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At least 667 records · Page 37Linked to original sources
PubMed1981

Effects of prostacyclin on the fetal pulmonary circulation.

The effects of prostacyclin (PGI2) and its metabolite, 6-keto-PGF1 alpha, on pulmonary and systemic circulations of anesthetized, unventilated fetal goats and sheep were evaluated in situ using an isolated perfused lower left lobe preparation. Results from infusions of PGI2 into the left pulmonary artery suggested dose-dependent decreases in pulmonary vascular resistance (PVR) and mean systemic arterial pressure (SAP). Two-minute infusions produced more pronounced reductions in PVR than 1-minute infusions, and fetal goats exhibited greater depressor responses to PGI2 (2-minute infusions) than fetal lambs. For every 10% decrease in mean pulmonary arterial pressure (PAP), SAP decreased by 3% in sheep receiving 1-minute infusions of PGI2. Systemic hypotensive responses and increases in heart rate were similar in both species. PGI2 appears to be a more powerful dilator of the fetal pulmonary circulation than PGE1 or PGE2; also, intrapulmonary infusions of PGI2 resulted in greater and more sustained systemic hypotensive effects than similar infusions of PGE1 and PGE2. The stable metabolite of PGI2, 6-keto-PGF1 alpha, produced attenuated pulmonary vasodilation. Since PGI2 may produce systemic hypotension, the use of this agent in treatment of persistent pulmonary hypertension should be considered with caution.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Clearance of vasoactive intestinal polypeptide (VIP) in the porcine pulmonary circulation.

The clearance of vasoactive intestinal polypeptide (VIP) in the lung was determined in pigs. To measure the first pass uptake, a bolus of VIP (0.9 pmol.kg-1 and 9 pmol.kg-1) with an inert intravascular marker, indocyanine green (ICG), was injected into the right atrium. The percent uptake of VIP after the higher bolus, as estimated by comparing the levels of VIP and ICG in the pulmonary artery and the aorta, was 36 +/- 6% during control infusion and 36 +/- 13% during continuous infusion of VIP (3 pmol.kg-1.min-1). The VIP concentrations in the pulmonary artery and the aorta were not different under baseline conditions, but during continuous VIP infusion the levels of plasma VIP in the pulmonary artery were higher than those in the aorta (24.3 +/- 1.6 pmol.l-1 and 20.4 +/- 1.3 pmol.l-1, resp. P less than 0.0001). These results indicate that the lung is not a source of plasma VIP, but the pulmonary circulation is a substantial contributor to the removal of VIP from plasma.

Animals↗
PubMed2000

Characterization of purine receptors in fetal lamb pulmonary circulation.

Activation of P1 purinergic receptors by adenosine and P2 receptors by ATP plays an important role in pulmonary vasodilation that occurs at birth in fetal lambs. Purine receptors occur in several subtypes, and the effects of their stimulation vary with the specific type involved. We characterized the subtypes of P1 receptors in fetal lamb pulmonary circulation at 128-132 d gestation by investigating the effects of the following adenosine analogs: N6-cyclopentyl adenosine (A1 selective), 2-phenylaminoadenosine (A2 selective), 2-p-(2-carboxyethyl)phenethyl-amino-5'-N-ethylcarboxamidoadenosine (A2A selective), N6-benzyl-5'-N-ethylcarboxamidoadenosine (A3 selective), and adenosine and 5'-N-ethylcarboxamidoadenosine (nonselective). We repeated the studies after treatment of animals with A1 antagonist 1,3-dipropyl-8-cyclopentylxanthine or A2 antagonist 1,3-dipropyl-7-methylxanthine. Identification of P2 receptors was done by investigation of the effects of P2x agonist beta,gamma-methylene-L-ATP and P2x and P2y agonist ATP. The studies were repeated after the treatment of animals with P2x antagonist suramin and the P2y antagonist cibacron blue. N6-cyclopentyl adenosine caused a significant decrease in heart rate and did not change pulmonary blood flow or pulmonary vascular resistance (PVR). The effect of N6-cyclopentyl adenosine on heart rate was abolished by 1,3-dipropyl-8-cyclopentylxanthine but not by 1,3-dipropyl-7-methylxanthine. 2-Phenylaminoadenosine, 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamidoadenosine, 5'-N-ethylcarboxamidoadenosine, and adenosine caused significant increases in pulmonary flow and decreases in PVR, and their vasodilator effects were attenuated by the A2 antagonist 1,3-dipropyl-7-methylxanthine and not by 1,3-dipropyl-8-cyclopentylxanthine. N6-benzyl-5'-N-ethylcarboxamidoadenosine did not alter pulmonary flow or PVR. The P2x agonist beta,gamma-methylene-L-ATP caused a decrease in heart rate and had no effect on pulmonary flow and PVR. ATP caused a significant increase in pulmonary flow and decrease in PVR without affecting heart rate. The vasodilator effects of ATP were attenuated by cibacron blue and not by suramin. These data demonstrate that adenosine and ATP cause pulmonary vasodilation by activation of A2A and P2y receptors, respectively, in fetal lambs.

