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Results for “Pulmonary Circulation”

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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↗
PubMed1989

[Effect of steroid therapy on pulmonary circulation in pulmonary sarcoidosis].

Effect of 12 month steroid therapy on pulmonary circulation at rest and during exercise was assessed in 24 patients with histologically confirmed stage II and III pulmonary sarcoidosis. Pulmonary hypertension was found in 3 patients before starting therapy. In the remaining 21 pulmonary artery pressure was within normal limits. In 18 of these an abnormal increase of pulmonary arterial pressure during exercise was found. After 12 months of steroid therapy in all except 2 patients radiological regression was observed. In most patients pulmonary function improved. Normal pulmonary arterial pressure was found in 22 patients. An abnormal increase of pulmonary arterial pressure during exercise was seen in 12 patients. No correlation could be demonstrated between radiological evaluation, respiratory function and effect of steroids on pulmonary circulation.

Adrenal Cortex Hormones↗
PubMed1990

Coronary artery fistula as source of pulmonary circulation in pulmonary atresia with ventricular septal defect.

Four patients are described with pulmonary atresia and ventricular septal defect, in whom the pulmonary circulation was dependent on a fistula from the left coronary artery to the pulmonary artery. The issue in this complex anomaly is complete preoperative diagnosis, including anatomic information on the coronary artery fistula and the pulmonary vasculature. This was achieved in the last 2 patients. In the last patient echocardiography turned out to be an important diagnostic tool in this rare anomaly and facilitated selective angiocardiography. All 4 patients were successfully operated by closing the fistula, closing other aortopulmonary connections and inserting a valved conduit between right ventricle and pulmonary artery. The ventricular septal defect was closed in 3 patients with a patch. In the setting of an already existing pulmonary hypertension and a possibly inadequate pulmonary arterial system at surgery, a perforated patch was inserted in the ventricular septal defect of the remaining patient.

Adolescent↗
PubMed1987

The Cushing responses in the systemic and pulmonary circulation: the role of adrenal glands, bronchial circulation and pulmonary innervation.

Systemic hypertension and increased total peripheral vascular resistance are the most consistent observations in the Cushing responses to an increase in intracranial pressure (ICP). In the present study, we evaluated the participation of adrenal glands, bronchial circulation and pulmonary innervation in the systemic and pulmonary hemodynamics following an intracranial hypertension (ICH). In a total of 18 anesthetized, vagotomized and open-chest dogs, total heart bypass was performed to perfuse the systemic and pulmonary circulation with constant flow. The venous outflows were diverted into reservoirs. The preparation allowed us to observe the simultaneous changes in the systemic vascular resistance (SVR) and capacity (SVC) as well as the pulmonary vascular resistance (PVR) and capacity (PVC). ICH was produced by inflation of an epidural balloon to elevate the ICP to a level of 165-175 mmHg for 1.5 min. Our data showed that ICH induced drastic increases in SVR and PVR accompanying decreases in SVC and PVC. Vascular occlusion of the adrenal glands (n = 6) did not affect the hemodynamic changes. Arrest of bronchial circulation (n = 6) or pulmonary denervation (n = 6) also did not affect the changes in systemic circulation (SVR and SVC), but greatly diminished the pulmonary hemodynamic changes (PVR and PVC). The results suggest that the adrenal glands are not involved in the systemic and pulmonary hemodynamic responses to this degree of ICH. The changes in the pulmonary vascular resistance and capacity require the integrity of bronchial blood supply and sympathetic innervation.

Adrenal Glands↗
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↗
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↗
PubMed1989

[Pulmonary circulation in embolic pulmonary edema].

The ultrasonic method was used in acute experiments on cats with open chest under artificial lung ventilation to obtain blood flow in low-lobar pulmonary artery and vein, the blood pressure in pulmonary artery, as well as the left atrial pressure in fat (olive oil) and mechanical (Lycopodium spores) pulmonary embolism. It is shown that pulmonary embolism produces the decrease in the blood flow in pulmonary artery and vein, the increase of the pressure in pulmonary artery and left atria, the increase of lung vessels resistance. The decrease is observed of systemic arterial pressure, bradycardia, and extrasystole. After 5-10 min the restoration of arterial pressure and heart rhythm occur and partial restoration of blood flow in pulmonary artery and vein. In many experiments the blood flow in vein outdoes that in the artery--it allows to suppose the increase of the blood flow in bronchial artery. After 60-90 min there occur sudden decrease of systemic arterial pressure, the decrease of the blood flow in pulmonary artery and vein. The pressure in pulmonary artery and resistance of pulmonary vessels remain high. Pulmonary edema developed in all animals. The death occurs in 60-100 min after the beginning of embolism.

Animals↗
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↗
PubMed1989

Failure of postnatal adaptation of the pulmonary circulation after chronic intrauterine pulmonary hypertension in fetal lambs.

To determine the effects of chronic intrauterine pulmonary hypertension on the perinatal pulmonary circulation, we induced chronic elevations of pulmonary artery pressure in 24 late-gestation fetal lambs by maintaining partial compression of the ductus arteriosus with an inflatable vascular occluder. Pulmonary artery pressure was increased from 44 +/- 1 to 62 +/- 3 mmHg for 3-14 d. Although left pulmonary artery blood flow initially increased during acute partial ductus compression, the increase in flow was not sustained during chronic ductus compression despite persistent elevations of pulmonary artery pressure (P less than 0.01). Chronic hypertension decreased the slope of the pressure-flow relationship from 3.4 +/- 0.3 (initial) to 0.9 +/- 0.1 ml/min per mmHg, and blunted the fetal pulmonary vascular response to small increases in PO2 (P less than 0.0001). Pulmonary hypertension for greater than 8 d increased the wall thickness of small pulmonary arteries (P less than 0.001). Compared with controls, hypertensive animals had higher pulmonary artery pressure, lower pulmonary blood flow, and predominant right-to-left ductus shunting after cesarean-section delivery (P less than 0.0001). We conclude that chronic pulmonary hypertension in utero, in the absence of hypoxemia or sustained increases in blood flow, causes abnormal fetal pulmonary vasoreactivity, structural remodeling, and the failure to achieve the normal decline in pulmonary resistance at birth.

Adaptation, Physiological↗
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↗