity and mortality (two years mortality 47%; 27/40). Pulmonary venous pressure increases to maintain the cardiac index (Starling's law) in cases of decline in cardiac function or mitral stenosis. It was shown that increases in pulmonary venous pressure cause changes in distribution of pulmonary perfusion, which in turn works to depress the cardiac index. A decline in cardiac function and changes in the distribution of pulmonary perfusion coexist, mediated by pulmonary venous pressure and cardiac index. The distribution of pulmonary perfusion reflects the severity of cardiac failure itself, so by using DPI the severity of cardiac failure can be easily evaluated.

Blood Pressure↗
PubMed1989

Acute effect of molsidomine on pulmonary circulation of patients with chronic obstructive pulmonary disease.

Chronic obstructive lung diseases (COLD) are very often complicated by pulmonary arterial hypertension and right heart failure. Several drugs including nitrates have been used to counteract this type of hypertension. Molsidomine (M) is a recent nitrates-like drug acting for a longer time than the classical nitrates. Our aim was to investigate whether M could significantly lower pulmonary arterial hypertension of patients suffering from COLD. Ten male patients were investigated before and after intake of 4.0 mg M given sublingually. Ventilatory and cardiocirculatory indices were measured at rest and during a 30 and a 50 watts exercise. During exercise, M significantly lowers pulmonary arterial pressure and pulmonary vascular resistance without detrimental effect on arterial blood gases. M seems to be a promising drug to counteract the pulmonary hypertension of patients with COLD.

Heart Failure↗
PubMed1988

[Hypoxia and pulmonary circulation. The importance of hypoxia in pulmonary arterial hypertension of chronic obstructive bronchopneumopathies].

In chronic airflow obstruction (CAO), there are grounds for distinguishing between the effects of acute alveolar hypoxia and those of chronic hypoxia. Acute hypoxia leads, in healthy subjects, to pulmonary vasoconstriction. In patients with CAO, there is however a great variability in the pulmonary vascular response to hypoxia. Chronic hypoxia leads in the long term to structural modifications in the pulmonary vessels (arteriolar muscularization, hypertrophy of the small arterial muscles, and intimal fibrosis), which are similar enough to those seen in residents at high altitude and which lead to an elevation of the pulmonary vascular resistance. These structural changes are potentially reversible but one does not know up to which point they are. This potential reversibility represents one of the justifications of long term oxygen therapy in these patients. The pulmonary arterial hypertension of CAO is generally moderated; it evolves slowly over years and years in the majority of cases; it certainly doesn't merit to be treated at any cost. Up to the present, pulmonary vasodilators have given rather disappointing results. Prolonged oxygen therapy (for greater than 16 hours in 24), which improves in other respects the expectation of life in patients is currently the most logical treatment for pulmonary hypertension in CAO.

Humans↗
PubMed1989

Regulation of the pulmonary circulation in the perinatal period and in children.

In the fetus, the pulmonary circulation is actively maintained in a constricted state due to low oxygen environment and perhaps leukotrienes. Pulmonary blood flow represents about 8% of fetal cardiac output. Shortly after birth, pulmonary vascular resistance (PVR) and pulmonary arterial pressure fall rapidly, whereas pulmonary blood flow reaches systemic levels. The exact mechanisms by which the dramatic changes in PVR occur with the onset of ventilation at birth are extensively reviewed. They include: oxygen environment and release of vasoactive substances such as bradykinin, PGI2 or PGD2. Thus, regulation of the fetal and immediate postnatal pulmonary circulation reflects a balance between factors producing active pulmonary vasoconstriction and those producing vasodilatation.

Bradykinin↗
PubMed1989

Ductal left-to-right flow and pulmonary circulation in normal neonates: pulsed Doppler echocardiographic evaluation.

