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We have shown in mouse models that hydrodynamic transfection of pBS-HCRII-HP-FIXA and pBS-HCRI/II-HP-FIXA was able to induce and maintain the expression and clotting activity of human factor IX for a long period of time at a potentially therapeutic level. With an appropriate delivery system, this type of plasmid vector could be clinically useful for the hepatic expression of therapeutic genes including human factor IX.

Background: Methylmethacrylate monomer (MMA) bone cement has been associated with sudden systemic hypotension. The present study was aimed to explore the mechanism of direct myocardial depressant actions of MMA.Methods: The isometric contraction of isolated guinea pig's right ventricular papillary muscle was measured. Normal and slow action potentials were evaluated by a conventional micro-electrode technique. The effects of MMA on sarcoplasmic reticulum (SR) function were evaluated by its effect on: rapid cooling contractures, rested state contraction of rat papillary muscle in normal Tyrode's solution and of guinea pig's papillary muscle in low Na + Tyrode's solution. To measure the inward calcium currents (ICa), whole cell patch clamp techniques were applied.Results: MMA caused a dose-dependent depression of the peak force (PF) and maximal rate of peak force (dF/dt-max). About a 30% depression of PF was shown at rested state (RS) contraction in rat myocardium and under low Na + Tyrode's solution in guinea pig myocardium, respectively. In the 26 mM K + Tyrode's solution, MMA caused dose-dependent depression of late force development without alteration in early force development. MMA depressed rapid cooling contracture accompanied by prolongation of time to peak contracture. MMA did not alter the amplitude or maximum depolarization rate of normal and slow action potentials. Action potential durations were significantly reduced. In patch clamp studies, MMA reduced ICa in a dose-dependent manner.Conclusions: MMA depressed cardiac contractility in a dose-dependent manner and may be partly related to the depression of Ca 2+ influx through the cardiac membrane. SR Ca 2+ release seems to be mildly inhibited by MMA. Based on common clinical concentrations, the direct myocardial depressant effect of MMA may not be a main cause of hypotension during an operation.

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