Objective Little is known about the influence of congenital heart disease on the phannacodynamies of neuromuscular blocking agents. The aim of this study was to compare the pharmacodynamics of rocuronium in children with cyanotic and acyanotic heart disease. Methods The study was conducted in two parts. In part Ⅰ , 36 children with congenital heart disease scheduled for open heart surgery were allocated into 3 groups (n=12) : acyanotic group; slightly cyanotic group and severely cyanotic group. Neuromuscular blockade was monitored after administration of 0.6 mg ? kg-1 rocuronium. In part Ⅱ , 40 children with congenital heart disease were allocated into acyanotic and cyanotic group ( n = 20). The children in each group were further divided into 4 subgroups of 5 patients according to the dose of rocuronium the children received : 120, 180, 240 and 300 ?g? kg-1 . The dose- response curve for neuromuscular blockade was constructed and ED50 , ED90 and ED95 were calculated. SPSS 8.0 software was used for statistical analysis.Results In part Ⅰ the onset time (the time from injection of rocuronium to 95% depression of neuromuscular transmission) was significantly longer in severely cyanotic group [(2.25 ? 1.27) Min] than in acyanotic group [(1.17 ? 0.15) min] . There was no significant difference in the duration of action and recovery time among the 3 groups. In part Ⅱ the dose-response curve shifted to the right in cyanotic group compared with acyanotic group. ED50, ED90 and ED95 were significantly higher in cyanotic group than in acyanotic group. Conclusion The onset time of rocuronium is prolonged and the sensitivity of the patients to rocuronium is decreased in patients with cyanotic heart disease.

Objective To investigate the effects of adenosine preconditioning on the expression of myocardial tumor necrosis factor-alpha (TNF-α) mRNA and intercellular adhesion molecule-1 (ICAM-1) mRNA in patients undergoing off-pump coronary artery bypass graft (OPCABG).Methods Forty patients, aged 44-68 yr, with more than three coronary artery obstructions and the ejection fraction≥40%,undergoing elective OPCABG, were randomly divided into 2 groups (n=20 each): control group and adenosine group. Adenosine group received adenosine preconditioning, with the initial infusion rate of 50 μg. kg-1.min-1, then increasing to 100μg.kg-1.min-1after 1 min, finally increasing to 150 μg. kg-1 . min-1 after 2 min and maintaining for 7 min. Vascular anastomosis was started at 5 min after preconditioning. While the control group received normal saline instead of adenosine. Tissue samples of the right auricle were taken before preconditioning (baseline) and at 15 min after blood current retum to measure the expression of myocardial TNF-α mRNA and ICAM-1 mRNA. The myocardial ultrastructure was observed and hemodynamic parameters were monitored.Results The myocardial damage was milder in the adenosine group than in the control group. The expression of myocardial TNF-α mRNA and ICAM-1 mRNA was significantly lower in the adenosine group than in the control group ( P＜0.05).Conclusion Adenosine preconditioning can attenuate myocardial ischemia-reperfusion injury in patients undergoing OPCABG through down-regulating the expression of myocardial TNF- mRNA and ICAM-1 mRNA.

Objective To investigate the effects of different doses of ulinastatin on platelet counts and function after normothermic cardiopulmonary bypass (CPB) in rabbits. Methods Fifty lung-ear white rabbits aged 5-6 months weighing 2.3-3.0 kg were randomly assigned to one of 5 groups (n = 10 each) : control group (group C) and4 ulinastatin groups (group U~1, U_2,U_3,U_4). The rabbits received ulinastatin 1×10~4, 3×10~4, 5×10~4 and 10×10~4 U/kg before CPB in group U~1, U_2, U_3 and U_4 respectively while equal volume of normal saline was given instead of ulinastatin in group C. All rabbits underwent CPB for 30 min at perfusion flow of 72-120 ml·kg~(-1) ·min~(-1). The rectal temperature was maintained at 36.5-37.5℃. Hemodynamic parameters were recorded and blood platelet count, platelet adhesion rate and platelet membrane glycopretein Gp Ⅰ b, Gp Ⅱ b, Gp Ⅲ a receptors were determined before CPB (baseline), at termination of CPB and at 1, 2 and 3 h after CPB. Results The platelet counts were significantly decreased after CPB in all 5 groups (P< 0.05), but there was no significant difference among the 5 groups. The platelet adhesion rates were significantly decreased after CPB as compared with the baseline value before CPB in all 5 groups but the platelet adhesion rates were significantly higher after CPB in group U_4 than in group C. The number of molecules of Gp Ⅰ b, Gp Ⅱ b and Gp Ⅲ a receptors was significantly decreased after CPB in all 5 groups. The number of molecules of Gp Ⅰ b, Gp Ⅱ b and Gp Ⅲ a receptors after CPB was significantly higher in group U_2, U_3 and U_4 than in group C, and there was no significant difference between group U_3 and U_4 . ConclusionUlinastatin 3×10~4-5×10~4 U/kg administered before CPB can inhibit breakdown of platelet membrane glycoprotein receptors. Ulinastatin 10×10~4 U/kg can preserve the platelet adhesion function.