Pretreating ES rats with CCK-8 led to lower mortality rate, amelioration of interstitial edema and inflammatory infiltration in lung, spleen and kidney, reduction in pulmonary arterial hypertension (PAH), and inhibition of TNF-α、IL-1β、IL-6 produced by lung and spleen;
Objective: To investigate the feasibility, safety, and initial clinicaloutcome of autologous endothelial progenitor cell (EPC)transplantation in children with idiopathic pulmonary arterial hypertension (IPAH).
CONCLUSION SanAoXiongTing combined dosage can reduce Pulmonary arterial hypertension of model mouse effectively, the lung blood vessel structure is rebuilt to reverse partly, improve the right heart function, its function mechanism may be with raising plasma CGRP notably, 6- Keto-PGF (la ) level, reduces TXB2 level and influence TXB2/6-Keto-PGF (1a) value to have something to do.
AIM: To study the relationship between the vasoconstrictor effect to 5-hydroxytryptamine (5-HT) and the expression of 5-HT1B-and 5-HT1D-receptors in pulmonary arteries (PA) from normal and pulmonary hypertensive (PHT) rats.
Pulmonary hypertension (PH) is a severe disease affecting both the pulmonary and systemic circulation.
Damage of the heart can further be aggravated in case of additional right ventricular impairment due to pulmonary hypertension in ARDS.
By use of chronic ambulatory PGI2-infusion, patients with primary pulmonary hypertension (PPH) may be bridged for (heart-) lung transplantation.
Repetitive aerosol application of the stable PGI2 analogue iloprost is under consideration for long-term treatment of patients with severe pulmonary hypertension such as primary pulmonary hypertension.
It also causes pulmonary hypertension, a generally undesired effect.
Exciting new surgical procedures, such as minimally invasive surgery, the Cox-Maze procedure for patients with atrial fibrillation, and lung transplantation for patients with severe pulmonary artery hypertension, are now available.
Noninvasive quantitative diagnosis of pulmonary artery hypertension with impedance rheopneumogram in patients with chronic obstr
The role of right ventricular function during acute pulmonary artery hypertension and the effect of acute myocardial injury upon right ventricular performance are examined.
Eight patients who developed pulmonary artery hypertension during the adult respiratory distress syndrome (ARDS) were treated with an infusion of prostacyclin (PGI2, 12.5-35.0 ng·kg-1·min-1) for 45 min.
To determine in the rat whether pulmonary artery hypertension accompanies thromboxane release, we sequentially monitored pulmonary and systemic artery pressures and cardiac output.
The maximal pulmonary hypertensive responses evoked by daltroban represented about half those induced by U-46619 (25.4 ± 1.0 vs.
Further experiments were carried out to determine whether daltroban antagonized the pulmonary hypertensive responses evoked by the high efficacy agonist, U-46619, or by itself as receptor theory would predict for a partial agonist.
Daltroban (10-2500 μg/kg) antagonized, although not fully, U-46619 (20 μg/kg)-evoked pulmonary hypertensive responses, since prominent intrinsic pulmonary hypertensive effects of daltroban were observed in the same range of doses.
Furthermore, in contrast to U-46619 (1.25 μg/kg), daltroban (80 μg/kg) failed to evoke a second pulmonary hypertensive response following a previous injection, as would be expected for a partial agonist.
Preliminary experience indicates that PGI2 can be useful in the treatment of pulmonary hypertensive disorders of the neonate.