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At least 19 recordsLinked to original sources
PubMed1992

Pulmonary circulation in pulmonary atresia associated with the asplenia cardiac syndrome.

OBJECTIVE: The goal of this study was to determine the patterns of the pulmonary circulation in patients with pulmonary atresia and asplenia. BACKGROUND: The asplenic cardiac syndromes characteristically have complex cardiac anomalies including pulmonary stenosis or atresia. Definition of the pulmonary artery circulation and pulmonary venous connections is needed for consideration of surgical procedures. METHODS: In 35 patients, the sources of pulmonary blood flow, anatomic features of pulmonary arteries and pulmonary venous connections were determined from angiograms or autopsy specimens. RESULTS: The main pulmonary artery was absent or hypoplastic in 91% of patients; most had a ductus arteriosus. The right and left pulmonary arteries were confluent in 90% and usually of normal size (right 71%, left 63%). Total anomalous pulmonary venous connections were present in 38%. CONCLUSIONS: The anatomic features of the pulmonary arteries in pulmonary atresia associated with the asplenic cardiac syndrome are usually favorable for palliative surgical procedures. Total anomalous pulmonary venous connection may exist as a complicating factor.

Child↗
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↗
PubMed1978

The pulmonary circulation in congenital heart disease. II. Pulmonary hypertension.

In young children with congenital heart disease the pulmonary circulation is exposed to abnormal haemodynamic conditions before it is fully developed. In the newborn infant the persistence or development of pulmonary hypertension rapidly leads to structural change. The speed with which an increase in muscularity can develop has hitherto been underestimated. In most children dying in early infancy with congenital heart disease and pulmonary hypertension the presence of thick walled small arteries is due not to persistence of the high wall thickness of foetal life, but to a rapid postnatal response of the pulmonary circulation to pulmonary hypertension. In older patients with a ventricular septal defect, aged between 3 months and 4 years, the presence of pulmonary hypertension has been shown to interfere with the growth and development of the pulmonary circulation, judging this by reduction in size and multiplication of intra-acinar arteries and an increase in muscularity of both pre and intra-acinar arteries and veins. In these patients elevation of pulmonary vascular resistance was associated with failure of the intra-acinar pulmonary circulation to develop normally and not with obliterative pulmonary vascular disease. Recent studies indicate that growth and development of the peripheral pulmonary circulation can be quantitated in lung biopsies taken from infants and young children with congenital heart disease. It should therefore be possibe to correlate structure and function at a critical period of lung development, before the changes of obliterative pulmonary vascular disease are established.

Aortic Coarctation↗
PubMed1978

Effects of prostaglandin E1 on pulmonary circulation in patients with pulmonary hypertension.

The effects of prostaglandin E1 on pulmonary circulation and left ventricular performance have been studied in 20 patients with mitral valve disease and pulmonary hypertension. Prostaglandin E1 was administered intravenously over a period of 30 minutes. The dose used was 0.01 microgram/kg per min during the first 15 minutes and 0.02 microgram/kg per min subsequently. The first dose led only to an insignificant fall in left ventricular end-diastolic pressure. Infusion of prostaglandin E1 in a dose of 0.02 microgram/kg per min resulted in a significant fall in the pulmonary arterial pressure (P less than 0.001), total pulmonary resistance (P less than 0.001), left ventricular end-diastolic pressure (P less than 0.001), and aortic pressure (P less than 0.01), and an increase in the pulmonary blood volume (P less than 0.01), cardiac index (P less than 0.01), and heart rate (P less than 0.05). No significant differences were noted in stroke volume index or left ventricular dP/dt at 50 mmHg after prostaglandin E1. These results indicate that exogenously administered prostaglandin E1 causes active vasodilatation of the pulmonary vascular bed and has no inotropic action on the cardiac muscle.

Adult↗
PubMed1977

Quantitative structural study of pulmonary circulation in the newborn with pulmonary atresia.

The lungs of eight newborn infants who had died from pulmonary atresia were studied by quantitative morphometric techniques. It was established for the first time that the abnormal pattern of blood flow through the heart and great vessels in a fetus with pulmonary atresia is associated with impaired lung development as shown by arteries that are too few, too small, and with an abnormally thin muscle coat, although the distribution of muscle along the arterial pathway is normal. Differences between the cases in the degree of impairment of lung development could be detected and related to the degree of reduction in pressure and flow before birth in the individual case. Although blood flow through the pulmonary circulation is small before birth lung development seems sensitive to any further reduction.

Blood Pressure↗
PubMed1977

Structural study of pulmonary circulation and of heart in total anomalous pulmonary venous return in early infancy.

