Objective To investigate the effects of ischemia reperfusion on the morphological changes of sinoatrial node(SAN) cells in rabbits in vivo . Methods Ninety healthy adult rabbits were randomly divided into 3 groups with 10 rabbits in control and every subgroup: control group [a suture passed under the root section of right coronary artery(RCA) without ligation], ischemia group(occluding the root section of RCA for 10, 30, 60 and 120 min respectively), ischemia reperfusion group(10, 30, 60 and 120 min ischemia after respectively followed by 4 hours′ reperfusion). Results ① Compared with control group, abnormal structure of SAN cells was not seen in 10 min ischemia group and 10 min ischemia reperfusion group with light microscopy, except slight mitochondrial swelling of SAN cells in former group with electron microscopy. ② There were morphological changes of SAN cells in 7, 6 and 8 rabbits in 30, 60 and 120 min ischemia group, presenting mainly as cellular swelling, karyopyknosis, and focal necrosis under a light microscope, and mitochodrial swelling, cristae disorganization or break under an electron microscope. The most severe cellular damages were found in 120 min ischemia group. ③ In ischemia reperfusion group, there were morphological abnormalities of SAN cells in 6, 8 and 7 rabbits in 30, 60 and 120 min ischemia reperfusion groups. The morphologic changes were similar to those in ischemia group, but injury degree was more severe than that in ischemia group with the same ischemic time. Conclusion Ischemia and ischemia reperfusion can induce morphological changes of SAN cells in a time dependent manner in rabbits in vivo , and the injury degree is more severe in ischemia reperfusion group than that in ischemia group with the same ischemic time.

OBJECTIVE： To analysis the adverse reactions of angiotension converting enzyme inhibitor（ ACEI） ， so as to deepen the understanding to the ARDs and improve the therapeutic effect of ACEI METHODS： The therapeutic effects and ARDs of ACEI were retrospectively reviewed and the incidence of ARDs induced by ACEI and the relationship between different ACEIs and their ARDs were analyzed RESULTS： （ 1） The incidence of ARDs of ACEI was 12％  Stimulating cough， parageusia， gastrointestinal tract discomfort， skin rash， itch of skin， hypotension， headache， dizziness， proteinuria and angioedema were the common symptoms （ 2） Of five kinds of ACEIs， captopril induced the highest incidence of ARDs and stimulating cough， parageusia， gastrointestinal tract discomfort， skin rash and itch of skin were the most common manifestations CONCLUSION： Stimulating cough， parageusia， gastrointestinal tract discomfort and skin rash are the most common symptoms of ARDs， and the symptoms will disappear when drug administration is discontinued

6 months (n=12), control group, without AF (n=8). Atrial muscle samples of the left and right atrial appendage were cut off during heart valve replacement. Expressions of Cx40 and Cx43 were detected by immunoblotting and immunohistologic analyses. Results ①No obvious change of Cx43 and Cx40 in the left and right atrium of each patient in each group was measured. ②Compared with that in the control group, the level of Cx40 was decreased signficantly in GroupⅠ (P

6 months; Control group (n=8) without AF. Atrial muscle samples of the left and right atrial appendage were cut off during heart valve replacement. Morphological changes were observed by light microscopy and electron microscopy. Results ① The incidence rates of Aschoff body were 37.5% (3/8), 46% (5/11) , and 50% (6/12) in Group Ⅰ, Group Ⅱ, and the control group. There was no difference in Aschoff body between the left and right atrial myocytes. ② There was no difference in myocytic degeneration, interstitial hyperplasia, and lymphocytes infiltration between the left and right atrial myocytes in each group. ③ Myolysis, accumulation of glycogen, and fibrosis were detected by electron microscopy in the 3 groups. Changes of myolysis and fibrosis were more obvious in patients with AF than patients without AF. Conclusion There are similar pathological changes in the left and right atria in rheumatic heart disease patients with or without AF. Fibrosis of atrial myocytes may be involved in the occurrence and maintenance of AF.

