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Objective:To investigate the effect of exercise both before and after myocardial infarction (MI) on microvessel density in the left ventricle, and on the mRNA and protein expression of vascular endothelial growth factor (VEGF) and its receptors.Methods:Ninety-six male Sprague-Dawley rats were randomly divided into a sedentary sham operation group (Sed-Sh), a pre-MI exercise sham operation group (PreE-Sh), a sedentary MI group (Sed-MI), a pre-MI exercise group (PreE-MI), a post-MI exercise group (PostE-MI) and a combined exercise group (ComE-MI). The rats of the exercise groups underwent 60min of treadmill training daily five times a week for five weeks, while those of the Sed-Sh and Sed-MI groups remained sedentary. Then all of the rats underwent either an operation to induce an acute MI (Sed-MI, PreE-MI, PostE-MI and ComE-MI groups) or a sham MI operation (Sed-Sh and PreE-Sh groups). Four weeks after the operation, the exercise groups underwent five days adaptive training, followed by 8 weeks of 60min of treadmill training daily, five times a week. All of the rats were then sacrificed. The microvessel densities in the infarcted and uninfarcted volumes were detected using Factor VIII-related antigen staining, while the mRNA expressions of VEGF and its receptors were examined using a real-time polymerase chain reaction. The protein expressions of VEGF and its receptors were measured using western blotting.Results:Compared with Sed-MI group, the average microvessel densities of the PostE-MI and ComE-MI groups had increased significantly, with the average density of the PostE-MI group significantly higher than that of the PreE-MI group, but significantly lower than the ComE-MI group′s average. Compared with the Sed-MI group, the average mRNA expression of VEGF and its receptors in the PostE-MI and ComE-MI groups was significantly higher, without significant differences between the two groups.Conclusions:Pre-MI exercise does not significantly improve left ventricular function or microvessel density, while post-MI exercise does, as it can upregulate the expression of VEGF and its receptors to activate VEGF signaling. The increase in microvessel density may benefit left ventricular remodeling and cardiac function.
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Objective To study the effects of exercise after myocardial infarction on the survival rate and the dynamic functioning of the left ventricle ( LV) . Methods Ninety-six male Sprague-Dawley rats were randomly assigned to a sedentary sham operation group ( Sed-Sh) , a previous exercise and sham operation group ( PreE-Sh) , a sedentary myocardial infarction ( MI) group ( Sed-MI) , a previous exercise MI group ( PreE-MI) , a post exercise MI group (PostE-MI) and a combined exercise MI group (ComE-MI), each of 16.All of the rats underwent either MI in-duction or a sham MI operation, the PreE groups after exercising for 5 weeks on a treadmill. The Sed groups did not exercise. The Post E-MI group did not exercise before the operation, but performed treadmill exercises for 4 weeks be-ginning 8 weeks after the operation. The ComE-MI group exercised for 5 weeks before and 4 weeks after the operation. All the exercising rats ran on the treadmill for 60 minutes daily, 5 d/wk. Life situation and spontaneous mortality were recorded, and echocardiographic measurements were performed on the4thday and 2, 4, 8 and 12weeks after the oper-ation. All of the rats were sacrificed at the end of the experiment. Results Compared with the Sed-Sh group, the Sed-MI group had significantly larger average LV dimensions at the end of both the diastol ( LVEDd) and the systol (LVEDs, but it had lower average fractional shortening (FS) and a smaller average ejection fraction(EF) at all of the different measuring times. The PreE-MI group had significantly lower average LVEDd and LVEDs, but a signifi-cantly higher FS and EF than the Sed-MI group on the 4th day. However, 2 weeks after the intervention the difference in LVEDd between the two groups was no longer significant. Significantly higher FS and EF were observed in the PostE-MI group at 12 weeks compared to the Sed-MI group. The ComE-MI group had significantly lower average LVEDd and LVEDs, but significantly higher FS and EF at all the time points than the Sed-MI group. The ComE-MI group had a significantly lower average LVEDs but a higher average FS and EF than the PreE-MI group at 12 weeks after the intervention. Conclusion Pre-MI exercise improves LV function significantly at the early stage, though the difference is temporary. Post-MI exercise improves LV function in the longer term. Combined exercise improves LV function the most effectively.
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Objective To investigate maternal risk factors for fetal congenital heart diseases (CHD). Methods A case-control study was conducted on 16 645 pregnant women who underwent cardiovascular malformation screening for fetal cardiovascular system,whose pregnancy outcomes were recorded,and whose newborns were scanned by an echocardiography in Peking University People's Hospital,Haidian,Changping,Mentougou and Daxing Maternal and Child Health Hospital from Nov.2006 to Oct.2009.One hundred and twelve pregnant women whose babies were found to be CHD (40 severe CHD and 72 simple CHD) before or after delivery were taken as study group.Women in control group (n =304) were randomly selected from those pregnant women who had infants without CHD.Logistic regression analysis and x2 test were used to analyze the maternal risk factors for fetal CHD. Results (1) The average age of women whose infants had severe CHD was 28.3 years (21-40 years),and it was 29.9 years (22-39 years) for women whose infants had simple CHD.There were no significant differences between the control group (29.5 years,20-44 years) and the above two groups (t=1.511 and -0.826,P=0.138 and 0.410 respectively).(2) Single factor analysis:during first trimester,the rate of upper respiratory infection (18/39,46.2 ％) and exposure to certain chemicals (13/40,32.5％) of severe CHD group were higher than those of control group [(14.9％ (45/303) and 2.0％ (6/304)] (x2 =22.399 and 62.678,OR=4.895 and 23.753,95％CI:2.419-9.905 and 8.358-67.506,P =0.000 respectively).Compared with control group (0.0％,0/304),the rate of pregnant women with CHD family history in simple CHD group was significantly higher (4.2％,3/72)(Fisher exact test,P=0.007).(3) Logistic regression analysis:maternal upper respiratory infections (OR =5.120,95％CI:2.340-11.206,P =0.000) and exposure to certain chemicals (f)R=23.030,95％CI:7.506-70.665,P=0.000) during first trimester were risk factors for fetal severe CHD. Conclusions Upper respiratory infection and exposure to certain chemicals during first trimester might play important roles in the occurrence of fetal severe CHD.Maternal family history of CHD might associate with fetal simple CHD.
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Objective To clear, amplify and detect the activity of the recombinant adeno-assoeiated virus vector with adiponectin( rAAV2/1-Aerp30 ). Methods Recombinant plasmid pSNAV2.0-Acrp30 was obtained. The recombinant plasmid was then transfected into BHK21 cells using LipofectAMINETM 2000. The G418 resistant cells were obtained consequently. These cells were infected with HSVI-rc/△UL2 which has the function of packaging and copying recombinant AAV. After purification, the construction of recombinant rAAV2/1-Aerp30 was collected. Results The construction of recombinant pSNAV2.0-Acrp30 was confirmed by PCR electrophoresis and digestion with restriction enzyme. The gene sequencing showed that the recombinant pSNAV2.0-Acrp30 was correct. The virus titer was about 1.0×1012 μg/ml. The purity f the recombinant AAV2/1 was fairly high using the SDS-PAGE method. Conclusion With this method, rAAV2/-Aerp30 with high virus titers and purity can be acquired successfully and it can meet the demands of the experimental study of Acrp30 gene therapy of GK rats.