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Results for “PULMONARY CIRCULATION”

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At least 847 records · Page 47Linked to original sources
PubMed1999

In vivo evidence for a myogenic response in the fetal pulmonary circulation.

In vitro studies have suggested that pulmonary arteries can exhibit a myogenic response and that this myogenic response may be potent during the perinatal period. However, whether a myogenic response can be demonstrated to exist in vivo and the potential role of the myogenic response on the regulation of pulmonary blood flow during fetal life is unknown. We hypothesized that an acute increase in pulmonary artery pressure resulting from partial compression of the ductus arteriosus (DA) in the fetus may simultaneously activate two opposing responses: 1) blood flow-induced vasodilation (owing to shear stress); and 2) pressure-induced vasoconstriction (owing to the myogenic response). To test this hypothesis, we studied the hemodynamic response to partial DA compression with and without inhibition of shear stress-induced vasodilation by nitric oxide synthase blockade in chronically prepared late-gestation fetal lambs. Without inhibition of nitric oxide synthase, pulmonary vascular resistance progressively decreased by 39 +/- 5% during the DA compression period (p < 0.05). In contrast, DA compression after nitric oxide synthase inhibition caused left pulmonary artery blood flow to initially increase and then steadily decrease toward a plateau value, and caused pulmonary vascular resistance to progressively increase by 28 +/- 4% above baseline (p < 0.05). The plateau value of pulmonary vascular resistance was reached in less than 5 min after the onset of DA compression. Left pulmonary artery blood flow after 10 min of partial DA compression did not change with the rise in pulmonary artery pressure; plateau values of pulmonary vascular resistance increased linearly with the increase in pulmonary artery pressure. These results support the hypothesis that the perinatal lung circulation has a potent myogenic response, and that this response may be masked in vivo under physiologic conditions by nitric oxide synthase activity. We speculate that the myogenic response may become a predominant regulatory mechanism of pulmonary vascular resistance when endothelium-dependent vasoreactivity is impaired, such as in persistent pulmonary hypertension of the newborn.

Animals↗
PubMed2002

Calcification of homograft valves in the pulmonary circulation -- is it device or donation related?

OBJECTIVE: Homograft valved conduits are used in the reconstruction of right ventricular outflow tract (RVOT), and calcification is a recognised phenomenon in these devices. The purpose of this study was to assess the effect of type (pulmonary and aortic) and mode of harvest of these cryopreserved homografts (cadaveric and beating heart) on the incidence of calcification of these conduits when used in the pulmonary circulation. METHODS: A retrospective study was carried out on 60 patients with congenital heart defects who underwent reconstruction of RVOT using cryopreserved homograft valved conduits. The homografts were harvested from two different groups of donors; beating heart donors and cadaveric donors. The period of study was from 1st January 1990 to 31st December 2000. There were 34 males and 26 females, and the median age was 75 months. The 30-day mortality was 10 (16.7%). The 50 survivors were followed-up 3-108 months (median 36 months). Twenty-four had aortic homografts and 26 pulmonary homografts. Twenty-four devices were from cadaveric donors and 26 from beating heart donors. RESULTS: There were 10 (20%) calcified devices, all aortic in origin. In a logistic regression analysis, aortic homografts were significant risk factor for calcification (P=0.0006). However, source of harvest was not significantly related to the incidence of calcification (P=0.6). CONCLUSION: Cryopreserved pulmonary homografts placed in the right side of the heart are less likely to undergo calcification. Homografts harvested from beating heart donors do not appear to reduce the incidence of calcification.

Adult↗
PubMed1978

Pulmonary circulation of the harbor seal.

Cardiac output (Q) and pulmonary arterial pressure (Ppa) were measured under various conditions in four harbor seals (Phoca vitulina) weighing 35--52 kg. In seals anesthetized with halothane, Q averaged 3.47 l/min; in awake resting seals, Q averaged 11.5 l/min; and during surface dives (i.e., at atmospheric pressure) Q averaged 1.99 l/min. Stroke volume was one-third and two-thirds of the awake resting value during anesthesia and diving, respectively. Systolic Ppa was usually 40--50 Torr in anesthetized and awake resting seals, but was about 10 Torr lower during both surface and compression (i.e., elevated ambient pressure) dives. Diastolic Ppa was constant and high during anesthesia and quite variable in awake resting seals. During both surface and compression dives the diastolic Ppa often fell to the same level as right atrial pressure. We conclude that Q and Ppa are high in awake resting seals and that pulmonary blood flow may cease between beats during diving.

Anesthesia, General↗
PubMed1978

[Effects of isometric exercise on the pulmonary circulation in aortic patients].

The hemodynamic changes of the pulmonary vascular system in patients with aortic stenosis, has been evaluated during isometric exercise (handgrip). Heart rate, left ventricular sistolic pressure and pulmonary artery sistolic pressure, increase significantly while pulmonary vascular resistences are uneffected. In conclusion, the pulmonary response to handgrip olso in patients with aortic stenosis shows the same.

Adult↗
PubMed1977

Prostaglandins and regulation of the pulmonary circulation in the perinatal period.

Effects of indomethacin on pulmonary vasodilation caused by ventilation of the fetal lungs with air were evaluated in anesthetized, exteriorized fetal goats by means of an open-chest pump perfused lung preparation. When fetal lungs are ventilated with air, pulmonary vascular resistance decreases in two steps: 1) a rapid decrease in pulmonary vascular resistance during the first 30 seconds of ventilation, and 2) a slower decline which continues through the first 10-20 minutes of more of ventilation. Indomethacin has minimal effect upon the first component. The second component is absent following treatment with indomethacin. Effects observed with indomethacin were more pronounced in immature fetuses (less than 90% gestation), than in mature fetuses. Prostaglandin synthetase activity appears to have a role in the pulmonary vasodilation resulting from ventilation of the fetal lungs with air.

Animals↗