Role of notch signal in angiotensin II induced pulmonary vascular remodeling.

Objective: Notch signal is particularly important to vascular remodeling during the process of embryonic development, vessel repair and tumor growth, but there are few studies about pulmonary vascular remodeling in pulmonary hypertension. This study was to explore the effect of inhibiting Notch signal on pulmonary vascular remodeling induced by angiotensin II.

Methods: Vessel strips taken from healthy Wistar rats were cocultured with extrogenous angiotensin II and the potent smooth muscle cell proliferation stimulators for 7 days.

[The influence of inhibiting notch signal on pulmonary vascular remodeling induced by PDGF].

Objective: To explore the influence of inhibiting Notch signal on pulmonary vascular remodeling induced by PDGF.

Methods: Vessel strips taken from healthy Wistar rats were cultured together with extrogenous PDGF, the potent smooth muscle cell proliferation stimulators, for 7 days. Some vessel strips were cultured with PDGF and gamma-secretase inhibitor DAPT, a Notch signaling inhibitor for 7 days.

[Effect of inhibition of Notch signal on pulmonary vascular remodeling induced by angiotensin Ⅱ].

Objective: It is known that Notch signal is very important to vascular remodeling during the process of embryonic development, vessel repair and tumor growth, but there are few studies about pulmonary vascular remodeling in pulmonary hypertension. This study was to explore the effect of inhibiting Notch signal on pulmonary vascular remodeling induced by angiotensin II.

Methods: Vessel strips taken from healthy Wistar rats were co-cultured with extrogenous angiotensin II and the potent smooth muscle cell proliferation stimulators for 7 days.

[Effects of simvastatin on proliferation and transition of phenotype in PDGF-BB-induced pulmonary artery smooth muscle cells].

Objective: To investigate the effects of simvastatin on inhibiting cell phenotype and potential mechanism in PASMC induced by PDGF-BB.

Methods: PASMC isolated from SD rats and cultured in vitro were induced by PDGF-BB and then intervened by simvastatin and Y-27632. Flow cytometry were performed to detect cell proliferation.

Simvastatin restores down-regulated GATA-6 expression in pulmonary hypertensive rats.

Vascular smooth muscle cell proliferation has been known to be predominant in vascular remodeling of pulmonary hypertensive. The GATA family proteins, a group of zinc finger transcription factors, play an important role during cell proliferation. The aim of present study was to investigate the expression of GATA-6 gene in experimental pulmonary hypertensive rats and explore the effect of regulation of GATA-6 expression by simvastatin on pulmonary vascular remodeling.

[Effect of polycythemia on hypoxia induced pulmonary hypertension and pulmonary vascular remodeling in rats].

Objective: To investigate the effect of polycythemia on hypoxia induced pulmonary hypertension and pulmonary vascular remodeling in rats.

Methods: The healthy female Sprague-Dawley rats were randomly divided into 3 groups: normoxia control group (C group), hypoxia group (H group), hypoxia + different doses of human recombine hemopoietin (rEPO) group. All rats in hyoxia groups were exposed to hypoxia, 8 hours every day, for 21 days.

[Effect of doxycycline on the development of pulmonary hypertension induced by four methods in rats].

Objective: Based on establishment of four rat models of experimental pulmonary hypertension (PH), the authors examined the inhibition of matrix metalloproteinases (MMPs) by doxycycline and its effect on the development of PH and associated pulmonary vascular remodeling.

Method: Healthy male Sprague-Dawley rats (weight 350 g to 400 g) were randomly divided into nine groups: Normal control group (N), four model groups (H, M, P, PM) and their corresponding drug intervention groups (HD, MD, PD, PMD) in which doxycycline was given by gavage at a 20 mg/kg daily dosage. On day 28 (day 35 for PM and PMD models), the animals were catheterized to record mean pulmonary arterial pressure (mPAP) and then sacrificed.

[Changes of MMP-2,9 and TIMP-1 expressions in rats with pulmonary arterial hypertension after captopril and losartan interventions].

Objective: To determine the effect of captopril and losartan on the expressions of matrix metalloproteinase-2,9 (MMP-2,9) and metalloproteinase-1 (TIMP-1) in rats with pulmonary arterial hypertension, and the mechanisms of captopril and losartan in intervening the development of pulmonary arterial hypertension.