Quantitative morphometric techniques have been applied to the injected and inflated lung and to the heart in 9 infants with total anomalous pulmonary venous return dying with obstruction to pulmonary venous return. In 5 (mean age at death 55 days) pge 20 days) to an infradiaphragmatic site. Structural changes were present in the pulmonary circulation in all patients, even in the youngest, an 8-day-old child. In both types of total anomalous pulmonary venous return increased arterial muscularity was severe, as shown by increase in wall thickness and by extension of muscle into smaller and more peripheral arteries than normal; these changes tended to increase with age. Where the pulmonary venous blood drained to a supradiaphragmatic site, the severity of arterial medial hypertrophy correlated inversely with the magnitude of the pulmonary: systemic flow ratio, increasing as the pulmonary blood flow fell. Vein wall thickness was increased and in all but the youngest child the veins were 'arterialised'. At the lung periphery the arteries and alveoli appeared to have multiplied normally. Arterial size varied according to whether pulmonary venous blood drained above or below the diaphragm; the diameter of pre- and intra-acinar arteries was increased only in cases where the pulmonary venous return drained to a supradiaphragmatic site, being normal when it drained to an infradiaphragmatic site. In the heart the left ventricle was of normal size in all but one case. Dilation and severe hypertrophy of the right ventricle and septum were present only in cases of drainage to a supradiaphragmatic site. In the older patients with the latter anomaly dilation of the pulmonary arteries and right ventricle suggested that a large left-to-right shunt had preceded the onset of obstruction to pulmonary venous return and that the more severe right ventricular and septal hypertrophy in these cases might be the result of a longer duration of pulmonary hypertension. In contrast, in total anomalous pulmonary venous return to an infradiaphragmatic site it appears that obstruction to pulmonary venous return develops soon after birth and prevents a large increase in pulmonary blood flow, and thus neither the pulmonary arteries nor the right ventricle become dilated. In infants with total anomalous pulmonary venous return and obstruction to pulmonary venous return, it is striking how rapidly the pulmonary circulation develops new muscle.

Anthropometry↗
PubMed1992

Endothelin dilates bovine pulmonary circulation and reverses hypoxic pulmonary vasoconstriction.

To assess the effects of endothelin 1 (ET) on the pulmonary and systemic vascular beds simultaneously, we examined the hemodynamic responses to ET in awake calves implanted with a Jarvik total artificial heart (TAH), a device that maintains constant cardiac output (CO). During basal conditions, successive incremental intravenous (i.v.) injections of 1, 3, and 10 micrograms ET caused a dose-dependent decrease in pulmonary arterial pressure (PAP), (from 24 +/- 3 to 15 +/- 1 mm Hg, p less than 0.05) while having no effect on systemic arterial (SAP), left atrial (LAP), and right atrial (RAP) pressures. Administration of 30 micrograms ET i.v. also decreased PAP, had no effect on LAP and RAP, but increased SAP from 100 +/- 6 to 118 +/- 4 mm Hg (p less than 0.05). The decrease in PAP was rapid, occurring within seconds and lasting 10 min, whereas the increase in SAP occurred after 2-5 min and was prolonged for greater than or equal to 20 min. As compared with injection in the right atrium, administration of 30 micrograms ET into the left atrium reduced PAP to a similar extent, but induced a greater increase in SAP (+32.5 +/- 4 vs +17.5 +/- 2 mm Hg, p less than 0.05). ET also dose-dependently reversed the acute pulmonary vasoconstriction induced by inhalation of an hypoxic gas mixture. In all cases, pulmonary vasodilation occurred without evidence of short-term tolerance. The results demonstrate that ET is a potent in vivo pulmonary vasodilator. In calves, the predominant hemodynamic response to ET is pulmonary vasodilation, with systemic vasoconstriction apparent only at higher concentrations of the peptide.

Acute Disease↗
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↗
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↗
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↗
PubMed1976

[Hemodynamic analysis of pulmonary circulation by microcatheter technique in healthy persons and in patients with pulmonary silicosis (author's transl)].

A comparison of hemodynamic analysis of pulmonary circulation in 18 healthy men (PM less than 20 Torr) and 19 patients with pulmonary silicosis (PM larger than or equal to 20 Torr) at rest and under work load gave following results: In most healthy persons pulmonary pressure rose under load while resistance of pulmonary circulation decreased significantly. In patients with silicosis pulmonary pressure being elevated at rest reached pathological values under load while resistance of circulation decreased less. There was no difference in cardiac time-volume between both groups. The authors found a linear correlation between cardiac time-volume and oxygen uptake related to body surface. They derived a formula of approximating cardiac time-volume by oxygen uptake and body surface.

Cardiac Output↗
PubMed1979

[Effects of isometric exercise on the right ventricular function and on the pulmonary circulation, in normal subjects (author's transl)].

The pulmonary circulatory response and right ventricular haemodynamics were assessed in normal subjects who sustained hand-grip exercise (HG) at 50% of the maximum voluntary contraction (M.V.C.) for 3 minutes. Ten normal subjects, aged 25 to 66 years, who underwent full right catheterization were studied. The following parameters were taken into consideration: heart rate (HR), end diastolic right ventricular pressure (EDRVP) end diastolic right ventricular volume (EDRVV), mean pulmonary arterial pressure (PAP), pulmonary wedge pressure (PWP), total pulmonary resistance (TPR), cardiac output (CO) and right ventricular sistolic work minute index (RVSWMI). These data were obtained by means of a tip-micromanometer connected with an polygraphic recorder and by means of thermodilution cardiac output computer. The statistical significance of the difference between the resting control values and those after isometric exercise was calculated with the Student's paired t test. A comparison of the control data with those obtained after isometric exercise, demonstrate a statistical significant (p less than 0,001) increase of the HR, PAP, PWP, TRP, CO, RVSWMI, a less significant (p less than 0.01) increase RVEDP. Our findings show that the HG causes changes in the pulmonary circulation and the right ventricular function. Our data seem to sustain that the pulmonary circulation respondes differently under isometric stress than it does under isotonic stress. The use of HG can thus be postulated as a useful means of evaluation of the response of the pulmonary circulation and right ventricular function.

Adult↗