Objectives To investigate the relation between hypertrophied myocardium and ventricular fibrillation threshold in spontaneously hypertensive rats （SHR）. Methods 20 male SHR were randomly divided into two groups： 10...Objectives To investigate the relation between hypertrophied myocardium and ventricular fibrillation threshold in spontaneously hypertensive rats （SHR）. Methods 20 male SHR were randomly divided into two groups： 10 week group （n= 10） and 18 week group （n=10）. 10 week male Wistar rats were controlled group （n=10）. The systolic blood pressure （SBP）, heart mass index （HMI）, ventricular effective refractory period （VERP） and ventricular fibrillation threshold（VFT） were measured respectively.① The SBP and HMI of SHR were significantly higher than those of Wistar rats（P 〈 0.001）. The VFT of SHR were significantly lower than that of Wistar rats （P 〈 0.001）.②In SHR, the SBP and HMI of 18 week SHR were significantly higher than those of 10 week SHR （P 〈 0.001）. The VFT of 18 week SHR were significantly lower than that of 10 week SHR （P 〈 0.001）. ③There were no significant difference of VERP among 10 week SHR, 18 week SHR and Wistar rats（P 〉 0.05）. ④There was no relationship between HMI and VFT or SBP in Wistar rats. There was significant relationship between HMI and VFT or SBP in different age spontaneously hypertensive rats. ⑤HMI, age and species of animal were the major influent factors of VFT. Conclusions The VFT of hypertrophied myocardium decreased. The higher the degree of hypertrophy of myocardium and the higher the systolic blood pressure were, the lower the ventricular fibrillation threshold was.展开更多
Speckle tracking echocardiography（STE） has been applied to the evaluation of cardiac contraction dysfunction. However, there were few studies on alteration of global and regional STE parameters in the process of myo...Speckle tracking echocardiography（STE） has been applied to the evaluation of cardiac contraction dysfunction. However, there were few studies on alteration of global and regional STE parameters in the process of myocardial hypertrophy and heart failure. In this study, STE was applied to evaluate the global and regional cardiac function under heart failure and hypertrophy in the mice model of pressure overload. Adult mice were subjected to mild or severe aortic banding with a 25 Gauge（G） or 27 G needle. After surgery, STE and conventional echocardiography were used in the sham group（n=10）, mild trans-aortic banding（TAB） group（n=14） and severe TAB group（n=10） for 8 weeks. The results showed that the mice subjected to severe TAB showed a significant change in fractional shortening（FS）, left ventricular（LV） mass, and left ventricular end diastolic diameter（LVEDD）（P〈0.05 for each）. Meanwhile, there were no significant differences in FS and LVEDD between the sham group and mild TAB group during the experimental procedures（P〉0.05 for both）. STE analysis revealed that longitudinal strain（LS） was significantly decreased in the severe TAB group as compared with the sham and mild TAB groups（P〈0.05 for both） from the postoperative week 1. LS in the mild TAB group was reduced as compared to the sham group（P〈0.05）. Radial strain（RS） and circumferential strain（CS） were significantly decreased in the severe TAB group as compared to the sham group and the mild TAB group（P〈0.05 for both） from the postoperative week 1（P〈0.05 for both）. Compared to the sham group, CS in the mild TAB group maintained unchanged during the test period, and RS was reduced only on the postoperative week 6（P〈0.05）. Finally, regional contraction dysfunction was analyzed in both hypertrophic and failing myocardium in longitudinal and radial directions. It was found that LS was largest in the apex region and RS was smallest in the apex region in the healthy and hypertrophic myocardium. It was also found that compared to the sham group, only base longitudinal strain in the mild TAB group was decreased. Each of regional strain in the severe TAB group was uniformly depressed in radial and longitudinal directions. It is concluded that STE has provided a non-invasive and highly feasible way to explore the global and regional contraction dysfunction in hypertrophic and heart failure myocardium in the murine model of pressure overload.展开更多
