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At least 199 records · Page 11Linked to original sources
PubMed1983

Cholinergic innervation of the human pulmonary circulation.

The cholinergic innervation of the pulmonary circulation was studied in man. Both extra- and intrapulmonary branches of the pulmonary artery and vein are provided with a cholinergic of the vein. In the main branches of the pulmonary vessels, the existence of two nerve plexuses, a superficial and a deep one, was observed. The superficial plexus is localized in the outer adventitial layer while the deeper plexus is localized in the adventitial-medial transitional zone. In smaller arteries and veins, the existence of a single plexus (adventitial-medial) was observed. In some specimens, the presence of diffuse masses of acetylcholinesterase (AChE)-positive material or elbow-shaped AChE-positive formations was observed. The nature of these formations as well as the possible functional role of a cholinergic system in the pulmonary circulation are discussed.

Acetylcholinesterase↗
PubMed2004

P2Y purine receptor responses and expression in the pulmonary circulation of juvenile rabbits.

The purine nucleotide ATP mediates pulmonary vasodilation at birth by stimulation of P2Y purine receptors in the pulmonary circulation. The specific P2Y receptors in the pulmonary circulation and the segmental distribution of their responses remain unknown. We investigated the effects of purine nucleotides, ATP, ADP, and AMP, and pyrimidine nucleotides, UTP, UDP, and UMP, in juvenile rabbit pulmonary arteries for functional characterization of P2Y receptors. We also studied the expression of P2Y receptor subtypes in pulmonary arteries and the role of nitric oxide (NO), prostaglandins, and cytochrome P-450 metabolites in the response to ATP. In conduit size arteries, ATP, ADP, and AMP caused greater relaxation responses than UTP, UDP, and UMP. In resistance vessels, ATP and UTP caused comparable vasodilation. The response to ATP was attenuated by the P2Y antagonist cibacron blue, the NO synthase antagonist N(omega)-nitro-l-arginine methyl ester (l-NAME), and the cytochrome P-450 inhibitor 17-octadecynoic acid but not by the P2X antagonist alpha,beta-methylene ATP or the cyclooxygenase inhibitor indomethacin in conduit arteries. In the resistance vessels, l-NAME caused a more complete inhibition of the responses to ATP and UTP. Responses to AMP and UMP were NO and endothelium dependent, whereas responses to ADP and UDP were NO and endothelium independent in the conduit arteries. RT-PCR showed expression of P2Y(1), P2Y(2), and P2Y(4) receptors, but not P2Y(6) receptors, in lung parenchyma, pulmonary arteries, and pulmonary artery endothelial cells. These data suggest that distinct P2Y receptors mediate the vasodilator responses to purine and pyrimidine nucleotides in the juvenile rabbit pulmonary circulation. ATP appears to cause NO-mediated vasodilation predominantly through P2Y2 receptors on endothelium.

Adenosine Triphosphate↗
PubMed1982

[Pulmonary circulation and right ventricular function in an experimental model of acute altitude-induced pulmonary edema].

The article deals with hemodynamic shifts that occur during the development of high-altitude pulmonary edema in rabbits. The principal hemodynamic disturbances occur in pulmonary circulation, while the main functional lead falls within the right heart. It was concluded that the increased pulmonary blood content and elevated pulmonary circulation pressure play a certain pathogenetic role in the origin of the syndrome under consideration.

Acute Disease↗
PubMed2005

Role of O(2)-sensitive K(+) and Ca(2+) channels in the regulation of the pulmonary circulation: potential role of caveolae and implications for high altitude pulmonary edema.

High altitude pulmonary edema (HAPE) is a potentially fatal complication in response to exposure to low O(2) at high altitudes. Hypoxia, by causing pulmonary vasoconstriction, increases pulmonary vascular resistance and pulmonary arterial pressure, both of which are features in the pathogenesis of HAPE. Uneven hypoxic pulmonary vasoconstriction is thought to be responsible for increased capillary pressure and leakage, resulting in edema. O(2)-sensitive ion channels are known to play pivotal roles in determining vascular tone in response to hypoxia. K(+), Ca(2+) and Na(+) channels are ubiquitously expressed in both endothelial and smooth muscle cells of the pulmonary microvasculature, subfamilies of which are regulated by local changes in P(O(2)). Hypoxia reduces activity of voltage-gated K(+) channels and down-regulates their expression leading to membrane depolarization, Ca(2+) influx in pulmonary artery smooth muscle cells (by activating voltage-dependent Ca(2+) channels) and vasoconstriction. Hypoxia up-regulates transient receptor potential channels (TRPC) leading to enhanced Ca(2+) entry through receptor- and store-operated Ca(2+) channels. Altered enrichment of ion channels in membrane microdomains, in particular in caveolae, may play a role in excitation-contraction coupling and perhaps in O(2)-sensing in the pulmonary circulation and thereby may contribute to the development of HAPE. We review the role of ion channels, in particular those outlined above, in response to low O(2) on vascular tone and pulmonary edema. Advances in the understanding of ion channels involved in the physiological response to hypoxia should lead to a greater understanding of the pathogenesis of HAPE and perhaps in the identification of new therapies.