To determine whether ductal left-to-right flow affects pulmonary circulation in the neonatal period, ductal patency and flow patterns of the right ventricular outflow tract were studied using Doppler echocardiography in 40 normal neonates. The ductus arteriosus was defined as being patent when diastolic or continuous flow could be detected at the pulmonary end of the ductus. Evaluation of pulmonary circulation was carried out by examining the flow velocity pattern of the right ventricular outflow tract; pulmonary hypertension was considered to be present when the Doppler echocardiogram pattern was triangular with peak velocity in early systole. Neonates were initially examined within nine hours (mean 5.3 hrs) after birth, and two to three times daily thereafter, until no ductal flow could be detected. In all the neonates, the ductus arteriosus was patent at the initial examination. The predicted time of closure of the ductus arteriosus was within seven hours after birth in 5% of the neonates, within 21 hours in 50%, and within 65 hours in 95%. The flow velocity pattern of the right ventricular outflow tract changed from a triangular shape with peak velocity in early systole soon after birth to a dome-like contour with peak velocity in mid-systole: thus the mean ratio of acceleration time to right ventricular ejection time increased with age. In neonates with patent ductus arteriosus at age 13.6-20.7 hours, the mean ratio of acceleration time to right ventricular ejection time was less than in age-matched neonates with closed ductus arteriosus. These results indicate that the ductal left-to-right flow affects the pulmonary circulation.

Blood Flow Velocity↗
PubMed2006

Computational models of structure-function relationships in the pulmonary circulation and their validation.

The pulmonary airway, arterial, venous and capillary networks are vast complex branching and converging systems that are mechanically coupled to the surrounding lung tissue. Early studies that examined vascular or airway geometry relied on measurements from casts, but medical imaging now enables measurement of the lung in vivo, at controlled lung volumes. The high-quality data that imaging provides have prompted development of increasingly sophisticated models of the geometry of the airway and pulmonary vascular trees. The accurate spatial relationships between airway, vessel and tissue in these imaging-derived models are necessary for computational analysis that aims to elucidate regional airway-vessel-tissue interactions. Predictions of blood flow through multiscale imaging-derived models of the pulmonary arteries and capillary bed reveal geometry-dependent patterns of perfusion in response to gravity and lung orientation that cannot be predicted with simplified, summary representations of the pulmonary transport trees. Validation of such predictions against measures from functional imaging holds significant potential for explaining and differentiating normal and disease-related heterogeneity in regional blood flow calculated using perfusion imaging.

Computer Simulation↗
PubMed1995

D-penicillamine inhibits the action of reactive oxygen species in the pig pulmonary circulation.

Oxygen radicals produced by the hypoxanthine-xanthine oxidase (Hyp-XO) system potently constrict the pulmonary circulation of pigs. D-penicillamine (DPA) is thought to be a free radical scavenger. In the present work we have studied if DPA may influence the vasoactive action of Hyp-XO in pig lungs. Further, we have measured how this drug influences the output of cyclooxygenase and lipoxygenase products from the left atrium in pigs infused with XO into the pulmonary circulation. Twelve young pigs were divided into two groups. Group 1, the XO group, was infused 1 U/kg XO into right atrium. Group 2, the DPA group, was pretreated with DPA, 100 mg/kg intravenously before XO infusion as in group 1. Pulmonary artery pressure, left atrial pressure, pulmonary artery blood flow and systemic blood flow and pressure were recorded continuously. Plasma tromboxane B2 and prostaglandin (6-keto-PGF1 alpha) were determined with a radioimmunoassay method. Cysteinyl containing leukotrienes LTC4, LTD4, and LTE4, were measured together by RIA analyses of plasma samples, using a monoclonal antibody. There was a significant parallel decrease in paO2 and saO2 during the 130 minutes duration of the experiments in both groups without differences between the groups. Pulmonary vascular pressure and resistance increased sharply with a peak found after 25 minutes in the XO group. DPA attenuated the hemodynamic response. DPA inhibited the XO induced pulmonary blood pressure changes with 80% and inhibited the increase in pulmonary vascular resistance 68%. Plasma TXB2 increased two folds in the XO group reaching a maximum after 40 minutes, this effect was completely inhibited by DPA (92% inhibition). DPA also inhibited the XO induced increase in 6-keto-PGF1 alpha, however, not as efficient as with TXB2 (40% inhibition). Plasma cysteinyl leukotrienes increased after XO infusion reaching a peak at 20 minutes. DPA completely abolished this effect (100% inhibition). The study demonstrates that DPA attenuates or even abolishes the hemodynamic effects of XO on the pulmonary circulation in pigs. It seems that DPA inhibits the production of both lipoxygenase and cyclooxygenase products per se, and it is tempting to speculate that the observed DPA effect is caused by its action as an oxygen radical scavenger. It is further speculated that the vasoconstricting effect of XO is due to the fact that oxygen radicals may inactivate nitric oxide (NO), and that DPA stabilizes NO so it more efficiently possess its vasorelaxant activity. We conclude that DPA is an extremely potent inhibitor of XO induced pulmonary vascular effects. The mechanism of action is not fully understood, although its action as an oxygen radical scavenger may explain part of it.

