[Therapy for clearing heat and resolving phlegm in treatment of systemic inflammatory response syndrome in acute deterioration stage of chronic obstructive pulmonary disease: a randomized controlled trial].

OBJECTIVE: To investigate the effects of traditional Chinese medicine (TCM) therapy for clearing heat and resolving phlegm on systemic inflammatory response syndrome (SIRS) in acute deterioration stage of chronic obstructive pulmonary disease (COPD) and the serum procalcitonin (PCT) level. METHODS: One hundred patients suffering from SIRS in acute deterioration stage of COPD were included and randomly divided into treatment group (50 cases) and control group (50 cases). Patients in the treatment group were treated with routine Western medicine and Chinese herbal medicine for clearing away heat and eliminating phlegm, while patients in the control group were treated with routine Western medicine only. Patients in the two groups were treated for one week. The serum PCT levels in the two groups were measured at days 1, 3, and 7, and clinical symptom scores were recorded at days 1 and 7 in hospital to determine the effects. RESULTS: Clinical symptom scores in the two groups decreased after the treatment (P<0.05), and the symptom score in the treatment group was lower than that in the control group (P<0.05). The effect of integrated traditional Chinese and Western medicine treatment was obviously better than that of the Western medicine treatment when improving rates in clinical symptom score were divided into over 70% and less than 70% (P<0.05). Serum PCT concentration was in direct proportion to clinical symptom score (P<0.05). The patients with higher clinical symptom score were in more serious pathogenetic condition. There were no significant differences in the serum PCT concentrations among days 1, 3 and 7 in hospital. CONCLUSION: The effect of TCM therapy for clearing heat and removing phlegm combined with Western medicine treatment is better than that of the Western medicine treatment. TCM therapy has a satisfied effect in improving clinical symptoms. The serum PCT concentration is correlated with the severity of SIRS in acute deterioration stage of COPD.

[Effect of urotensin II on secretion of adrenomedullin from human vascular endothelial cells].

OBJECTIVE: To study the effect of human urotensin II (HU II) on secretion of adrenomedullin (ADM) from human vascular endothelial cells (HVEC) and its mechanism. METHODS: In cultured HVEC, different concentrations of HUII were used to stimulate the ADM secretion from HVEC, and the inhibitors of different signal transduction pathway were used to investigate their effects on ADM secretion. The contents of ADM in medium were determined by radio immunoassay. RESULTS: HUII stimulated secretion of ADM from HVEC in a time-dependent and concentration-dependent manner. The contents of ADM in the experiment groups were changed compared with that in control group (P < 0.05). The increase of ADM could be inhibited by inhibitor of extracellular signal-regulated protein kinase (PD(98059)), inhibitor of P38 kinase (SB(202190)), inhibitor of calmodulin (W(7)) and inhibitor of Ca(2+) (nicardipine) (P < 0.05). The inhibition ratio in those groups was 68%, 78%, 24% and 25% respectively. But the inhibitor of Calcineurin (CaN) and inhibitor of protein kinase C (H(7)) had no influence on the secretion of ADM from HVEC (P > 0.05). CONCLUSION: The stimulated effect of HUII on the ADM secretion from HVEC may be mediated by Ca(2+), ERKs, CaM-PK and P38 signal transduction pathways.

[Observation of short- and mid-term clinical outcome of percutaneous coronary intervention for acute myocardial infarction with heart failure or cardiogenic shock].

OBJECTIVE: To observe the short- and mid-term effects of percutaneous coronary intervention (PCI) in patients with ST-segment elevation acute myocardial infarction (AMI) complicated by heart failure and/or cardiogenic shock . METHODS: Altogether 90 patients with AMI were recruited, of whom 58 were treated by PCI, 20 by thrombolytic therapy, and the other received general treatment without reperfusion therapy. The length of hospital stay, major adverse cardiac events (MACE) and left ventricular ejection fraction (LVEF) were compared between PCI and thrombolysis groups. The relationship between the patency time of the infarct-related artery (IRA), thrombolysis in myocardial infarction (TIMI) grade after PCI and prognosis were analyzed in PCI group. RESULTS: The patency rate of IRA was significantly improved in patients receiving PCI therapy in comparison by those with thrombolytic therapy (98.3% vs 65.0%, P<0.01), and the LVEF was also higher in PCI group with lower mortality (6.9% vs 25.0%, P<0.05) during in-hospital and follow-up period. CONCLUSION: PCI can be a more effective therapy than thrombolytic therapy in the treatment of ST-segment elevation AMI accompanied with heart failure and/or cardiogenic shock.

[Mechanism of urotensin II-stimulated adrenomedullin secretion in human vascular endothelial cells].

OBJECTIVE: To study the mechanism of urotensin II(U II)-stimulated adrenomedullin secretion in human vascular endothelial cells. METHODS: In cultured human vascular endothelial cells (HEVCs), different concentrations of U II was used to stimulate the secretion of Adm, and different inhibitors were used to study the changes in the secretion after block of different signal transduction pathways. The contents of Adm in the medium were detected with radioimmunoassay. RESULTS: U II-stimulated Adm secretion in the HEVCs in a time- and concentration-dependent manner. Adm contents of the treatment groups were comparable with that of the control group (P<0.05 ), and the secretion of Adm could be inhibited by the inhibitor of extracellular signal-regulated protein kinases (PD098059), p38 kinase inhibitor (SB202190), calmodulin inhibitor (W7) and Ca(2+) inhibitor (nicardipine)(P<0.05), but calcineurin inhibitor and protein kinase C inhibitor (H7) had no such effect (P>0.05). CONCLUSION: Ca(2+), MAPK, CaM-PK and p38 signal transduction pathways may play major roles in U II-stimulated secretion of Adm in HVECs.