No abstract available.
Female ; Humans ; Hypertension, Pulmonary/*drug therapy/*etiology ; Phentermine/*adverse effects/*therapeutic use

Animals ; Humans ; Hypertension, Pulmonary ; etiology ; Inflammation Mediators ; physiology ; Neutrophil Activation ; Platelet Activating Factor ; antagonists & inhibitors ; physiology ; Pulmonary Edema ; etiology ; Respiratory Distress Syndrome, Adult ; drug therapy ; etiology

AIMTo investigate whether pulmonary vascular remodeling in hypoxic pulmonary hypertensive rats could be prevented by treatment with a selective K(ATP)CO, iptkalim (Ipt).

METHODSRats were fed in hypoxic and normobaric environment (10% +/- 0.5% O2, 8 h/day and 6 day/week) and divided into control group, hypoxia group (hypoxic rat treated with ig NS 5.0 ml x kg(-1) x d(-1)), treated group I (hypoxic rat treated with ig Ipt 0.75 mg x kg(-1) x d(-1)), treated group II (hypoxic rat treated with ig Ipt 1.5 mg x kg(-1) x d(-1)). After 4 wk, the mean pulmonary arterial pressure (mPAP), right ventricle/left ventricle and septum [RV/(LV + S)] were measured, and the small pulmonary arterial morphologic changes were observed with morphometric analysis under microscopes in four groups.

RESULTSThe level of mPAP and RV/(LV+ S) was significantly higher in the hypoxic group than those in control group (P < 0.01). Morphometric analysis revealed that the ratio of vascular medial wall thickness to external diameter (MT%) and the ratio of vascular medial cross-sectional area to total arterial cross-sectional area (MA%) were also significantly increased in the hypoxic group than those in control group (P < 0.01) and the ratio of vessel lumen cross-sectional area to total arterial cross-sectional area (VA%) was significantly lower in the hypoxic group than those in control group (P < 0.01). Ipt 0.75 mg x kg(-1) x d(-1) or 1.5 mg x kg(-1) x d(-1) decreased the level of mPAP(mmHg), RV/(LV+ S), and inhibited the small pulmonary arterial remodeling significantly. Ipt 1.5 mg x kg(-1) x d(-1) reversed all pathological indices.

CONCLUSIONK(ATP)CO iptkalim can be a very promising candidate for the treatment of hypoxic pulmonary hypertension.

Animals ; Hypertension, Pulmonary ; drug therapy ; etiology ; physiopathology ; Hypoxia ; physiopathology ; KATP Channels ; agonists ; Male ; Propylamines ; pharmacology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the effect of oral bosentan in the treatment of congenital heart disease-associated pulmonary arterial hypertension.

METHODS24 patients with congenital heart disease-associated pulmonary arterial hypertension, including 4 receiving heart surgery and 20 with surgical contraindications, were enrolled in this study. All the patients were given oral bosentan and followed up regularly for analyzing the outcomes and side effects.

RESULTSOne patient was lost to follow up and one patient died. Systolic pulmonary artery pressure showed no significant changes at 2 (93.6 ± 17.2 mmHg) and 4 months (85.7 ± 25.5 mmHg) of bosentan treatment compared to that before the medication (97.8 ± 14.9 mmHg) (P=0.096), but decreased significantly after a 6-month therapy (80.9 ± 25.0 mmHg, P=0.029). The 6-minute walking distance increased significantly after a 2, 4, and 6-month therapy [(488 ± 98.8, 496.3 ± 89.0, and 491.3 ± 114.2 m, respectively; P=0.004, 0.003, and 0.004 vs the distance before medication (317.0 ± 134.1)]. The New York heart functional classification was improved significantly after a 2, 4, and 6-month therapy [(2.0 ± 0.5, 1.8 ± 0.4, and 1.7 ± 0.5, respectively; P<0.001 vs pre-medication score (2.9 ± 0.5)). Hepatic and renal function remained normal, and ALT and AST showed no significant variations during the medication (P>0.05).

CONCLUSIONOral bosentan can effectively relieve the symptoms, decrease pulmonary artery hypertension, and improve exercise tolerance and cardiac function classification in patients with pulmonary artery hypertension associated with congenital heart disease with good safety and mild side effects.