Objective To study the effects of heart ischemia reperfusion on conductive function of atrioventricular node (AVN) in rabbits. Methods Animal models of ischemia reperfusion of AVN were established by ligating and reopening the right coronary artery of rabbits. A total of 60 adult rabbits were divided into control groups ( n =10), right coronary artery occlusion group ( n =10), and ischemia reperfusion groups with ligation of the right artery occlusion for 10, 30, 60 and 120 min respectively ( n =10 for every subgroup). The hemodynamics, His bundle electrography and epicardial electography were carried out and recorded. Results After occlusion of right coronary artery, 94.8% animals in experimental groups were found to have prolonged atrial His interval (AH) ( P

Objective To investigate the mechanism of affecting smooth muscle cells apoptosis after balloon injury to vessel Methods The percentage of vascular smooth muscle cells (VSMC) apoptosis and the expression of angiotensin Ⅱ subtype 1 receptor (AT 1R) was measured by terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labeling (TUNEL) and immunohistochemical technique after balloon injury Results Compared with sham's, the expression of AT 1R protein in vascular media was significantly increased at 3 days after balloon injury ( P

Objective To explore the regularity of dynamic morphologic changes of the sinoatrial node (SAN) cells of rabbits after the constitution was damaged by formaldehyde wet dressing. Methods Sixty rabbits were randomly divided into 6 groups (n=10 in each group): the control group and 5 experimental groups observed at 2 h, 1, 2, 3, and 4 weeks respectively after the operation. The SAN constitution of rabbits was damaged by 20% formaldehyde wet dressing. The constitutions of SAN were cut quickly at 2 h after wet dressing in the control group and at the corresponding time points in other experimental groups respectively. The specimens were made for light microscopical and electron microscopical observations. The apoptosis of SAN cells was detected by TUNEL method. Results Compared with those in the control group, SAN cells in all experimental groups were damaged at various degrees observed by light microscopy and electron microscopy. Distinct cell tumefaction, soak of grain cells, cytoclasis, hyperplasia of collagen fibers, and other pathological changes were detected. Electron microscopical observation showed distinct pathological changes of the super-micro construction of cells. Apoptosis was not detected in the control group, but various degrees of apoptosis in all experiment groups. The apoptotic rates in all experimental groups were significant as compared with that in the control group (P

0.05), and HC lead ECG was more useful than Wilson lead when applied to localize the right free wall and right-anteroseptal accessory pathway (P

Objective To investigate the potassium currents of the cardiac pacemaking cells induced and differentiated from rat mesenchymal stem cells (MSCs) modified by HCN4 gene. Methods Identified cardiac pacemaking cells were adopted as the experiment group, and the sinoatrial node cells of original infant rat cultured in the same period were regarded as the control group. Whole cell patch was used to measure the action potential of the pacemaking cells and sinoatrial node cells. Results Action potential of automatic depolarization at dilatation was recorded in both the differentiated cardiac pacemaking cells and sinoatrial node cells. There was no significant difference on amplitudes of resting potential, amplitudes and cycle of action potential [(-50?2.8) vs (-55?5.5),(-60?2.5) vs (-65?2.5),(240?57) ms vs (250?60) ms], but the field potential was much lower in cardiac pacemaking cells than the control group[(-30?2.5) vs (-55?5.5),P

Objective To investigate the effects of electrical stimulation on the differentiation of rat bone marrow mesenchymal stem cells (MSCs) to cardiomyocyte induced by 5-azacytidine in vitro. Methods MSCs from Sprague-Dawley (SD) rats were cultured and passed repeatedly to P3. MSCs were treated with 5-azacytidine (10 ?mol/L) and incubated for 24 h.The induced MSCs were divided to stimulated group and non-stimulated group, and every groups divided by incubated for 1,2,3 and 4 weeks were named as subgroup Ⅰ,Ⅱ, Ⅲ and Ⅳ respectively.MSCs of stimulated group were stimulated for 30 min every day by supra-threshold square biphasic pulses (2 ms duration, 1.5 Hz, 20 ?A), and the stimulation was initiated 1 d after inducing. Light and electronic microscope were used to identify the influences of characteristic morphological of MSCs in every subgroups,and immunocytochemistry was used to identify the expression of ?-actin,cTnT, Cx43 in MSCs. Results The growth of MSCs in stimulated group was better than that of non-stimulated group. MSCs of stimulated group exhibited differentiation into cardiomyocyte-like cell at 1 week after inducing, earlier than that of no-stimulated group (2 weeks). In stimulated subgroup Ⅰ, scattered myogenic structure was observed in the plasma of some cells under electronic microscope, and ?-actin,cTnT expressed in some cells, but not that be observed in non-stimulated subgroup Ⅰ. In cells of stimulated subgroups Ⅱ to Ⅳ, the expression level of ?-actin, cTnT, Cx43 of were all higher than that of non-stimulated subgroups respectively. Conclusion Electrical stimulation (simulating the heart beating) could redound differentiation of rat bone marrow mesenchymal stem cells (MSCs) to cardiomyocyte induced by 5-azacytidine in vitro.