To observe the possibility of differentiation of bone marrow stromal stem cells of adult dog into myogenic cells. In a hope of providing a new cell line for treatment of myocardial infarction and heart failure. Bone marrow stromal stem cells were isolated by their adherence to plastic in vitro . 5 azacytidine was used to induce stem cells to differentiate into cardiomyotes in the experimental group, and same volume of culture media was used in the control group. The cultured cells were exarnined with inverted contrast phase microscope and immunochemistry. 4 weeks after induction, the shape of most of cultured cells changed from fusiform into rod like contiguration in experimental group, immunohistochemistry showed that the induced cells were positive for Desmin, ? smooth muscle actin, and Troponin I. The shape of cultured cells remained fusiform in control group, immunohistochemistry showed that they were mildly positive for Desmin and ? smooth muscle actin and negative for Troponin I. Adult canine bone marrow stromal stem cells were able to differentiate into myogenic cells after induction in vitro .

To investigate whether insulin enhances canine myocardial GLUT4 translocation and glucose uptake during ischemia in vivo, physiological parameters of myocardial metabolism were measured with an autoanalyzer, and GLUT4 distribution was assessed by immunoblot analysis and immunofluorescence. The results showed insulin significantly increased ischemic myocardial sarcolemmal GLUT4 content, and it was associated with up regulation of myocardial glucose uptake. Insulin increased coronary arterio venous difference by 4 fold in ischemic region. It suggested that insulin enhances ischemic myocardial GLUT4 translocation and glucose uptake. Insulin might contribute to increase myocardial glucose uptake and utilization during ischemia.

AIM: To investigate the effect of intraventricular pressure change by volume overload (VOL) on expression of proto-oncogene c- fos ,c- jun ,c- myc and egr-1 . METHODS: Left ventricular systolic pressure(LVSP) and left ventricular end diastolic pressure (LVEDP) of rat with VOL induced by aortacaval fistula operation and rats of control group were measured at 30 min, 1, 4, 6, 12 and 48 h after the operation,these mRNAs at the foregoing time points were measured by slot bloting method and quantified with densitometry. RESULTS: Be compared with the control group, VOL rats LVSP decreased ( P 0.05) after the operation.The proto-oncogene expression signals were not detected in the control,negative controls and VOL rats at 30 min after the operation. The c- fos, c- jun and egr-1 mRNA signals appeared earlier,at 1 h, and c- myc mRNA increased later at 4 h.All reached peak value at 4 h and then declined gradually.The c- fos mRNA were not detected at 48 h. The c- myc ,c- 0jun and egr-1 mRNA persisted throught the entire observation period from 1 h to 48 h. CONCLUSIONS: During VOL early phase the overload have effect on expression of the proto-oncogene mRNA,c- fos, c- jun and egr-1 mRNA appear earlier, c- myc later, egr -1,c- jun and c- myc persist longer period, but the expressions do not strengthen with the ventricule wall load increase.This sequential induction pattern may reflect the time course regularity of the proto-oncogenes expression induced by VOL,and indicate the proto-oncogenes expression initiate while the heart load accumulate some extent and duration and the load magnitude may not play a critical role.

AIM: To determine the alterations of myocardial ? 1-adrenergic receptor (? 1-AR) and cardiac sympathetic norepinephrine transporter (NET) mRNA expression, which is upstream modulator of ? 1-AR, in rats with longterm volume overload (VOL).METHODS: Left ventricular systolic (LVSP) and end diastolic pressure (LVEDP) of rats with VOL induced by aortacaval fistula operation and control group were measured at 3, 14,30 and 60 d after the operation, the mRNA at the time points was measured by RT-PCR and Northern blot analysis and quantified by densitometry.RESULTS: The cardiac sympathetic NET specific expression is in the cardiac sympathetic ganglia. Be compared with the control group, LVSP of VOL rats decreased most dramatically by 24%( P