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At least 91 records · Page 5Linked to original sources
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↗
PubMed2005

Obstructive sleep apnea syndrome and the pulmonary circulation.

The pulmonary hemodynamic consequences of obstructive sleep apneas have been investigated by several groups during the last 30 years. The earlier data have been obtained by measuring the intravascular pulmonary arterial pressure (PAP) and have shown a rise of PAP during apneas, the highest PAP being observed at the end of apneas. Actually, during obstructive apneas the only reliable measurements are those of transmural PAP which increases throughout the apneas, as a consequence of hypoxic vasoconstriction, and decreases after ventilation has resumed. The link between episodic (nighttime) and permanent (daytime) pulmonary hypertension is poorly understood. Recent studies have clearly indicated that daytime hypoxemia, generally due to an associated chronic airflow obstruction, is the major determinant of permanent pulmonary hypertension and cor pulmonale, and that nocturnal hypoxemia is not sufficient per se.

Circadian Rhythm↗
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↗
PubMed1989

Effect of prolonged inhibition of angiotensin converting enzyme by captopril on some hemodynamic parameters of pulmonary circulation in patients with secondary pulmonary hypertension.

The effect of prolonged treatment with captopril on some parameters of pulmonary circulation was studied in a group of 17 patients with secondary pulmonary hypertension due to mitral stenosis. Each patient received 25 mg of captopril four times daily for mean time of means = 12.5 +/- 2.1 days. A drop in pulmonary artery mean pressure of at least 20% was observed in 5 patients (29.4%). In 4 patients (23.5%) captopril had adverse effect on the hemodynamics of the pulmonary circulation, and in 8 patients no effect of captopril on the pulmonary hypertension was noticed. Our model of the experiment did not allow us to select before the treatment the group of patients in whom positive effects of captopril could be expected.

Adult↗
PubMed2000

Hypotensive effect of endothelin-1 via endothelin-B-receptor pathway on pulmonary circulation is enhanced in rats with pulmonary hypertension.

The pharmacological characterization of endothelin-1 (ET-1) in the pulmonary circulation in pulmonary hypertension (PH) is not known precisely. We investigated the effect of intravenous injection of ET-1 (1000 pmol/kg) on right ventricular systolic pressure (RVSP) (which is equal to systolic pulmonary arterial pressure) in rats with monocrotaline-induced PH. ET-1 decreased RVSP in PH rats; however, ET-1 did not alter RVSP in control rats, suggesting that ET-1 causes dilatation of the pulmonary artery in PH rats. Under pretreatment with the endothelin-A- (ET(A)) receptor antagonist BMS 193884, ET-1 decreased RVSP in PH rats more than in control rats, suggesting that pulmonary vasodilator action of ET-I mediated via the ET(B)-receptor pathway is augmented in PH rats. Under pretreatment with the ET(A/B)-receptor antagonist SB 209670, the effect of ET-1 in lowering pulmonary arterial pressure was abolished in both groups of rats. These results suggest that the hypotensive effect of ET-1 on pulmonary circulation mediated via the ET(B)-receptor pathway is enhanced in PH rats compared with control normal rats. It is considered that the blockade of only the ET(A)-receptor pathway is preferable to the blockade of both the ET(A)- and ET(B)-receptor pathways in the treatment of PH.

Animals↗