Heart Diseases ; complications ; Humans ; Hypertension, Pulmonary ; etiology

Female ; Humans ; Hypertension, Portal ; complications ; Hypertension, Pulmonary ; etiology ; Middle Aged

Animals ; Cardiovascular Diseases ; etiology ; Coronary Disease ; etiology ; Humans ; Hydrogen Sulfide ; metabolism ; Hypertension ; etiology ; Hypertension, Pulmonary ; etiology ; Myocardial Reperfusion Injury ; etiology

Animals ; Humans ; Hydrogen Sulfide ; Hypertension, Pulmonary ; etiology ; pathology ; physiopathology ; Pulmonary Artery ; physiopathology ; Pulmonary Circulation

Humans ; Hypertension, Pulmonary ; complications ; physiopathology ; Ventricular Dysfunction, Right ; etiology

Heart Defects, Congenital ; complications ; surgery ; Humans ; Hypertension, Pulmonary ; etiology ; surgery

Female ; Humans ; Hypertension, Pulmonary ; etiology ; Middle Aged ; Sjogren's Syndrome ; complications

Humans ; Hypertension, Pulmonary ; etiology ; Male ; Middle Aged ; POEMS Syndrome ; complications

This paper aimed to investigate the effects of high mobility group box 1(HMGB1)-mediated pulmonary artery smooth muscle cell pyroptosis and immune imbalance on chronic obstructive pulmonary disease-associated pulmonary hypertension(COPD-PH) in rats and the intervening mechanism of Compound Tinglizi Decoction. Ninety rats were randomly divided into a normal group, a model group, low-dose, medium-dose, and high-dose Compound Tinglizi Decoction groups, and a simvastatin group. The rat model of COPD-PH was established by fumigation combined with lipopolysaccharide(LPS) intravascular infusion, which lasted 60 days. Rats in the low, medium, and high-dose Compound Tinglizi Decoction groups were given 4.93, 9.87, and 19.74 g·kg~(-1) Compound Tinglizi Decoction by gavage, respectively. Rats in the simvastatin group were given 1.50 mg·kg~(-1) simvastatin by gavage. After 14 days, the lung function, mean pulmonary artery pressure, and arterial blood gas of rats were analyzed. Lung tissues of rats were collected for hematoxylin-eosin(HE) staining to observe the pathological changes. Real-time fluorescent quantitative polymerase chain reaction(qRT-PCR) was used to determine the expression of related mRNA in lung tissues, Western blot(WB) was used to determine the expression of related proteins in lung tissues, and enzyme linked immunosorbent assay(ELISA) was used to determine the levels of inflammatory factors in the lung tissues of rats. The ultrastructure of lung cells was observed by transmission electron microscope. The forced vital capacity(FVC), forced expiratory volume in 0.3 second(FEV_(0.3)), FEV_(0.3)/FVC, peek expiratory flow(PEF), respiratory dynamic compliance(Cdyn), arterial partial pressure of oxygen(PaO_2), and arterial oxygen saturation(SaO_2) were increased, and resistance of expiration(Re), mean pulmonary arterial pressure(mPAP), right ventricular hypertrophy index(RVHI), and arterial partial pressure of carbon dioxide(PaCO_2) were decreased by Compound Tinglizi Decoction in rats with COPD-PH. Compound Tinglizi Decoction inhibited the protein expression of HMGB1, receptor for advanced glycation end products(RAGE), pro caspase-8, cleaved caspase-8, and gasdermin D(GSDMD) in lung tissues of rats with COPD-PH, as well as the mRNA expression of HMGB1, RAGE, and caspase-8. Pulmonary artery smooth muscle cell pyroptosis was inhibited by Compound Tinglizi Decoction. Interferon-γ(IFN-γ) and interleukin-17(IL-17) were reduced, and interleukin-4(IL-4) and interleukin-10(IL-10) were incresead by Compound Tinglizi Decoction in lung tissues of rats with COPD-PH. In addition, the lesion degree of trachea, alveoli, and pulmonary artery in lung tissues of rats with COPD-PH was improved by Compound Tinglizi Decoction. Compound Tinglizi Decoction had dose-dependent effects. The lung function, pulmonary artery pressure, arterial blood gas, inflammation, trachea, alveoli, and pulmonary artery disease have been improved by Compound Tinglizi Decoction, and its mechanism is related to HMGB1-mediated pulmonary artery smooth muscle cell pyroptosis and helper T cell 1(Th1)/helper T cell 2(Th2), helper T cell 17(Th17)/regulatory T cell(Treg) imbalance.
Animals ; Rats ; Caspase 8 ; Pyroptosis ; HMGB1 Protein/genetics* ; Hypertension, Pulmonary/etiology* ; Pulmonary Disease, Chronic Obstructive/genetics*

OBJECTIVETo identify the causes of respiratory complications following liver transplantation (LT) and to discuss the management of these complications.

METHODSOne hundred and twenty four cases with pulmonary complications in the first two weeks after LT were identified among 163 patients admitted to the First Affiliated Hospital, College of Medicine, Zhejiang University from February, 1999 to March, 2003.

RESULTSThe incidence rate of complications was 76%(124/163) with the total cure rate of 92%(114/124). The cure rates of the various complications were as follows: pleural effusion 100%(113/113), pneumonia 92%(76/83), respiratory insufficiency 91%(59/65), pulmonary hypertension 98%(101/103), pulmonary edema 98(58/59), atelectasis 100%(4/4) and pneumothorax 100%(2/2).

CONCLUSIONTo drainage the pleural effusion with an unicameral venous catheter is safety and effective. To cure or prevent pneumonia and atelectasis, aseptic manipulating, aspiration of sputum and keeping respiratory channel open were the key measurements of treatment. Restrictive ventilatory functional disturbance (RVFD) and dysfunction of ventilation are two major types of respiratory insufficiency in early stage of post-transplantation. The causes of pulmonary hypertension and edema are associated with pulmonary angiotasis and blood flow volume, and the vasodilator and diuretic often introduced in the therapy.

Female ; Humans ; Hypertension, Pulmonary ; etiology ; therapy ; Liver Transplantation ; adverse effects ; Male ; Pleural Effusion ; etiology ; therapy ; Pneumonia ; etiology ; therapy ; Postoperative Complications ; etiology ; therapy ; Pulmonary Atelectasis ; etiology ; therapy ; Pulmonary Edema ; etiology ; therapy ; Respiratory Insufficiency ; etiology ; therapy ; Respiratory Tract Diseases ; etiology ; therapy