Methods: Forty male Spraque-Dawley rats were divided into 4 groups randomly: pulmonary arterial hypertension (created by pneumonectomy plus MCT injection) model group (PAH Model), PAH model treated with captopril [PAH+Cap 10 mg/(kg x d)], losartan group [PAH+Los 15 mg/(kg x d)] and normal control group(Control). The mPAP, weight ratio of RV to LV+S, neointima formation, relative thickness of small pulmonary arteries, and degree of muscularization of non-muscular arterioles were measured at day 35.

[Expression of connective tissue growth factor and its down-regulation by simvastatin administration in pulmonary hypertensive rats].

Objective: To explore the role of expression of connective tissue growth factor (CTGF) in pulmonary vascular remodeling of pulmonary hypertensive rats, and investigate the regulation of CTGF expression by simvastatin in this animal model.

Methods: Eighty male Sprague-Dawley rats (350 to 400 g) were randomized to 7 groups. The rats in group PM(1 - 21) (n = 10) and PM(1 - 35) (n = 12) were treated with pneumonectomy + monocrotaline (MCT), and sacrificed at the 21st or 35th experimental day;those in groups PMS(1 - 35) (n = 12), PMS(21 - 35) (n = 12), PMV(1 - 35) (n = 12) and PMV(21 - 35) (n = 12) were given daily lavage of simvastatin (or vehicle) as intervention measure which began from the 1st and 21st experimental days, respectively; additional 10 rats were used as control without any intervention.

[Effect of triptolide on the development of monocrotaline-induced pulmonary hypertension in pneumonectomized rat].

Objective: To investigate the effect of Triptolide on the development of monocrotaline(MCT)-induced pulmonary hypertension and right ventricular hypertrophy in pneumonectomized rat.

Methods: Sixty male Sprague-Dawley rats were randomly divided into continuous Triptolide therapy group, delayed Triptolide therapy group, two placebo groups, model group and normal group, of which the mean pulmonary arterial pressure (mPAP), right ventricular index (RV/LV+S) were observed or checked. The light microscope, image analysis and immunohistochemistry were used to show percent vascular wall thickness (WT%), the degree of muscularization and vascular occlusion score in pulmonary arteries.

[Effect of triptolide on the expression of matrix metalloproteinases 2 and 9 in lungs of experimental pulmonary hypertension].

Objective: It has been shown that triptolide can attenuate pulmonary arterial hypertension in rats. This study was designed to investigate the therapeutic effect of triptolide on pulmonary hypertension in rats and possible mechanisms.

Methods: Sixty Sprague-Dawley (SD) rats were randomly divided into 6 groups: normal control, model, continuous triptolide-treated, delayed triptolide-treated and two placebo groups for continuous and delayed fashions (n=10 each).

[Effect of simvastatin on rat pulmonary hypertension induced by high pulmonary blood flow and injected monocrotaline].

Objective: To explore the therapeutic effect of simvastatin on the pulmonary hypertension induced by injected monocrotaline combining with high pulmonary blood flow of rats.

Methods: Forty male SD rats were randomly divided into the placebo group, simvastatin 1 mg/(kg x d) group, simvastatin 2 mg/(kg x d) group and control group. The arterial-venous shunt rats were injected with monocrotaline at day 7 and developing the pulmonary hypertension after shunting operation.

[Expression of GATA6 gene in lung tissue of rat with pulmonary hypertension].

Objective: To investigate the expression of GATA6 gene in lung tissue of rat with pulmonary hypertension.

Methods: Male Sprague-Dawley rats (350 to 400 g) were received monocrotaline (MCT) (60 mg/ kg) subcutaneous injection on day 7 after left lung resection. Mean pulmonary artery pressure (mPAP), right ventricle (RV) / [left ventricle (LV)+ interventricular septum (S)] ratio and pulmonary artery wall thickness (WT%) were detected on day 1, 21, 35 after left lung resection, respectively.

[Interventional approach to the treatment of aneurysms of the perimembranous ventricular septal defects].

Objectives: To explore applicable protocol for the positioning of ventricular septal defect (VSD) occluder and the selection of the device by retrospective analysis of transcatheter closure approach to the aneurysms of the perimembranous VSD.

Methods: Thirty-five cases of perimembranous VSD with septal aneurysm (19 males and 16 females) from May, 2004 to May, 2005 were included, with a mean age of 5.3 y and mean weight of 17.

[Effect of captopril on pulmonary vascular remodeling induced by left-to-right shunt in rats].

Objective: To investigate the therapeutic effect of angiotensin converting enzyme inhibitor on pulmonary vascular remodeling of pulmonary hypertension induced by high pulmonary blood flow.