Hearts of pressure-overload hypertrophy show an increased activation of intracardiac renin-angiotensin system which may contribute to ischemia and reperfusion injury. The purpose of this study is to evaluate whether t...Hearts of pressure-overload hypertrophy show an increased activation of intracardiac renin-angiotensin system which may contribute to ischemia and reperfusion injury. The purpose of this study is to evaluate whether the hypertrophied myocardium is more vulnerable to ischemia and reperfusion injury and to find out its relation to the cardiac renin-angiotensin system. Hypertrophied rat hearts induced by abdominal aortic banding for 6 weeks were subjected to 2 hours of hypothermic ischemic arrest followed by 30 minutes of reperfusion, and their cardiac function recovery was compared with that of sham-operated normal control hearts. The cardiac renin activity and angiotensin II content before ischemia and after reperfusion were determined. It was found that both the pre-ischemic renin activity and angiotensin II level were higher in hypertrophied myocardium than those in the control: ischemia and reperfusion injury increased both renin activity and angiotensin II content in the two groups, but the renin activity and angiotensin II level were further elevated after reperfusion in the hypertrophied hearts than those in the control hearts. Meanwhile, the cardiac function recovery after 30 minutes reperfusion in the hypertrophied hearts was poorer than that in the control. Correlation analysis revealed that there was a negative correlation between the cardiac output recovery and the myocardial angiotensin II content (r=-0.841), P<0.001), It is concluded that ischemia and reperfusion injury can activate cardiac renin-angiotensin system in isolated rat heart, which may be responsible for the increased susceptibility of the hypertrophied myocardium to ischemia and reperfusion injury.展开更多
To study the difference in membrane ionic currents between hypertrophied and normal myocytes and to explore the electrical remodeling of hypertrophied myocytes Methods Membrane ionic channels were studied in enzymat...To study the difference in membrane ionic currents between hypertrophied and normal myocytes and to explore the electrical remodeling of hypertrophied myocytes Methods Membrane ionic channels were studied in enzymatically dispersed spontaneously hypertensive rats (SHRs) left ventricular myocytes using the whole cell configuration of patch clamp technique, with normal Wistar rats ventricular myocytes as controls We observed depolarizing currents (sodium current, I Na ; L type calcium current, L I Ca ) and repolarizing currents (inward rectifier potassium current, I K1 ; delayed rectifier potassium current, I K; transient outward potassium current, I to ) and compared the differences between normal and hypertrophied myocytes Results The heart to body weight ratio of Wistar rats and SHRs was 3 70±0 29?mg/g and 5 66±0 46?mg/g, respectively ( P <0 001), and the mean cell membrane capacitances were 189 94±56 59?pF and 280 68±67 98?pF, respectively ( P <0 05) These differences suggest that SHRs have heart hypertrophy and hypertrophied myocytes The amplitude of L I ca of SHRs (1944±466 8?pA) was significantly greater than that of Wistar rats (1136±383 3?pA) ( P <0 001), and the current density was 6 93±1 71?pA/pF and 6 19±2 85?pA/pF respectively when normalized to cell capacitance, and the slow inactivation time constant of SHRs was significantly prolonged (56 01±13 36?ms vs 43 63±17 89?ms, P <0 001) The amplitude of I Na of SHRs (6132 5±1162 9?pA) was significantly greater than that of Wistar rats (3613 9±794 44?pA) ( P <0 001), but there was no difference when normalized to cell capacitance (24 61±6 72?pA/pF vs 24 95±6 99?pA/pF) Channel activation and inactivation time constants were also the same The amplitude of I K of SHRs (3461 5±1967 10?pA) was greater than that of Wistar rats (2302 4±893 72?pA) ( P <0 05), but there was no difference when normalized to cell capacitance (12 38±5 46 ?pA/pF vs 11 86±3 59?pA/pF) The inward portion of I K1 of SHRs was significantly lower than that of Wistar rats (11 3±2 26?pA/pF vs 14 3±3 00?pA/pF, P <0 05), but there was no difference in the outward portion (2 360±0 86?pA/pF vs 2 957±1 27? pA/pF) The current density of I to of SHRs (8 21±6 64?pA/pF) was significantly lower than that of Wistar rats (19 16±6 17?pA/pF) ( P <0 001), but channel kinetics were similar, suggesting that the reduction of I to may result from the decrease in channel number Conclusions Membrane ionic current changes of hypertrophied left ventricular myocytes in SHRs include: 1 there was an increase of L I ca , I Na and I k, but the current density was similar to that in normal myocytes, indicating that channel numbers increase as the myocytes become hypertrophied; 2 I to was small in hypertrophied ventricular myocytes and its current density was even smaller, indicating that channel numbers decrease as the myocytes enlarge The former is recognized as a physiologically compensatory change which does not lead to electrophysiological disturbance; the latter is viewed as pathological change, where the reduction of I to may lead to a repolarizing delay in myocytes, prolongation of the action potential and the occurrence of arrhythmias because of repolarizing heterogeneity Therefore, the reduction of I to in hypertrophied myocytes should be recognized as a significant or substantial change of electrical remodeling展开更多