Altitude Sickness↗
PubMed2003

Gender differences in the long-term effects of perinatal hypoxia on pulmonary circulation in rats.

Some effects of perinatal hypoxia on pulmonary circulation are permanent. Since pulmonary vascular sensitivity to hypoxia in adults differs between sexes, we hypothesized that gender-based variability also exists in the long-term effects of perinatal hypoxia. Rats spent 1 wk before and 1 wk after birth in hypoxia (12% O2) and then lived in normoxia. When adult, females, but not males, with the perinatal experience of hypoxia had right ventricle hypertrophy. To assess the role of sex hormones, some rats were gonadectomized in ether anesthesia as newborns. Compared with intact, perinatally normoxic controls, muscularization of peripheral pulmonary vessels in adulthood was augmented in perinatally hypoxic, neonatally gonadectomized males (by 85%) and much more so in females (by 533%). Pulmonary artery pressure was elevated in perinatally hypoxic, neonatally gonadectomized females (24.4 +/- 1.7 mmHg) but not males (17.2 +/- 0.6 mmHg). Gonadectomy in adulthood had no effect. We conclude that female pulmonary circulation is more sensitive to late effects of perinatal hypoxia, and these effects are blunted by the presence of ovaries during maturation.

Animals↗
PubMed2003

The pulmonary circulation in bronchopulmonary dysplasia.

Abnormalities of the pulmonary circulation are increasingly being recognized as a major contributor to the high morbidity and mortality of bronchopulmonary dysplasia. Historically, studies have focused on the importance of pulmonary hypertension to the pathophysiology of BPD, with the assumption that pulmonary vascular abnormalities are a secondary consequence of primary injury to the airspace. Recent studies suggest, however, that abnormalities of the pulmonary vasculature, including altered growth and structure, may directly contribute to the abnormal alveolarization that characterizes the condition. In this article, we briefly outline mechanisms of pulmonary vascular injury in infants at risk of BPD. We then focus on the recognition and management of pulmonary hypertension in these infants. Finally, we review how disordered pulmonary vascular growth may contribute to the pathogenesis of BPD and emphasize the importance of the reciprocal development of the airspace and the pulmonary circulation.

Bronchopulmonary Dysplasia↗
PubMed1981

Hemodynamics of pulmonary circulation in asbestosis: study of 16 cases.

Pulmonary circulation hemodynamics was studied by microcatheterization at rest and during exercise in 16 workers with asbestosis. There was pulmonary arterial hypertension owing to increased total pulmonary resistance even in the early stages of pneumoconiosis, sometimes without impairment of lung function. In two cases, a partial reduction in pulmonary hypertension and total pulmonary resistance was obtained with aminophylline. The pathogenesis of pulmonary circulation impairment has been attributed in previous work to periarteriolar fibrosis originating in the lymphatic vessels, until now insufficiently emphasized as the anatomical basis of these physiological alterations.

Adult↗
PubMed1983

[Effects of methysergide on pulmonary circulation].

The effects of methysergide (a serotonin antagonist) on the pulmonary circulation were investigated experimentally. Twenty-eight mongrel dogs were anesthetized with sodium pentobarbital, and thoracotomy was carried out. A micro-tip pressure transducer was inserted into the pulmonary trunk and an electromagnetic flow probe was placed around it. Aortic and left atrial pressure were also measured. Three different doses (100, 250 and 1000 micrograms/kg) of methysergide and a dose of 3 micrograms/kg of serotonin were infused rapidly into the right atrium through a catheter inserted transvenously. Then, all parameters were continuously recorded. Furthermore, moduli of pulmonary vascular input impedance were calculated from pulmonary pressure and flow waves by means of Fourier analysis. The administration of each dose of methysergide resulted in an increase in pulmonary arterial pressure and resistance and a decrease in heart rate. With the highest dose of methysergide, the aortic pressure was decreased moderately. No increase in pulmonary vascular resistance was observed even after serotonin administration under the treatment with methysergide(1000 micrograms/kg). Although the characteristic impedance did not change significantly with methysergide, the impedance modulus at 0-frequency and low frequencies increased slightly in magnitude. The shift of the frequency of the impedance minimum was slight in comparison with the case of serotonin. These findings were similar to those obtained with serotonin, in general, The results have shown that methysergide produces serotonin-like effects on the pulmonary circulation, and have suggested that it may stimulate serotonin receptors in the pulmonary vascular smooth muscles as a partial agonist. It is desirable that serotonin antagonist have little effect by itself on the pulmonary circulation, in order to determine the role of serotonin in some pulmonary circulatory disturbances.

