Massive cryptogenic hemoptysis undergoing pulmonary resection: clinical and pathological characteristics and management.

Massive cryptogenic hemoptysis is a common presenting symptom and cause of hospitalization for respiratory diseases, and represents a challenging condition in the clinical. This study aimed to analyze the clinical and pathologic data and management of patients with massive cryptogenic hemoptysis. We retrospectively reviewed 12 patients with massive cryptogenic hemotysis in our hospital between January 2003 and December 2012.

Roxithromycin suppresses airway remodeling and modulates the expression of caveolin-1 and phospho-p42/p44MAPK in asthmatic rats.

Roxithromycin (RXM) expresses anti-asthmatic effects that are separate from its antibiotic activity, but its effects on airway remodeling are still unknown. Here, we evaluated the effects of RXM on airway remodeling and the expression of caveolin-1 and phospho-p42/p44mitogen-activated protein kinase (phospho-p42/p44MAPK) in chronic asthmatic rats. The chronic asthma was induced by ovalbumin/Al(OH)3 sensitization and ovalbumin challenge, RXM (30mg/kg) or dexamethasone (0.

[Functional role of caveolin-1 in airway smooth muscle cells proliferation and regulatory effect of roxithromycin].

Objective: To explore the functional role of caveolin-1 in airway smooth muscle cells (ASMCs) proliferation and examine the regulatory effect of roxithromycin.

Methods: The rat model of bronchial asthma was established. Electron microscope was employed to observe the status of caveolae and light microscope for the histological changes in pulmonary tissues.

Impaired iNOS-sGC-cGMP signalling contributes to chronic hypoxic and hypercapnic pulmonary hypertension in rat.

Nitric oxide (NO) is an important vascular modulator in the development of pulmonary hypertension. NO exerts its regulatory effect mainly by activating soluble guanylate cyclase (sGC) to synthesize cyclic guanosine monophosphate (cGMP). Exposure to hypoxia causes pulmonary hypertension.

[Changes of airway smooth muscle cell apoptosis in asthmatic airway remodeling and the effect of dexamethasone in rats].

Objective: To observe the changes of airway smooth muscle cells (ASMC) apoptosis in the airway remodeling process of asthma, and to evaluate the effect of dexamethasone on ASMC apoptosis and the possible mechanisms.

Methods: Thirty six male Sprague-Dawley rats were randomly divided into 3 groups, including a control group, an asthma group and a dexamethasone treated group. The rats were sensitized with ovalbumin and Al(OH)(3), and repeatedly exposed to aerosolized ovalbumin.

[Influence of the agents which maintain the coordination between spontaneous breathing and mechanical ventilation on haemodynamics and respiration].

Objective: To investigate the haemodynamic and respiratory changes following intravenous administration with midazolam, pavulon or both of them in the patients having incoordination between spontaneous breathing and mechanical ventilation.

Methods: Thirty patients having incoordination between spontaneous breathing and mechanical ventilation were randomly assigned to receiving intravenous injection of pavulon (group 1), midazolam (group 3), and both (group 2) respectively with 10 cases in each group. The degree of coordination between spontaneous breathing and mechanical ventilation, blood pressure (BP), heart rate (HR), respiration frequency (RF), oxygen saturation of pulse (SpO(2)) were observed before the medication and at 5, 15, 30 and 60 minutes following the administration of drugs in all the patients.

[Study on soluble guanylate cyclase in pulmonary hypertension rat model].

Objective: To investigate the mRNA and protein expressions of soluble guanylate cyclase (sGC) and its enzyme activity in pulmonary hypertension rat model which was reproduced by hypoxia and hypercapnia.

Methods: Male Sprague-Dawley rats were randomly divided into hypoxic and hypercapnic group (HH group) and control group (C group). The protein expressions of sGC alpha(1) and sGC beta(1) subunits in medial and small pulmonary arteries was measured by immunohistochemistry method with a polycolonal antibody.