文摘Objectives To investigate the relation between hypertrophied myocardium and ventricular fibrillation threshold in spontaneously hypertensive rats （SHR）. Methods 20 male SHR were randomly divided into two groups： 10 week group （n= 10） and 18 week group （n=10）. 10 week male Wistar rats were controlled group （n=10）. The systolic blood pressure （SBP）, heart mass index （HMI）, ventricular effective refractory period （VERP） and ventricular fibrillation threshold（VFT） were measured respectively.① The SBP and HMI of SHR were significantly higher than those of Wistar rats（P 〈 0.001）. The VFT of SHR were significantly lower than that of Wistar rats （P 〈 0.001）.②In SHR, the SBP and HMI of 18 week SHR were significantly higher than those of 10 week SHR （P 〈 0.001）. The VFT of 18 week SHR were significantly lower than that of 10 week SHR （P 〈 0.001）. ③There were no significant difference of VERP among 10 week SHR, 18 week SHR and Wistar rats（P 〉 0.05）. ④There was no relationship between HMI and VFT or SBP in Wistar rats. There was significant relationship between HMI and VFT or SBP in different age spontaneously hypertensive rats. ⑤HMI, age and species of animal were the major influent factors of VFT. Conclusions The VFT of hypertrophied myocardium decreased. The higher the degree of hypertrophy of myocardium and the higher the systolic blood pressure were, the lower the ventricular fibrillation threshold was.
基金supported by grants from the National Natural Science Foundation of China(No.81400255)the Hubei Science&Technology Pillar Program of China(No.2012DCA12007)the Hubei Public Welfare Science Research Program of China(No.2013BCB023)
文摘Speckle tracking echocardiography（STE） has been applied to the evaluation of cardiac contraction dysfunction. However, there were few studies on alteration of global and regional STE parameters in the process of myocardial hypertrophy and heart failure. In this study, STE was applied to evaluate the global and regional cardiac function under heart failure and hypertrophy in the mice model of pressure overload. Adult mice were subjected to mild or severe aortic banding with a 25 Gauge（G） or 27 G needle. After surgery, STE and conventional echocardiography were used in the sham group（n=10）, mild trans-aortic banding（TAB） group（n=14） and severe TAB group（n=10） for 8 weeks. The results showed that the mice subjected to severe TAB showed a significant change in fractional shortening（FS）, left ventricular（LV） mass, and left ventricular end diastolic diameter（LVEDD）（P〈0.05 for each）. Meanwhile, there were no significant differences in FS and LVEDD between the sham group and mild TAB group during the experimental procedures（P〉0.05 for both）. STE analysis revealed that longitudinal strain（LS） was significantly decreased in the severe TAB group as compared with the sham and mild TAB groups（P〈0.05 for both） from the postoperative week 1. LS in the mild TAB group was reduced as compared to the sham group（P〈0.05）. Radial strain（RS） and circumferential strain（CS） were significantly decreased in the severe TAB group as compared to the sham group and the mild TAB group（P〈0.05 for both） from the postoperative week 1（P〈0.05 for both）. Compared to the sham group, CS in the mild TAB group maintained unchanged during the test period, and RS was reduced only on the postoperative week 6（P〈0.05）. Finally, regional contraction dysfunction was analyzed in both hypertrophic and failing myocardium in longitudinal and radial directions. It was found that LS was largest in the apex region and RS was smallest in the apex region in the healthy and hypertrophic myocardium. It was also found that compared to the sham group, only base longitudinal strain in the mild TAB group was decreased. Each of regional strain in the severe TAB group was uniformly depressed in radial and longitudinal directions. It is concluded that STE has provided a non-invasive and highly feasible way to explore the global and regional contraction dysfunction in hypertrophic and heart failure myocardium in the murine model of pressure overload.
