Cardiovascular disease,predominantly coronary heart disease and stroke,leads to high morbidity and mortality not only in developed worlds but also in underdeveloped regions.The dominant pathologic foundation for cardi...Cardiovascular disease,predominantly coronary heart disease and stroke,leads to high morbidity and mortality not only in developed worlds but also in underdeveloped regions.The dominant pathologic foundation for cardiovascular disease is atherosclerosis and,as to coronary heart disease,coronary atherosclerosis and resulting lumen stenosis,even total occlusions.In translational research,several animals,such as mice,rabbits and pigs,have been used as disease models of human atherosclerosis and related cardiovascular disorders.However,coronary lesions are either naturally rare or hard to be fast induced in these models,hence,coronary heart disease induction mostly relies on surgical or pharmaceutical interventions with no or limited primary coronary lesions,thus unrepresentative of human coronary heart disease progression and pathology.In this review,we describe the progress of animal models of coronary heart disease following either spontaneous or diet-accelerated coronary lesions.展开更多
Objective To explore the molecular mechanism underlying the decreased velocity of tension rise in rat myocardium during congestive heart failure (CHF) and left ventricular hypertrophy (LVH) induced by aortic stenosis...Objective To explore the molecular mechanism underlying the decreased velocity of tension rise in rat myocardium during congestive heart failure (CHF) and left ventricular hypertrophy (LVH) induced by aortic stenosis.Methods The maximum velocity of tension rise (+dT/dtmax) was measured in left ventricular papillary muscle and the mRNA level of myosin heavy chain (MHC) isoforms in the left ventricle were detected by Northern blot analysis.Results The value of +dT/dtmax in CHF and LVH group were 64.17% and 37.15% lower than sham-operated controls (Sham) (P<0.01); values in the CHF group were 42.99% lower than that of LVH (P<0.01). The level of α-MHC mRNA in LVH was not different from that of the Sham (P>0.05), but decreased significantly in CHF to 42.3% of Sham and 56.1% of LVH (P<0.01). The level of β-MHC mRNA was up-regulated by 88.3% (P<0.01) in LVH compared with Sham and the level of β-MHC in CHF was 1.5-fold and 3.7-fold higher than that in LVH and Sham respectively (P<0.01). The ratio of α-MHC/β-MHC mRNA in LVH and CHF decreased to 42.4% and 9.8% respectively of the value in Sham (P<0.01). Correlation between α-MHC/β-MHC mRNA level and +dT/dtmax was analyzed which showed that these values were positively correlated with a correlation coefficient of 0.875 (P<0.01).Conclusion The decreased ratio of α-MHC/β-MHC mRNA was the major molecular mechanism underlying the decreased +dT/dtmax in CHF and LVH myocardium. The decreased ratio of α-MHC/β-MHC mRNA in LVH was mainly due to the up regulation of β-MHC mRNA while in CHF both down regulation of α-MHC and up regulation of β-MHC were involved.展开更多
文摘Cardiovascular disease,predominantly coronary heart disease and stroke,leads to high morbidity and mortality not only in developed worlds but also in underdeveloped regions.The dominant pathologic foundation for cardiovascular disease is atherosclerosis and,as to coronary heart disease,coronary atherosclerosis and resulting lumen stenosis,even total occlusions.In translational research,several animals,such as mice,rabbits and pigs,have been used as disease models of human atherosclerosis and related cardiovascular disorders.However,coronary lesions are either naturally rare or hard to be fast induced in these models,hence,coronary heart disease induction mostly relies on surgical or pharmaceutical interventions with no or limited primary coronary lesions,thus unrepresentative of human coronary heart disease progression and pathology.In this review,we describe the progress of animal models of coronary heart disease following either spontaneous or diet-accelerated coronary lesions.
文摘Objective To explore the molecular mechanism underlying the decreased velocity of tension rise in rat myocardium during congestive heart failure (CHF) and left ventricular hypertrophy (LVH) induced by aortic stenosis.Methods The maximum velocity of tension rise (+dT/dtmax) was measured in left ventricular papillary muscle and the mRNA level of myosin heavy chain (MHC) isoforms in the left ventricle were detected by Northern blot analysis.Results The value of +dT/dtmax in CHF and LVH group were 64.17% and 37.15% lower than sham-operated controls (Sham) (P<0.01); values in the CHF group were 42.99% lower than that of LVH (P<0.01). The level of α-MHC mRNA in LVH was not different from that of the Sham (P>0.05), but decreased significantly in CHF to 42.3% of Sham and 56.1% of LVH (P<0.01). The level of β-MHC mRNA was up-regulated by 88.3% (P<0.01) in LVH compared with Sham and the level of β-MHC in CHF was 1.5-fold and 3.7-fold higher than that in LVH and Sham respectively (P<0.01). The ratio of α-MHC/β-MHC mRNA in LVH and CHF decreased to 42.4% and 9.8% respectively of the value in Sham (P<0.01). Correlation between α-MHC/β-MHC mRNA level and +dT/dtmax was analyzed which showed that these values were positively correlated with a correlation coefficient of 0.875 (P<0.01).Conclusion The decreased ratio of α-MHC/β-MHC mRNA was the major molecular mechanism underlying the decreased +dT/dtmax in CHF and LVH myocardium. The decreased ratio of α-MHC/β-MHC mRNA in LVH was mainly due to the up regulation of β-MHC mRNA while in CHF both down regulation of α-MHC and up regulation of β-MHC were involved.
