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http://scihub22266oqcxt.onion/ 17386161!ä!17386161 Warning: Undefined variable $yww in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 538 Warning: Undefined variable $yww in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 538       Zhonghua+Xin+Xue+Guan+Bing+Za+Zhi 2007 ; 35 (1): 33-6 Nephropedia Template TP {{tp|p=17386161|t=2007. The effects of calmodulin kinase II inhibitor on ventricular arrhythmias in rabbits with cardiac hypertrophy |pdf=|usr=}}{{17386161}} gab.com Text The effects of calmodulin kinase II inhibitor on ventricular arrhythmias in rabbits with cardiac hypertrophy JO: Zhonghua Xin Xue Guan Bing Za Zhi http://www.kidney.de/pget.php?&tw=1&pmid=17386161 #FOAvip OBJECTIVE: To investigate the effect of KN-93, a calmodulin kinase II inhibitor, on ventricular arrhythmias in rabbits with cardiac hypertrophy. METHODS: Female New Zealand white rabbits were randomly divided into four groups (n = 10 each): Sham; LVH; LVH + KN-92 and LVH + KN-93 group. LVH was induced by partially constricting the abdominal aorta. In Sham group, the abdominal aorta was exposed without constriction. Eight weeks later, the arterially perfused left ventricular wedge preparations were made and transmembrane action potentials (TAP) from epicardium and endocardium and transmural ECG were simultaneously recorded. Incidence of early after depolarization (EAD) and torsade de pointes (Tdp), QT interval, action potential duration (APD) and transmural depolarization dispersion (TDR) at different cycle lengths were observed under slow stimulation (2000 - 4000 ms), hypokalemic (2 mmol/L) and hypomagnesaemic (0.25 mmol/L) Tyrode's solution perfusion. RESULTS: Left ventricular hypertrophy was detected in LVH group by echocardiography and not affected by KN-92 and KN-93. Perfused with hypokalemic, hypomagnesaemic Tyrode's solution and under slow stimulation (2000 - 4000 ms), the incidences of EAD and Tdp in Sham group, LVH group, LVH + KN-92 group (0.5 micromol/L) and LVH + KN-93 group (0.5 micromol/L) were 0/10, 10/10, 9/10, 5/10 and 0/10, 5/10, 4/10, 1/10, respectively. With 1 micromol/L KN-92 and KN-93, the incidences of EAD and Tdp in LVH + KN-92 and LVH + KN-93 group were 9/10, 3/10 and 4/10, 1/10 respectively. The QT interval, APD and TDR were not affected by KN-93. CONCLUSION: The calmodulin kinase II inhibitor KN-93 can effectively suppress ventricular arrhythmias in rabbits with cardiac hypertrophy by decreasing EAD. Twit Text FOAVip The effects of calmodulin kinase II inhibitor on ventricular arrhythmias in rabbits with cardiac hypertrophy ????Zhonghua Xin Xue Guan Bing Za Zhi http://www.kidney.de/pget.php?&tw=1&pmid=17386161 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=17386161 #FOAvip English Wikipedia <ref>{{Cite pmid|17386161}}</ref> The effects of calmodulin kinase II inhibitor on ventricular arrhythmias in rabbits with cardiac hypertrophy #MMPMID17386161 Ke J; Zhang CT; Ma YX; Liu J; Zhang QY; Liu N; Ruan YF; Lin L Zhonghua Xin Xue Guan Bing Za Zhi 2007[Jan]; 35 (1): 33-6 PMID17386161show ga OBJECTIVE: To investigate the effect of KN-93, a calmodulin kinase II inhibitor, on ventricular arrhythmias in rabbits with cardiac hypertrophy. METHODS: Female New Zealand white rabbits were randomly divided into four groups (n = 10 each): Sham; LVH; LVH + KN-92 and LVH + KN-93 group. LVH was induced by partially constricting the abdominal aorta. In Sham group, the abdominal aorta was exposed without constriction. Eight weeks later, the arterially perfused left ventricular wedge preparations were made and transmembrane action potentials (TAP) from epicardium and endocardium and transmural ECG were simultaneously recorded. Incidence of early after depolarization (EAD) and torsade de pointes (Tdp), QT interval, action potential duration (APD) and transmural depolarization dispersion (TDR) at different cycle lengths were observed under slow stimulation (2000 - 4000 ms), hypokalemic (2 mmol/L) and hypomagnesaemic (0.25 mmol/L) Tyrode's solution perfusion. RESULTS: Left ventricular hypertrophy was detected in LVH group by echocardiography and not affected by KN-92 and KN-93. Perfused with hypokalemic, hypomagnesaemic Tyrode's solution and under slow stimulation (2000 - 4000 ms), the incidences of EAD and Tdp in Sham group, LVH group, LVH + KN-92 group (0.5 micromol/L) and LVH + KN-93 group (0.5 micromol/L) were 0/10, 10/10, 9/10, 5/10 and 0/10, 5/10, 4/10, 1/10, respectively. With 1 micromol/L KN-92 and KN-93, the incidences of EAD and Tdp in LVH + KN-92 and LVH + KN-93 group were 9/10, 3/10 and 4/10, 1/10 respectively. The QT interval, APD and TDR were not affected by KN-93. CONCLUSION: The calmodulin kinase II inhibitor KN-93 can effectively suppress ventricular arrhythmias in rabbits with cardiac hypertrophy by decreasing EAD. |Animals[MESH] |Arrhythmias, Cardiac/complications/*drug therapy[MESH] |Benzylamines/*pharmacology[MESH] |Calcium-Calmodulin-Dependent Protein Kinase Type 2/*antagonists & inhibitors[MESH] |Cardiomegaly/complications/*drug therapy[MESH] |Disease Models, Animal[MESH] |Male[MESH] |Protein Kinase Inhibitors/*pharmacology[MESH] |Rabbits[MESH] The effects of calmodulin kinase II inhibitor on ventricular arrhythm(epmc).pdf DeepDyve Pubget Overpricing