文摘Hearts of pressure-overload hypertrophy show an increased activation of intracardiac renin-angiotensin system which may contribute to ischemia and reperfusion injury. The purpose of this study is to evaluate whether the hypertrophied myocardium is more vulnerable to ischemia and reperfusion injury and to find out its relation to the cardiac renin-angiotensin system. Hypertrophied rat hearts induced by abdominal aortic banding for 6 weeks were subjected to 2 hours of hypothermic ischemic arrest followed by 30 minutes of reperfusion, and their cardiac function recovery was compared with that of sham-operated normal control hearts. The cardiac renin activity and angiotensin II content before ischemia and after reperfusion were determined. It was found that both the pre-ischemic renin activity and angiotensin II level were higher in hypertrophied myocardium than those in the control: ischemia and reperfusion injury increased both renin activity and angiotensin II content in the two groups, but the renin activity and angiotensin II level were further elevated after reperfusion in the hypertrophied hearts than those in the control hearts. Meanwhile, the cardiac function recovery after 30 minutes reperfusion in the hypertrophied hearts was poorer than that in the control. Correlation analysis revealed that there was a negative correlation between the cardiac output recovery and the myocardial angiotensin II content (r=-0.841), P<0.001), It is concluded that ischemia and reperfusion injury can activate cardiac renin-angiotensin system in isolated rat heart, which may be responsible for the increased susceptibility of the hypertrophied myocardium to ischemia and reperfusion injury.
文摘To study the difference in membrane ionic currents between hypertrophied and normal myocytes and to explore the electrical remodeling of hypertrophied myocytes Methods Membrane ionic channels were studied in enzymatically dispersed spontaneously hypertensive rats (SHRs) left ventricular myocytes using the whole cell configuration of patch clamp technique, with normal Wistar rats ventricular myocytes as controls We observed depolarizing currents (sodium current, I Na ; L type calcium current, L I Ca ) and repolarizing currents (inward rectifier potassium current, I K1 ; delayed rectifier potassium current, I K; transient outward potassium current, I to ) and compared the differences between normal and hypertrophied myocytes Results The heart to body weight ratio of Wistar rats and SHRs was 3 70±0 29?mg/g and 5 66±0 46?mg/g, respectively ( P <0 001), and the mean cell membrane capacitances were 189 94±56 59?pF and 280 68±67 98?pF, respectively ( P <0 05) These differences suggest that SHRs have heart hypertrophy and hypertrophied myocytes The amplitude of L I ca of SHRs (1944±466 8?pA) was significantly greater than that of Wistar rats (1136±383 3?pA) ( P <0 001), and the current density was 6 93±1 71?pA/pF and 6 19±2 85?pA/pF respectively when normalized to cell capacitance, and the slow inactivation time constant of SHRs was significantly prolonged (56 01±13 36?ms vs 43 63±17 89?ms, P <0 001) The amplitude of I Na of SHRs (6132 5±1162 9?pA) was significantly greater than that of Wistar rats (3613 9±794 44?pA) ( P <0 001), but there was no difference when normalized to cell capacitance (24 61±6 72?pA/pF vs 24 95±6 99?pA/pF) Channel activation and inactivation time constants were also the same The amplitude of I K of SHRs (3461 5±1967 10?pA) was greater than that of Wistar rats (2302 4±893 72?pA) ( P <0 05), but there was no difference when normalized to cell capacitance (12 38±5 46 ?pA/pF vs 11 86±3 59?pA/pF) The inward portion of I K1 of SHRs was significantly lower than that of Wistar rats (11 3±2 26?pA/pF vs 14 3±3 00?pA/pF, P <0 05), but there was no difference in the outward portion (2 360±0 86?pA/pF vs 2 957±1 27? pA/pF) The current density of I to of SHRs (8 21±6 64?pA/pF) was significantly lower than that of Wistar rats (19 16±6 17?pA/pF) ( P <0 001), but channel kinetics were similar, suggesting that the reduction of I to may result from the decrease in channel number Conclusions Membrane ionic current changes of hypertrophied left ventricular myocytes in SHRs include: 1 there was an increase of L I ca , I Na and I k, but the current density was similar to that in normal myocytes, indicating that channel numbers increase as the myocytes become hypertrophied; 2 I to was small in hypertrophied ventricular myocytes and its current density was even smaller, indicating that channel numbers decrease as the myocytes enlarge The former is recognized as a physiologically compensatory change which does not lead to electrophysiological disturbance; the latter is viewed as pathological change, where the reduction of I to may lead to a repolarizing delay in myocytes, prolongation of the action potential and the occurrence of arrhythmias because of repolarizing heterogeneity Therefore, the reduction of I to in hypertrophied myocytes should be recognized as a significant or substantial change of electrical remodeling
