大鼠肥厚心肌缩短速度和肌凝蛋白重链同功酶谱的变化

CHANGES IN MYOSIN ISOENZYMES COMPOSITION AND THE MAXIMUM SHORTENING VELOCITY IN HYPERTROPHIC LEFT VENTRICULAR MUSCLE OF RATS

用聚丙烯酰胺电泳分离并测定了大鼠左室肌凝蛋白ＡＴＰ酶活性依次降低的同功酶Ｖ_１，Ｖ_２和Ｖ_３的百分比（ＭＩ谱），从乳头肌力－速度曲线读取心肌最大缩短速度（Ｖ_（ｍａｘ）），观察到：（１）正常大鼠出现增龄性Ｖ_１向Ｖ_３迁移和Ｖ_（ｍａｘ）下降，与８周龄组（Ｓ_０）相比，１６周和２４周龄组（Ｓ_８和Ｓ_（１６））的Ｖ_１／Ｖ_３比，分别下降３８．９％和６１．０％；Ｖ_（ｍａｘ）下降８．３％和１３．３％。（２）高血压肥厚心肌ＭＩ谱的迁移和Ｖ_（ｍａｘ）下降的程度大大超过增龄效应：高血压８周和１６周组（Ｈ_８和Ｈ_（１６））的Ｖ_１／Ｖ_３比值较术前对照Ｓ_０分别下降８４．４％和９３．５％，较同龄假手术对照Ｓ_８和Ｓ_（１６）组也分别低７４．５％和８３．３％，而Ｖ_（ｍａｘ）则比Ｓ_０组下降３３．３％和４８．３％。（３）６组４８只大鼠结果相关分析表明，Ｖ_（ｍａｘ）与Ｖ_１％高度正相关，与Ｖ_３％高度负相关。（Ｐ均小于０．０１）。上述结果提示：高血压肥厚心肌收缩速度明显下降，其主要生化机制似与同功酶谱由Ｖ_１优势向Ｖ_３迁移有关。

Changes in unloaded maximum shortening velocity (Vmax) and myosin isoenzymes (MI) composition of rat left ventricular muscle were examined in the 8-week or 16week Goldblatt hypertensive (H8, H16 ) and hypertension-regressive rats (R8). The Vmax was estimated by extrapolation to zero afterload from the tension-velocity curve of left ventricular papillary muscle, while the MI composition (V1, V2 and V3) was separated by polyacrylamide gel electrophoresis and determined by densitometry. The resuits showed that: (1 ) A slow age-dependent shift to V3 and a decrease in Vmax were observed in 16- and 24-week-old rats (S8, S16), in which V1/V3 ratio was decreased respectively by 38. 9 % and 61. 0% and Vmax was decreased respectively by 8. 3% and 1 3. 3 % when compared with that of the 8-week-old rats (S0). (2) There was a significant decrease in V1/V3 ratio and Vmax in 8-week (H8) and 1 6-week (H16) hypertension induced hypertrophic left ventricular muscle as evidenced by the fact that the V1/V3 rano decreased by 84. 4 % and 93. 5% and Vmax decreased by 33. 3% and 48. 3 % in H8 and H16 as compared with that of the control rats (S0). (3) There was a partial recovery in Vmax and V1/V3 ratio in (R8) group rats. (4) The Vmax was positively correlated with the level of V1 (r=0. 921 5, P<0. 01 ) and negatively with the level of V3 (r=0. 9071, P<0.01) as analyzed in all the six experimental groups of a total of 48 rats (S0, S8, S16, H8, H16, R8 ). In conclusion, a significant shift of the myosin isoenzymes towards low ATPase activity V3 might be the biochemical mechanism responsible, at least in part, for the decrease in maximum shortening velocity in the hypertrophic left ventricular muscle induced by pressure overload.