Animals↗
PubMed1999

Regulation of pulmonary circulation by alveolar oxygen tension via airway nitric oxide.

The effects of airway (AH) and vascular hypoxia (VH) on the production of nitric oxide (NO; VNO) were tested in isolated buffer-perfused (BFL) and blood-perfused rabbit lungs (BLL). To produce AH and/or VH, the lung was ventilated with 1% O(2) gas, and/or the perfusate was deoxygenated by a membrane oxygenator located on the inlet limb to the pulmonary artery. We measured exhaled NO (VNO), accumulation of perfusate NOx, and pulmonary arterial pressure (Ppa) during AH (inspired O(2) fraction = 0.01) and/or VH (venous PO(2) = 26 Torr). In BFL, a pure AH without VH caused decreases in VNO and NOx accumulation with a rise in Ppa. However, neither VNO, NOx accumulation, nor Ppa changed during VH. Similarly, in BLL, only AH reduced VNO, although NOx accumulation was not measurable because of Hb. When alveolar PO(2) was gradually reduced from 152 to 0 Torr for 20 min, AH reduced VNO curvilinearly from 73.9 +/- 8 to 25.6 +/- 8 nl/min in BFL and from 26.0 +/- 2 to 5. 2 +/- 1 nl/min in BLL. This plot was analogous to that of a substrate-velocity curve for an enzyme obeying Michaelis-Menten kinetics. The apparent Michaelis-Menten constant for O(2) was calculated to be 23.2 microM for BLL and 24.1 microM for BFL. These results indicate that the VNO in the airway epithelia is dependent on the level of inspired O(2) fraction, leading to the tentative conclusion that epithelial NO synthase is O(2) sensitive over the physiological range of alveolar PO(2) and controls pulmonary circulation.

Animals↗
PubMed2005

Hemodynamic evaluation of the peripheral pulmonary circulation by cine phase-contrast magnetic resonance imaging.

PURPOSE: To describe the normal flow patterns in peripheral pulmonary vessels with phase-contrast (PC) magnetic resonance imaging (MRI). MATERIALS AND METHODS: Twelve healthy adults (age = 33 +/- 7 years) underwent cine PC MRI of the segmental and central pulmonary arteries and veins by means of a breath-held segmented k-space technique. Flow patterns were analyzed on time-velocity curves and compared between the peripheral and central vessels. RESULTS: The pulsatile flow patterns in the segmental arteries and veins were similar among individuals. When compared with the central pulmonary arteries, the segmental arteries had a delay in the systolic and diastolic flow velocity waves, and an increased magnitude of the diastolic peaks, in relation to the systolic peaks. A prominent notch was present during the deceleration phase of the systolic flow velocity wave in 79% of the segmental arteries investigated. The segmental veins showed a typical pulmonary venous flow pattern, as seen in the central veins, with similar systolic-to-diastolic peak velocity ratios. CONCLUSION: Noninvasive evaluation of blood flow in intraparenchymal pulmonary vessels is feasible with PC MRI. This first description of normal flow patterns in segmental pulmonary arteries and veins can serve as basis for further investigation in the setting of altered pulmonary blood flows.

Adult↗
PubMed1989

Occlusion pressures vs. micropipette pressures in the pulmonary circulation.

Because of the discrepancies between the arterial and venous occlusion technique and the micropuncture technique in estimating pulmonary capillary pressure gradient, we compared measurements made with the two techniques in the same preparations (isolated left lower lobe of dog lung). In addition, we also obtained direct and reliable measurements of pressures in 0.9-mm arteries and veins using a retrograde catheterization technique, as well as a microvascular pressure made with the double-occlusion technique. The following conclusions were made from dog lobes perfused with autologous blood at normal flow rate of 500-600 ml/min and pressure gradient of 12 mmHg. 1) The double-occlusion technique measures pressure in the capillaries, 2) a small pressure gradient (0.5 mmHg) exists between 30- to 50-micron arteries and veins, 3) a large pressure gradient occurs in arteries and veins greater than 0.9 mm, 4) the arterial and venous occlusion techniques measure pressures in vessels that are less than 900 microns diam but greater than 50 microns, very likely close to 100 microns, 5) serotonin constricts arteries (larger and smaller than 0.9 mm) whereas histamine constricts veins (larger and smaller than 0.9 mm). Thus three different techniques (small retrograde catheter, arterial and venous occlusion, and micropuncture) show consistent results, confirming the presence of significant resistance in large arteries and veins with minimal resistance in the microcirculation.

