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PubMedDate not supplied

[Pulmonary alveolar microlithiasis. Study of pulmonary circulation].

Pulmonary alveolar microlithiasis is a rare disease of unknown etiology which consists of alveolar deposit of calcium microspheres. We report the procedures for the diagnosis of this disease, as well as the hemodynamic features of the pulmonary circulation. Pulmonary arterial hypertension (PAH), and cor pulmonale were documented. The active and passive factors involved in PAH are analyzed. We conclude that alveolar hypoxia and estructural vascular changes play a major role in the genesis of PAH.

Calculi↗
PubMed1980

Effect of prostaglandin E1 on pulmonary circulation in pulmonary atresia. A quantitative morphometric study.

The structural effect of prostaglandin E1 on the pulmonary circulation in pulmonary atresia has been studied by applying quantitative morphometric techniques to the injected and inflated lungs of eight babies who had received prostaglandin E1 for between 30 hours and 12 days. The most striking effect was on the pulmonary arterial smooth muscle. Relative arterial medial thickness was reduced and muscle did not extend as far along the arterial pathway as compared with the normal and with untreated cases of pulmonary atresia, dying at a similar age. The reduction in muscularity tended to increase the longer the duration of infusion. In all cases the thin arterial media was less compact than normal, and localised aneurysmal dilatations occurred, varying in extent and severity between cases. The preacinar arteries were dilated in comparison with the untreated cases, but, by contrast, the intra-acinar arteries remained abnormally small. The number of intra-acinar arteries per unit area of lung was greater in prostaglandin E1 treated than in untreated cases. Infusion of prostaglandin E1 is now the ideal emergency treatment for pulmonary atresia, but the findings in the present study suggest that it should be given for as short a time as possible before the pulmonary blood flow is increased by surgical treatment.

Humans↗
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↗
PubMed1995

NO and H2O2 mechanisms of guanylate cyclase activation in oxygen-dependent responses of rat pulmonary circulation.

Pulmonary hypoxic vasoconstriction appears to have both endothelium-dependent and -independent regulatory pathways. We have previously described a mechanism of guanylate cyclase activation in isolated pulmonary arteries that is smooth muscle contained and oxygen tension dependent. In this study we examine this mechanism, involving H2O2 metabolism by catalase, and its relationship to endothelial-derived nitric oxide in the regulation of pulmonary artery pressure (PAP) by oxygen tension. Using probes selective for these two distinct mechanisms of guanylate cyclase activation, we found in the isolated buffer-perfused rat lung that 100 microM nitro-L-arginine (NLA), an inhibitor of NO formation, increased baseline PAP from 4.8 +/- 0.6 to 6.0 +/- 0.6 mmHg and hypoxic PAP from 6.8 +/- 0.8 to 8.56 +/- 0.6 mmHg. Aminotriazole (AT), an inhibitor of H2O2 metabolism by catalase, also increased PAP from 4.5 +/- 0.9 to 6.1 +/- 2.0 mmHg (P < or = 0.05) and hypoxic PAP from 6.0 +/- 1.7 to 8.7 +/- 2.7 mmHg (P < or = 0.05). Additionally, while NLA did not affect the vasodilation that occurs upon reoxygenation, AT inhibited the immediate response to reoxygenation. In the presence of both NLA and AT, baseline PAP increased from 4.25 +/- 0.8 to 9.9 +/- 0.92 mmHg (P < or = 0.05), but hypoxia did not significantly increase PAP and the reoxygenation response was inhibited. These data suggest that both NO and H2O2-catalase mechanisms contribute to a similar degree to maintain low PAP under normoxic conditions. The removal of either mediator may contribute to hypoxic vasoconstriction.

Amino Acid Oxidoreductases↗
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↗