Animals↗
PubMed1975

[Proceedings: The effect of volume manipulation (bloodletting or dextran administration) on pressure in the pulmonary circulation and on the hematocrit].

In a clinical survey the respective effects have been compared of venesection and of hypervolemic hemodilution on hematocrit and pressure in the pulmonary circulation. Whereas after venesection the pressure in the pulmonary circulation and the hematocrit decrease slightly, infusion of 1000 ml Macrodex is followed by marked hemodilution and a distinct increase in pressure in the pulmonary circulation.

Adult↗
PubMedDate not supplied

[Relation between mitral orifice surface area and extent of hemodynamic disorder of the pulmonary circulation in patients with mitral stenosis].

UNLABELLED: Mitral annulus and valves form the mitral orifice area with the size between 4.0-6.0 cm2. Every area which is smaller than this, represents mitral stenosis. As a consequence of mitral stenosis hemodynamic gradients occur over the mitral orifice with circulation disturbances below and above the stenotic mitral valve. The size of transmitral gradient is important in the evaluation of functional or/and structural changes in the blood vessels of pulmonary circulation. This investigation included 40 patients with mitral stenosis (or accompanying minimal mitral regurgitation). All patients underwent echocardiographic examination: area of the mitral orifice was determined and hemodynamic procedure with the left and right heart catheterization was performed. The following hemodynamic parameters were measured: mean capillary wedge pressure, left ventricular filling pressure, left ventricular mean diastolic pressure, mean pulmonary artery pressure. According to these parameters resistance in the pulmonary circulation was measured. The size of the mitral orifice was determined according to oximetry blood analyses and hemodynamic parameters. All patients were divided into 4 groups: minimal (2.5-4.0 cm2), mild (1.5-2.5 cm2), moderate (1.0-1.5 cm2) and severe mitral stenosis (1.0 cm2). The comparison of echocardiographic and hemodynamic parameters revealed a high and positive correlation between the area of mitral orifice. There was also a negative and moderate correlation between the values of stenotic mitral orifice area and total pulmonary resistance, i.e. in all patients with severe mitral stenosis there was an increased pulmonary arteriolar resistance. CONCLUSION: Noninvasive echocardiographic method is valid in the evaluation of stenotic mitral valve area. In the evaluation of hemodynamic parameters in the pulmonary circulation the index of arteriolar pulmonary systemic vascular resistance is very important. In all patients with the area of stenotic mitral orifice 1.0 cm2, there are functional or pathomorphologic changes in the pulmonary circulation of the blood vessel wall.

Echocardiography↗
PubMed1978

[Embryogenesis of the venous portion of the pulmonary circulation].

The wall of the cardiac venous sinus and splanchnic plexus participate in the formation of the venous part of the pulmonary circulation. At the 4th week of the intrauterine life, splanchnic and sinusal parts come into contact. At this stage, the venous part of the pulmonary circulation is represented only by the primary pulmonary vein. Further, from the splanchnic plexus, common and lobar pulmonary veins are formed. At the 6th week of the intrauterine development, assimilation of the primary and common pulmonary veins by the heart is started--the process resulting in the formation of the primary interatrial septa at the expense of the sinusal wall and the walls of the assimilated vessels. By the end of the 8th week of the intrauterine development, the common atrium is separated into the right and left halves up to the auricular canal, the primary and common pulmonary veins are completely assimilated and the venous part of the pulmonary circulation is represented by four pulmonary veins discharging into the left atrium.

Gestational Age↗
PubMed1986

Bronchial venous plexus and its communication with pulmonary circulation.

This study was undertaken to clarify the microvascular anatomy of the normal human bronchial circulation, focusing on the bronchial venous system and its communication with the pulmonary circulation. Ten normal lungs obtained at autopsy were studied. Bronchial arteriography was performed in six lungs, pulmonary arteriography in two lungs, and pulmonary venography in another two. Using radiologic methods, including microradiography, and serial histologic sections, we found numerous bronchial venous plexuses around the airways and blood vessels into which the bronchial capillaries drained. Frequent communications of the venous plexuses with the pulmonary veins and neighboring alveolar capillaries were also demonstrated. The bronchial venous plexus and its close connection with the pulmonary circulation may be important in various pathologic conditions involving the interstitial space, such as interstitial pulmonary edema.

