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Objective: To investigate the changes of myo cardial contractile function during myocardial stunning in calcium overload rats and the protective effects of tetrandrine. Methods: Forty-six rats were randomized into control, myocardial ischemia, myocardial stunning, low and high dose of tetrandrine groups. Another 10 rats were used to identify the calcium overload. vitamin D3 (0.3 million Unit/kg) and nicotinic acid were adm inistered. After 16 d when calcium overload occured, left anterior descending ar tery was ligated. Twenty minutes of myocardial ischemia followed by 60 min of re perfusion was induced. The contractile function parameters were determined dynam ically. At the end of experiment, myocardial cytosolic ［Ca2+］i was deter mined in various groups. In tetrandrine groups, tetrandrine (62.2 or 93.6 μmol/ kg ) was administered by gastrogavage daily.After 16 d, the rats undergone the e xperiments mentioned above. Results: Sixteen days after vitamin D3 , nicotinic acid were given, ［Ca2+］i increased by 2.6 folds (146.8±10.8 ) vs (368.5±22.6) nmol/L, (P<0.01). Whereas, ［Ca2+］i in tetrand rine groups were (210.8±16.4) and (198.6±15.3) nmol/L, which were significantl y lower than that of calcium overload group. Twenty minutes of myocardial ische mia resulted in the decrease of dp/dtmax and Vmax in all groups with the most si gnificant in stunning and calcium overload groups. The contractile function rest ored gradually after reperfusion. At all time points, dp/dtmax and Vmax in both tetrandrine groups were higher than those in both stunning and calcium overload groups. And effect with higher dose of tetrandrine were more significant than in low dose of tetrandrine. After 60 min of reperfusion, dp/dtmax in stunning, cal cium overload, low and high dose of tetrandrine groups were 49.7%, 51.5%, 71.0% and 83.4% of that in control, respectively， and Vmax were 55.0%, 49.8%, 73.9% and 77.5% of that in control, respectively. Conclusion: T he myocardial contractile function in vitamin D3-induced calcium overload gro up is impaired. On basis of myocardiocyte calcium overload, transient ischemia l eads to myocardial stunning. At the stage of ischemia, the impaired degree of my ocardial contractile function is similar to that in stunning group, suggesting a t this stage the effect of ischemia on myocardial function is greater than that of calcium overload. Tetrandrine chronically improves the myocardial function in Vitamin D3-induced calcium overload rats.
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AIM: To evaluate the therapeutic efficacy of intratracheal instillation of porcine pulmonary surfactant(PPS) in rats with lipopolysaccharides(LPS)-induced early-stage ALI in this study.METHODS: SD rats weighing 200 g-300 g were randomly divided into 4 groups: LPS(1.5 mg?kg-1)+saline,LPS+PPS 100 mg?kg-1,LPS+PPS 150 mg?kg-1,LPS+PPS 200 mg?kg-1.The PaO2 and PaCO2,as well as survival rate of rats were examined for 6 h after the start of PPS-instillation.Then,rats were killed and lungs were immediately removed for lung index(LI) and histological analysis.The bronchoalveolar lavage fluid(BALF) was collected for measurement of total protein(TP) contents,TNF-? level and white blood cell(WBC) numbers.RESULTS: Significantly increased PaO2,reduced mortality rate,decreased total protein and TNF-? contents in BAL,as well as lung index and meliorated histological appearance were observed in three PPS-treated groups compared with group given saline after LPS(P
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AIM: To study the effect of dexamethasone(Dex) on the expression of CD18. METHODS: Quantitative RT-PCR analysis, Northern blotting technique were used to measure the expression of CD18 in U937 cells treated by PMA. RESULTS : Dex could significantly attenuated the effects of PMA in a dose-dependent manner (10 -6 mol/L-10 -10 mol/L). These effects of Dex (10 -7 mol/L) were completely aborted by RU-486 (10 -6 mol/L).CONCLUSION: Dex, via GR, could inhibit CD18 mRNA expression in U937 cells treated by PMA. The effects of Dex might be possibly depended on the counteracting action on the NF-?B.
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AIM: To investigate the effect of PMA(phorbol 12-myristate 13-acetate) on the expression of CD18 and the mechanism. METHODS: The technique of quantitative RT-PCR analysis was used to measure the expression of CD18 mRNA in U937 cells treated by PMA. RESULTS: PMA could significantly induce CD18 mRNA expression in a dose and time-dependent manner. The induction effects of PMA on CD18 mRNA could be inhibited obviously by Myr (2 ?mol/L), a specific inhibitor of PKC, and APDC, an inhibitor of NF-?B, but not be inhibited by curcumin, a inhibitor of transcriptional factor AP-1. CONCLUSION: PMA enhanced the expression of CD18 via the pathway of PKC. Transcriptional factor NF-?B, but not AP-1, was essential for the gene transcription of CD18 in U937 cells treated by PMA.