开搏通逆转高血压性心肌肥大过程中心肌超微结构的变化(PDF)
《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]
- 期数:
- 2003年第6期
- 页码:
- 504-507
- 栏目:
- 实验研究
- 出版日期:
- 2003-11-01
文章信息/Info
- Title:
- The changes in ultramicro-structure during regression of hypertensive cardiac hypertrophy by Captopril in rats
- Author(s):
- TONG Chang-qing; WANG Yi-he; QI Li; LI Hai-ying; LIU Zi-quan
- Department of Physiology, Medical College of the Chinese People‘s Armed Police Forces, Tianjin 300162, China
- 分类号:
- Q463; R331.3
- DOI:
- -
- 文献标识码:
- A
- 摘要:
- 目的:探讨开搏通逆转高血压性心肌肥大对心脏超微结构的作用。方法: 用多道生物信号系统记录血压和心率, 用电子显微镜观察心肌超微结构。结果: 第4、8、12 周, 高血压组的SBP, DBP, MAP 比对照组高, 第16周差别不明显, 假手术组和对照组的差别无统计学意义; 在第4、8、12周, T 管和肌浆网扩张, 第16周大部T 管和肌浆网恢复正常; 在第4周, 粗、细肌丝溶解, 第16周, 大部分粗、细肌丝清晰, 排列正常。结论: 开搏通能降低腹主动脉缩窄大鼠的血压和逆转心肌肥大; 在第4周, 高血压组肌纤维和肌管出现病理变化, 在第16周大多数粗、细肌丝和T管、肌浆网恢复正常。
- Abstract:
- AIM: To investigate the action of Captopril on ultramicro-structure in regression of left ventricular hypertrophy induced by hypertension in rats. METHODS: Blood pressure and heart rate were recorded with polygraph channel system, and the ultramicro structure of myocardium was observed by transmission electromicroscopy. RESULTS: SBP, DBP, MAP in hypertension group (H) at 4th, 8th, 12th weeks were higher than those of the control group (C) ; at 16th week difference among groups was not remarkable, and no statistics significance was found between the pseudooperation group (P) and the control group. At 4th, 8th, 12th weeks enlarging of T tubl and sarcoplasmic reticulum (SR) was found, at 16th week T tubl, SR for the most part were normal. At 4th week dissolving of thick and thin filaments in myofibrils was obsered. At 16th week thick and thin filaments in myofibrils were clear, ranking and their was normal. CONCLUSION: Captopril reduced blood pressure and reversed cardiac hypertrophy of abdomonal aortic banding rats. At 4th week pathological changes in myofibrils were seen, in the hypertension group , at 16th week thick and thin filaments, T tuble and SR were normal for the great part.
参考文献/References
[1] Agabiti RE, Muiesan ML. Left ventricular hypertrophy: how to influence an important risk factor in hypertension [J] . J Hypertens Suppl, 1998, 16(1):S53-58.
[2] 王长谦, 谢秀兰, 丁弘毅, 等. 压力负荷增高性心肌肥厚大鼠心肌胶原网络重构及? , ? 型mRNA 表达的变化 [J] . 心脏杂志, 2001, 13(5):369-371, 376.
[3] 佟长青, 张引国, 陈莉. 运动性和高血压性心脏肥大心肌间血管超微结构的对比研究 [J] . 武警医学, 2001, 12(1):7-9.
[4] Thurmann PA. Left ventricular and microvascular hypertrophy in essential hypertension: clinical relevance and prognostic implications [J] . Int J Clin Pharmacolther, 1997, 35(5):181-187.
[5] Raman-V K, Lee YA, Lindpaintner KV. The cardiac renin-angiotensin-aldosterone system and hypertensive cardiac hypertrophy [J] . Am J Cardiol, 1995, 76(13):18D-23D.
[6] Sharma JN, Kesavarao U. Effect of captopril on urinary kallikrein, blood pressure and myocardial hypertrophy in diabetic spontaneously hypertensive rats [J] . Pharmacology, 2002, 64(4):196-200.
[7] Callewaert G. Excitation-contraction coupling in mammalian cardiac cells [J] . Cardiovasc Res, 1992, 26:923-932.
[8] Bootman MD, Berridge MJ. The elemental principles of calcium signaling [J] . Cell, 1995, 83(5):675-678.
[9] Kohmoto O, Levi AJ, Bridge JH. Relation between reverse sodium-calcium exchange and sarcoplasmic reticulum calcium release in guinea pig ventricula cells [J] . Circ Res, 1994, 74(3):550-554.
[10] Gwathmey JK, Morgan JP. Altered calcium handling in experimental pressure-overload hypertrophy in the ferret [J] . Circ Res, 1985, 57:836-843.
[11] Aoki H, Sadoshima J, Izumo S. Myosin light chain kinase mediates sarcomere organization during cardiac hypertrophy in vitro [J] . Nat Med , 2000, 6(2):183-188
[12] Kent RL, McDermott PJ. Passive load and angiotensin ? evoke differential responses of gene expresion and protein synthesis in
cardiac myocytes [J] . Circ Res, 1996, 78(5):829-838.
备注/Memo
- 备注/Memo:
- 收稿日期：2002-12-25.
常用功能
统计/Statistics
- 摘要浏览/Viewed1001
- 全文下载/Downloads697
- 评论/Comments