Methods: An arterial-venous shunt was surgically created between abdominal aorta and inferior vena cava in the rat of all groups except the control group. Captopril was given to all of the rats.

[The change of mast cells and macrophages in the lung of rat with pulmonary hypertension].

Objective: To investigate the change of mast cells and macrophages in lung tissue of rats with pulmonary hypertension (PH) and the effect of simvastatin on it.

Methods: Pulmonary hypertension was established as follow, a shunt between abdominal aorta and inferior vena cava was created in rats, 8 days later, the rats were injected with monocrotaline (60 mg/kg). Moreover, a subgroup of rats were given simvastatin 2 mg/ (kg x d).

[Differences of Angiotensin II receptor expression between systemic and pulmonary circulation in children with left-to-right shunt congenital cardiac lesions].

Objective: It has been shown that angiotensin converting enzyme inhibitors (ACEI) can reduce the ratio of pulmonary and systemic circulation blood flow (Qp/Qs) and thus decrease the blood flow of left-to-right shunt in children with left-to-right shunt congenital cardiac lesions. This suggests that there are differences in the expression of Angiotensin II receptors between systemic and pulmonary circulation. This study aimed to explore the differences of Angiotensin II receptors type 1 and type 2 (AT1 and AT2 receptors) expression between systemic and pulmonary circulation in children with left-to-right shunt congenital cardiac lesions.

[Protection of HOE642 against cardiomyocyte injury caused by anoxia and reoxygenation].

Objective: To investigate the protective effect of calcium antagonists (A/R) injury of cardiomyocytes.

Methods: Primary-cultured cardiomyocytes were divided A/R, A/R+nicardipine(Nic), A/R+HOE642, A/R+H7, A/R+PD98059 and control parameters were measured in all groups, intracellular calcium concentration ([Ca2+]i), content, lactate dehydrogenase (LDH) and creative phosphokinase(CK) activity in the activity. The calpain (u-calpain and m-calpain) protein expression levels were measured In comparison with A/R group, A/R + nicardipine (Nic) and A/R + Nic groups showed [Ca2+]i, m-calpain protein expression, LDH and CK content in the medium, a higher activity of PKC and MAPK (P < 0.

[Effects of Losartan on expression of heme oxygenases in volume-overloaded rats with left-to-right shunt].

Objective: To study the expression of heme oxygenase-1 mRNA and pulmonary remodeling before and after surgical establishment of left-to-right shunt in volume-overloaded SD rats and rats with Losartan intervention.

Methods: Left-to-right shunt volume-overloaded SD rat models were established by aortocaval shunt operation. Seven rats with shunt were placed on Losartan (Losartan group), 7 rats with but not given Losartan were included in the operation group, and 4 rats after sham operation served as controls.

[Clinical value of serum matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 for the prediction and early diagnosis of coronary artery lesion in patients with Kawasaki disease].

Objective: Kawasaki disease (KD) complicated with coronary artery lesion (CAL) seriously threatens survival quality and life of patients, suggesting that it is very important to early predict the risk of CAL and to early diagnose the disease. Nevertheless, up to now there has been no specific clinical biochemical marker for it because of the poor understanding of the pathological process of KD with CAL. Matrix metalloproteinases (MMPs) and their specific tissue inhibitor of metalloproteinases (TIMPs) play an important role in arterial wall extracellular matrix breakdown and remodeling and are involved in CAL in other diseases.

[The change of angiotensin II receptors in children with left-to-right shunt].

Objective: To explore the change of AT1 and AT2 receptors in children with left-to-right shunt.

Methods: Lung tissue was obtained from 20 children with left-to-right shunt by biopsy during operation, and lung tissue from 5 children by autopsy was used as control. The above specimens were stained by immunohistochemistry techniques for detecting AT1 and AT2 receptors.

[Expression and variation of angiotensin II type 1 receptor on vascular smooth muscle cells of systemic and pulmonary circulations in experimental ventricular septal defect in pigs].

Objective: To investigate the expression of angiotensin II type 1 receptor (AT1R) on the vascular smooth muscle cells (VSMC) of both systemic and pulmonary circulations and their variation caused by intracardiac left to right shunting using an animal model of the ventricular septal defect (VSD).

Methods: Nineteen young pigs were divided into 3 groups: operation (experimental VSD), sham-operation, and normal control. One month after operation, the pigs were catheterized and then put to death.