Animals↗
PubMed1991

[Effects of prostaglandins on pulmonary circulation].

Effects of prostacyclin (PGI2) and thromboxane A2 (TxA2) on pulmonary circulation and pulmonary edema were studied in 24 dogs. The heart and lungs were provided with an autoperfusion circulation. Mean aortic pressure and cardiac output were maintained at 80 mmHg and 40 ml.kg-1.min-1, respectively. The animals were divided evenly into 4 groups: group 1, control; group 2, PGI2-analog loaded; group 3, TxA2-analog loaded; and group 4, TxA2-antagonist loaded. The heart-lung tissues were autoperfused for 4 hours. During the experimental period, respiratory parameters (PaCO2 and PaO2) showed no significant change, but significant elevations of mean pulmonary arterial pressure and mean left atrial pressure were observed in group 3. The radiological pulmonary dilution curve changed significantly during autoperfusion. The half-life and the mean transit time were both prolonged significantly in groups 1, 3 and 4, but unchanged in group 2. Characteristic pathological pulmonary vascular changes, intravascular leukocyte sequestration, capillary dilatation and perivascular edema were observed in groups 1 and 3. Those changes were attenuated in group 4 and prevented in group 2. In conclusions, pulmonary circulation was impaired by TxA2, whereas maintained by PGI2. These findings show that TxA2 and PGI2 may modify blood-vessel interaction, and organ damage may occur in the case of TxA2 and organ may be preserved in the case of PGI2.

Animals↗
PubMed1998

Pulmonary circulation.

Evaluation of the pulmonary vasculature is mainly indicated in patients with suspected pulmonary thromboembolism. The routine procedure so far is ventilation-perfusion scintigraphy alone or in combination with diagnostic assessment of the legs to rule out deep venous thrombosis. The results are still not reliable for the majority of patients. In the case of equivocal diagnosis, invasive conventional angiography is considered the gold standard. With steady improvements in tomographic imaging techniques, such as computed tomography (CT) or magnetic resonance imaging (MRI), non-invasive alternatives to the routine diagnostic work-up are given. Helical CT and CTA techniques are already in clinical use and estimated to sufficiently serve the demands for detection/exclusion of pulmonary thromboembolism. The disadvantages mainly concern peripheral disease and reconstruction artifacts. MRI and MR angiography have been implemented in the diagnosis of pulmonary vascular disease since the introduction of contrast-enhanced MRA. In breath-hold techniques, the entire lung vascularization can be delineated and thromboemboli can be detected. The clinical experience in this field is limited, but MRI has the potential to demonstrate its superiority over CT due to its improved delineation of the vascular periphery and the more comprehensive three-dimensional reconstruction.

Aged↗
PubMed1988

Dynamics of the pulmonary circulation in systemic hypertension.

Pulmonary and systemic hemodynamics in 28 mild to moderate hypertensive patients (group II) with left ventricular (LV) hypertrophy (ECG and echo criteria) and 22 severe hypertensive patients with LV hypertrophy (group III) were compared with 20 patients with mild-to-moderate hypertension in WHO stage I (group I). Mean right atrial pressure was equivalent in groups II and III and significantly higher in the last group than in group I. An increased pulmonary arterial resistance (PAR) in group II and, to a large extent, in group III accounted for the elevation of diastolic and mean pulmonary arterial pressure in both groups in comparison with group I. Cardiac index (CI) was lower and systemic vascular resistance (SVR) higher in group III than in group I. Pulmonary capillary wedge pressure (PCWP) values were within the normal range and equivalent between groups II and III, and both significantly higher than in group I. PAR showed a positive relation with SVR (r = 0.30, P less than 0.01) and an inverse relation with CI (r = -0.561, P less than 0.001). Findings indicate that in systemic hypertension with LV hypertrophy there is an elevation of the right ventricular filling pressure and the pulmonary arterial pressure whose degree is even higher in severe hypertension. This increase is not necessarily a consequence of impairment of LV function as suggested by the normal range of PCWP values.

Blood Pressure↗