Animals↗
PubMed1991

Oral prostaglandin E1 derivative (OP-1206) in an infant with double outlet right ventricle and pulmonary stenosis. Effect on ductus-dependent pulmonary circulation.

A small-for-gestational-age infant with cyanosis due to double outlet right ventricle with severe pulmonary stenosis and patent ductus arteriosus was treated with oral prostaglandin E1 derivative (OP-1206). The constricting ductus arteriosus dilated and the ductus-dependent pulmonary blood flow increased. The recommended dosage was 1.5-2.0 micrograms/kg/day which was lower than that of intravenous PGE1 or of oral PGE2. The administration interval was 6 hours, which was longer than that of oral PGE2. The patient was treated as an out-patient because continuous intravenous infusion was not necessary. Treatment was continued for 2 months without complication, at which time a Blalock-Taussig shunt operation was performed. Orally administered PGE1 derivative (OP-1206) was found to be equally effective to intravenous infusion of PGE1 for both short and long-term management of cyanotic heart disease in which the pulmonary blood flow is mostly dependent on the patency of the ductus arteriosus. Oral PGE1 derivative (OP-1206) may be a possible substitute for intravenous PGE1 infusion therapy.

Administration, Oral↗
PubMed2004

Effects of perinatal exposure to hypoxia upon the pulmonary circulation of the adult rat.

The hypothesis on Fetal and Infant Origins of Adult Disease proposes that an altered in utero environment may impair fetal development and physiological function, increasing susceptibility to disease in adulthood. Previous studies demonstrated that reduced fetal growth predisposes to adult cardiovascular diseases. Maternal smoking and high altitude are also linked to reduced fetal growth and adult disease, and both cause fetal hypoxia. We therefore wanted to determine whether fetal hypoxia produces alterations in the adult pulmonary vasculature. Body and ventricular weight, pulmonary arterial compliance and vasoreactivity to potassium chloride (KCl), prostaglandin F2alpha (PGF2alpha), acetylcholine (ACh) and sodium nitroprusside (SNP) were studied in adult rats exposed to 10 % hypoxia throughout the perinatal period, compared to age-matched controls. Rats exposed to perinatal hypoxia had reduced body weight (199+/-15 vs. 294+/-10 g, P<0.001), elevated right ventricular weight (70.3+/-8.8 vs. 51.4+/-1.2 mg/100 g, P<0.05), elevated left ventricular weight (281+/-27 vs. 232+/-5 mg/100 g, P<0.05), reduced pulmonary arterial compliance (35.2+/-2.0 vs. 46.4+/-2.4 microm/mN, P<0.05) and reduced maximal pulmonary vasoconstriction to KCl (1.74+/-0.14 vs. 2.63+/-0.31 mN/mm, P<0.01), and PGF2(2alpha) (1.40+/-0.14 vs. 2.47+/-0.44 mN/mm, P<0.05). Perinatal exposure to hypoxia had a profound effect upon the adult pulmonary circulation, which could predispose to cardiopulmonary diseases in adulthood.

Age Factors↗
PubMed1994

Functional and structural changes with hypoxia in pulmonary circulation of spontaneously hypertensive rats.

Chronic hypoxic pulmonary hypertension involves both vasoconstriction and vascular remodeling. Spontaneously hypertensive rats (SHR) have an increased systemic vascular resistance and a greater responsiveness to constricting stimuli. We hypothesized that, in contrast to age-matched normotensive Wistar-Kyoto rats (WKY), SHR also display spontaneous pulmonary hypertension in normoxia and increased vascular response to acute and chronic hypoxia. Baseline mean pulmonary arterial pressure (PAP) and total pulmonary resistance (TPR) were higher in SHR than in WKY. With acute hypoxia (10% O2 for 15 min), PAP increased to the same extent in SHR and WKY and cardiac output (CO) was unchanged in WKY but increased in SHR. Thus, the rise in PAP in the SHR might be accounted for by the rise in CO, as TPR did not rise, but not that in the WKY, as TPR increased. After 12 days in hypoxia (10% O2), mean arterial pressure was unchanged in WKY but decreased significantly in SHR without a change in CO. PAP increased by 59% in SHR and 54% in WKY when the rats were taken from the hypoxic chamber for 1 h. Acute hypoxic challenge caused a further increase in PAP only in WKY. Medial wall thickness of alveolar duct and terminal bronchial vessels was similar in WKY and SHR after chronic hypoxia. We conclude that SHR exhibit mild baseline pulmonary hypertension in normoxia and that chronic hypoxia does not produce a disproportionate increase in SHR pulmonary vascular remodeling and pulmonary hypertension.

Animals↗