[On angiotensin II receptor distribution after myocardial infarction in dogs].

OBJECTIVE: To investigate the effects of valsartan on expression of angiotensin II receptors in different regions of heart after myocardial infarction (MI). METHODS: Canines were divided into sham-operated control group (n=7), infarction group (n=7) and Valsartan group (10 mg x kg(-1) x day(-1) for 4 weeks after MI operation, n=7). Four weeks after operation, Doppler tissue imaging (DTI) was used to evaluate regional ventricular function in the noninfarcted myocardium (apical and basal near to the infarction region). The mRNA and protein expressions of angiotensin II type 1 receptor (AT1-R) and angiotensin II type 2 receptor (AT2-R) on the corresponding regions were detected by competitive reverse-transcriptase polymerase chain reaction technique and immunohistochemical technique respectively. Results The protein and mRNA expressions of AT1-R were significantly increased in both apical and basal regions near to the infarction in dogs with MI compared with those in control group (P < 0.05) which could be downregulated by valsartan (P < 0.05). AT2-R expressions were significantly upregulated in infarction group in both apical and basal regions compared with those in control group and valsartan further increased AT2-R expressions in both areas (P < 0.05). Myocardial peak systolic velocity (Sm), myocardial peak early diastolic velocity (Em) and myocardial peak late diastolic velocity (Am) at both apical and basal regions near to the infarction regions were significantly lower in MI group than those in the control group which could be significantly improved by valsartan. CONCLUSION: Both mRNA and protein expressions of AT1-R and AT2-R are upregulated in noninfarcted regions near MI, valsartan improved myocardial function via inhibiting AT1-R upregulation and enhancing AT2-R upregulation.

[Effect of chronic myocardial infarction on the distribution of beta-adrenoceptors in heart: experiment with dogs].

OBJECTIVE: To investigate the distribution of beta-adrenoceptors at different sites of heart after myocardial infarction (MI). METHODS: 14 dogs were randomly divided into 2 equal groups: MI group, undergoing ligation of the left anterior descending coronary artery, and control group undergoing sham-operation. Four weeks later metoprolol, a beta 1-adrenergic receptor antagonist, was injected intravenously. Doppler tissue imaging (DTI) was used to evaluate the peak systolic myocardial velocity (Sm) of the regions apical and basal to the infarction region before and after the injection. Then the dogs were killed with their hearts taken out. Reverse-transcriptase polymerase chain reaction was used to examine the mRNA expression of beta 1-receptor and beta 2-receptor in the non-infracted myocardial tissues apical and basal to the infarction region. RESULTS: The Sm values at the regions apical and basal to the infarction region of the MI group were 3.93 +/- 0.47 and 0.81 +/- 0.19 cm/s respectively, both significantly lower than those of the control group (10.84 +/- 1.97 and 5.85 +/- 1.15 cm/s respectively, both P < 0.05). After injection of metoprolol, the Sm values at the regions apical and basal to the infarction region of the MI group were 3.43 +/- 0.37 and 0.73 +/- 0.14 cm/s respectively, not significantly different from those before the injection; however, the corresponding Sm values of the control group were 8.69 +/- 1.14 and 4.33 +/- 0.29 cm/s respectively, both significantly lower than those before the injection (both P < 0.05). The mRNA expression levels of beta 1-receptor decreased in both apical and basal regions in the MI group compared with those in the control group, and the degree of expression decrease at the apical region was significantly greater than that at the basal region. However, there was no significant difference in the expression level of beta 1-receptor mRNA between the apical and basal regions in the control group. There was no significant difference in the mRNA expression of beta 2-receptor in different regions of the heart in both groups. CONCLUSION: After MI regional variation occurs for the beta 1-receptor mRNA expression, but not to the beta 2-receptor.

[Regional denervation after myocardial infarction and its effect on ventricular repolarization].

OBJECTIVE: To investigate whether myocardial infarction (MI) causes heterogeneity of sympathetic innervation and to evaluate the effects of sympathetic stimulation on myocardial repolarization in the regions of denervation after MI. METHODS: Fourteen dogs were randomly divided into 2 equal groups: MI Group, undergoing ligation of the left anterior descending coronary artery, and Control Group, undergoing sham operation. Four weeks later thoracotomy was performed for the second time, the effective refractory period (ERP) of the non-infarcted myocardium at the base of heart proximal to the infarcted myocardium and the ERP of the non-infarcted myocardium at the cardiac apex distal to the infarcted myocardium by S(1)S(2) programmed stimulation. Then the left satellite ganglion was exposed, ligated, cut, and stimulated at the proximal end, and ERP was determined at the above mentioned regions again. After the ERP measurement the heart was taken out to undergo immunohistochemistry to observe the distribution of tyrosine hydroxylase (TH) positive nerve fibers. RESULTS: The ERP of the non-infarcted myocardium at the base of heart proximal to the infarcted myocardium was not significantly different from that of the non-infarcted myocardium at the cardiac apex distal to the infarcted myocardium before sympathetic stimulation in both groups. In MI Group, however, the ERP of the non-infarcted myocardium at the base of heart proximal to the infarcted myocardium was significantly shortened after stimulation at the satellite ganglion (141 ms +/- 10 ms) in comparison with that before the stimulation (162 ms +/- 9 ms, P < 0.01); and the ERP of the non-infarcted myocardium at the cardiac apex distal to the infarcted myocardium after sympathetic stimulation (157 ms +/- 8 ms) was not significantly different from that before sympathetic stimulation (161 ms +/- 6 ms), however, was significantly longer than that of the non-infarcted myocardium at the base of heart proximal to the infarcted myocardium (P < 0.05). In Control Group the ERP values of both the basal and apical regions were significantly shorter than those before stimulation at the same region (both P < 0.01), however, there were no significant differences in the ERP values at the same region before and after the stimulation for the 2 regions. Immunohistochemistry showed that TH positive nerve fibers were distributed in the whole heart of Control Group and in the heart base of MI Group, and no TH positive nerve fiber was seen in the cardiac apex of MI Group. CONCLUSION: Regional denervation occurs after MI; Spatial variation of regional sympathetic innervation leads to heterogeneity in cardiac repolarization after sympathetic stimulation.