Adult↗
PubMed1975

The functional anatomy of the pulmonary circulation of the domestic fowl.

The architecture of the pulmonary circulation in the domestic fowl was studied in 30 birds of different breeds by injection techniques and serial sections. The branches of the cranial, caudomedial and caudolateral rami of the pulmonary artery form interparabronchial arteries which are essentially transverse to the long axis of the parabronchi. At the periphery of the parabronchus they give rise to intraparabronchial arterioles which form capillaries in the exchange tissue. Most of the capillaries drain into atrial veins via intraparabronchial venules. The atrial veins lie near the parabronchial lumen below the interatrial septa. Some of the capillaries empty into septal venules which form a network underneath the atrial muscles and empty into the atrial veins. The atrial veins draining any particular region converge into a single intraparabronchial vein which penetrates the exchange tissue radially to join an interparabronchial vein. The interparabronchial veins contribute to the cranial and caudal radices of the pulmonary vein. The anatomical pathways of blood and gas indicate a cross-current relationship between pulmonary arterial blood and bulk parabronchial gas flow, and a counter-current relationship between capillary blood and gas in the air capillaries.

Animals↗
PubMed1998

The requirement of intercellular adhesion molecule-1 for neutrophil respiratory burst in the pulmonary circulation of rats infused with endotoxin.

Recently, we demonstrated direct evidence of respiratory burst of the neutrophil in the pulmonary circulation of the endotoxin-infused rat (Am. J. Respir. Crit. Care Med. 1995;152:348-354). To determine the role of intercellular adhesion molecule-1 (ICAM-1) in this model, we neutralized ICAM-1 using antirat ICAM-1 monoclonal antibody (mAb) 1A29. We observed and measured the number of sticking leukocytes and the amount of hydrogen peroxide (H2O2) in the pulmonary circulation of the endotoxin-infused rat by means of a fluoro-imaging technique. The rats received 4.5 mg/kg/h of endotoxin for 2 h. Ten rats received 2 mg/kg of mAb 1A29 20 min before the intravenous infusion of endotoxin. Although the pretreatment with mAb 1A29 did not reduce the number of leukocytes sticking to the pulmonary capillaries, it almost completely inhibited the H2O2 production of leukocytes in the rat lung infused with endotoxin. We confirmed that the leukocytes that produced H2O2 were neutrophil by an electron microscopic cerium technique. We conclude that, although ICAM-1 is not necessary for neutrophil to stick to the capillary in the rat pulmonary circulation infused with endotoxin, ICAM-1 is required for neutrophil H2O2 production in this model.

Animals↗
PubMed1989

Acute effects of partial compression of ductus arteriosus on fetal pulmonary circulation.

To determine the acute effects of increased pulmonary artery pressure and flow on the fetal pulmonary circulation, we studied the response of pulmonary blood flow and vascular reactivity to partial compression of the ductus arteriosus in 22 chronically prepared late-gestation fetal lambs. An inflatable occluder was placed loosely around the ductus arteriosus for compression. Partial compression of the ductus rapidly increased mean pulmonary artery pressure from 45 +/- 1 to 60 +/- 1 mmHg (mean +/- SE) and left pulmonary artery blood flow from 65 +/- 6 to 151 +/- 11 ml/min at 30 min (P less than 0.001; 12 animals). Despite keeping pulmonary artery pressure constant, pulmonary blood flow steadily declined and by 2 h was not different from base-line values. Pulmonary vascular resistance initially fell during the first 30 min of partial compression but then steadily increased and remained elevated above base-line values for at least 30 min after the release of the occluder (P less than 0.001). The decline of pulmonary vascular resistance during the first 30 min of compression was blunted after treatment with the cyclooxygenase inhibitor, meclofenamate (P less than 0.001; 6 animals). Rapid incremental ductus compressions demonstrated a decrease in the slope of the pressure-flow relationship from 3.30 +/- 0.27 (control) to 1.59 +/- 0.21 ml.min-1.mmHg-1 during the postcompression period (P less than 0.001; 12 animals). The vasodilation response to small increases of fetal PO2 was markedly blunted during the postcompression period (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