ABSTRACT
Objective To evaluate the impact of different doses of recombinant human B-type natriuretic peptid (rh-BNP) within the dosage of clinical rage on oxygen consumption during acute myocardial infarction (AMI) with heart failure (HF). Methods AMI-HF model of York pig was established by occluding coronary artery with balloon combined with in-jecting microthrombus. Then animals were randomized into rhBNP group and control group. Clinical dose of rhBNP ( 1.5μg/kg bolus followed by a continuous infusion with speed of 0.01, 0.02 and 0.03μg · kg-1 · min-1 for 60 minutes respectively in turn) was administrated in rhBNP group while equal volume of saline was given in the control group. Myocardial oxygen up-take (MOU) was measured by drawing blood from coronary artery and coronary sinus using a catheter. Coronary diameter was determined using quantitative coronary angiography. The observation points were at baseline (T0), instant after the mod-el establishment (T1), 60 min after continuous rhBNP infusion of 0.01, 0.02, 0.03μg·kg-1·min-1 (T2-T4) respectively. Re-sults Compared with the control group, pulmonary capillary wedge pressure, central venous pressure, heart rate, systolic blood pressure and MOU were significantly decreased after rhBNP administration. And cardiac output and coronary diame-ter were obviously increased with addition of rhBNP. There is a interaction of drug intervention and time. In rhBNP group, MOU was significantly decreased with drug administraion (T2-T4 vs T1,mL O2/L: 10.61 ± 0.35,9.85 ± 0.60,9.79 ± 0.31 vs 11.59 ± 0.37). Conclusion Intravenous administration of rhBNP in AMI-HF model could decrease MOU and PCWP while increase the cardiac output.
ABSTRACT
<p><b>OBJECTIVE</b>To study the influence of hepatitis B virus (HBV) replication and expressions of different viral genes on CDC37 level in hepatocytes.</p><p><b>METHODS</b>We amplified and cloned 6 HBV genes (P, preS1, preS2, S, C and X) into pCMV expression vectors, which were transfected in Huh7 and HepG2 hepatoma cell lines, and CDC37 expression level in the cells was detected using Western blotting. Wealso cloned the promoter sequence of CDC37 into pGL3 vector, and co-transfected pGL3 with pCMV recombinant plasmids into Huh7 and HepG2 cells and the fluorescent signals were detected. To study the influence of HBV replication on CDC37 expression, we constructed 1.28-copy overlength genomes of HBV genotypes B, C, D and CD recombinant. The overlength HBV genomes were transformed into Adeasier-1 cells for recombination and into 293 cells for packaging. Huh7 and HepG2 cell lines infected with the packaged HBV recombinant adenoviruses were examined for CDC37 expression with Western blotting.</p><p><b>RESULTS</b>Western blotting showed that the expression of different HBV genes did not obviously affect the protein level of CDC37 in the hepatocytes. The protein expression of HBV genes had no effect on the activity of CDC37 promoter. Huh7 and HepG2 cells infected with 1.28-copy HBV replicon showed no significant changes in the expression level of CDC37.</p><p><b>CONCLUSION</b>HBV replication and its gene expression have no effect on the level of CDC37 in hepatocytes in vitro.</p>