Administration, Oral ; Antihypertensive Agents ; therapeutic use ; Heart Defects, Congenital ; complications ; Humans ; Hypertension, Pulmonary ; drug therapy ; etiology ; Sulfonamides ; therapeutic use

OBJECTIVETo observe simvastatin treatment of pulmonary hypertension in patients with coal workers pneumoconiosis (CWP).

METHODS96 CWP patients with pulmonary hypertension were randomly divided into treatment and control groups. The control group was treated with 2.5 mg warfarin, once a day for four months; the treatment group was treated with 20 mg simvastatin, taken in evening, for 4 months. 6 min walking distance (6MWD) test and inspection pulmonary artery pressure were measured by echocardiography before and after treatment.

RESULTSIn the treatment group, the 6MWD were (258 ± 26) m after treatment and (225 ± 19) m before treatment, respectively. Compared with control group, pulmonary artery pressure was (41 ± 9) mm Hg in the treatment group before treatment, (36 ± 3) mm Hg in the treatment group after treatment, and (39 ± 5) mm Hg in control group, respectively, the difference was statistically significant (P < 0.05).

CONCLUSIONSSimvastatin can improve pulmonary hypertension in coal workers pneumoconiosis, and shows a definite curative effect.

Aged ; Aged, 80 and over ; Anthracosis ; complications ; drug therapy ; Coal Mining ; Humans ; Hypertension, Pulmonary ; drug therapy ; etiology ; Male ; Middle Aged ; Simvastatin ; therapeutic use

Pulmonary arterial hypertension (PAH) secondary to chronic obstructive pulmonary disease (COPD) is incurable and it has an unpredictable survival rate. Two men who suffered from COPD presented with progressive dyspnea and edema, respectively. PAH, as estimated by the peak velocity of tricuspidal regurgitation, and the depressed myocardial performance index (MPI) of the right ventricle (RV) were noted on echocardiography. In addition to the baseline therapy for their depressed ventilatory function, we prescribed tadalafil 10 mg orally every other day for 2 weeks and then we doubled the dosage. They well tolerated the medication without any notable side effects. After 4 weeks of tadalafil treatment, the patients' pulmonary arterial pressure was decreased and the MPI of the RV was improved in both. The exercise capacity, as measured by the respiratory oxygen uptake, also improved from 10.9 mL/kg/min to 13.8 mL/kg/min in one patient. We report here on 2 patients with PAH secondary to COPD, and they showed notable improvement of their pulmonary hemodynamics and exercise capacity with the administration of tadalafil.
Pulmonary Disease, Chronic Obstructive/*complications ; Pulmonary Artery/drug effects/*pathology ; Phosphodiesterase Inhibitors/*therapeutic use ; Oxygen Consumption/drug effects ; Middle Aged ; Male ; Hypertension, Pulmonary/*drug therapy/etiology ; Humans ; Exercise Tolerance/drug effects ; Carbolines/*therapeutic use

Enbucrilate ; adverse effects ; therapeutic use ; Female ; Humans ; Hypertension, Portal ; diagnosis ; etiology ; Liver Cirrhosis, Biliary ; drug therapy ; Middle Aged ; Pulmonary Embolism ; chemically induced ; diagnosis ; Sepsis ; chemically induced ; etiology

Weight-control drugs (known as anorexigens) such as fenfluramine have been linked with pulmonary hypertension in previous reports. In our case, a 29 year old woman was admitted for shortness of breath and was diagnosed with pulmonary hypertension. Three months ago, she had been taking phentermine for five weeks. Other factors that might have contributed to the development of pulmonary hypertension were excluded. With treatment, her symptoms improved. This is the first case that can suggest a possible connection between phenermine single medication with pulmonary hypertension. Phentermine has been considered a relatively safe drug to treat obesity, and further investigation is needed to decide the safety and dosage of phentermine.
Adult ; Antihypertensive Agents/therapeutic use ; Electrocardiography/methods ; Female ; Humans ; Hypertension, Pulmonary/*drug therapy/*etiology ; Models, Chemical ; Obesity/drug therapy ; Phentermine/*adverse effects/*therapeutic use ; Radiography, Thoracic/methods ; Safety ; Sulfonamides/therapeutic use

OBJECTIVETo investigate the effects of rapamycin (RAP) on pulmonary hypertension (PH) in rats, and to provide new insights into medication selection for the clinical treatment of PH.

METHODSFifty male Sprague-Dawley rats were randomly divided into blank control, PH model, solvent control, RAP 1, and RAP 2 groups. A rat model of PH was induced by left pneumonectomy (PE) and monocrotaline (MCT). At 5 days after PH model establishment, the solvent control group and the RAP 1 group received an intramuscular injection of solvent and RAP, respectively. At 35 days after PH model establishment, the RAP 2 group received an intramuscular injection of RAP. The mean pulmonary artery pressure (mPAP) and the right ventricle/left ventricle plus septum weight ratio (RV/LV+S) were measured in each group. Histopathological changes in the right lung were evaluated by hematoxylin-eosin (HE) staining. The relative expression of alpha-smooth muscle actin (α-SMA) and smooth muscle protein 22-alpha (SM22α) in each group was determined using real-time PCR.

RESULTSAt 35 days after surgery, the PH model and the solvent control groups had significantly higher mPAP and RV/LV+S than the blank control group, while the RAP 1 and the RAP 2 groups had significantly lower mPAP than the solvent control group (P<0.05). The RV/LV+S in the RAP 1 group was significantly lower than that in the solvent control group (P<0.05); however, there was no significant difference in RV/LV+S between the RAP 2 and the solvent control groups (P>0.05). HE staining in the right lung showed the substantially thickened pulmonary artery wall and narrowed arterial lumen in the PH model and the solvent control groups compared with the blank control group. Different degrees of reversal of the pulmonary artery wall thickening were observed after RAP administration. The results of real-time PCR revealed that the relative expression of α-SMA and SM22α in the PH model and the solvent control groups was significantly lower than in the blank control group, while the relative expression of α-SMA and SM22α in the RAP 1 and the RAP 2 groups was significantly higher than in the solvent control group (P<0.05).

CONCLUSIONSRAP can reverse the increase in pulmonary artery pressure and the right ventricular hypertrophy probably by regulation of the phenotypic conversion of vascular smooth muscle cells.

Actins ; genetics ; Animals ; Hemodynamics ; Hypertension, Pulmonary ; drug therapy ; physiopathology ; Hypertrophy, Right Ventricular ; etiology ; Male ; Microfilament Proteins ; genetics ; Muscle Proteins ; genetics ; Pulmonary Artery ; pathology ; RNA, Messenger ; analysis ; Rats ; Rats, Sprague-Dawley ; Sirolimus ; therapeutic use

OBJECTIVETo investigate the role of angiotensin converting enzyme inhibitor (ACEI) in the treatment of acute respiratory distress syndrome (ARDS).

METHODSChanges in physiological and biochemical indexes, and circulating endothelial cells (CEC) were observed in rats of oleic acid-induced ARDS with ACEI-Captopril (Cap) therapy and controls, respectively.

RESULTSUnder the normal systemic blood pressure, Captopril therapy showed good effect on ARDS in rats. Two hours after administration of Captopril, their pulmonary arterial pressure reduced to (14.43 +/- 1.51) mm Hg (1 mm Hg = 0.133 kPa), approximating to normal level, from (23.50 +/- 5.79) mm Hg. The number of CEC, which reflected injuries in pulmonary capillaries, decreased to (4.25 +/- 0.20)/0.9 micro l from (6.88 +/- 1.90)/0.9 micro l. Value of oxygen pressure in arterial blood (PaO(2)) increased to (70.48 +/- 9.54) mm Hg from (35.08 +/- 4.59) mm Hg. In the mean time, ratio of wet to dry lung weight was returned to nearly normal. So, it indicated that high-dose of oleic acid could only induce mild lung injury, and the development of ARDS was obviously inhibited by ACEI.

CONCLUSIONSACEI may effectively depress pulmonary arterial hypertension, block the development of ARDS, and have certain good protective effect on pulmonary capillary endothelia.

Acute Disease ; Angiotensin-Converting Enzyme Inhibitors ; therapeutic use ; Animals ; Captopril ; therapeutic use ; Disease Models, Animal ; Endothelium, Vascular ; drug effects ; physiopathology ; Hypertension, Pulmonary ; complications ; drug therapy ; Male ; Oleic Acid ; Rats ; Rats, Wistar ; Respiratory Distress Syndrome, Adult ; chemically induced ; etiology ; prevention & control