间隙结解器heptanol可以防止细胞对细胞的超收缩进展,并限制心肌再输液期间的亡
D Garcia-Dorado1, J Inserte, M Ruiz-Meana
1Servicio de Cardiología, Hospital General Universitari Vall d'Hebron, Barcelona, Spain. dgdorado@ar.vhebron.es
Circulation
|December 13, 1997
概括
化学物质在心脏细胞之间传播过度收缩,导致心脏病发作的大小. 像赫普坦醇这样的间隙结阻剂阻止了这种传播,减少了在再注射期间的心脏损伤,并提供了一种新的治疗方法.
科学领域:
- 心血管生物学 心血管生物学
- 细胞生理学 细胞生理学
- 药理学 药理学是指药理学的学科.
背景情况:
- 通过间隙结进行细胞对细胞的通信在心脏组织中至关重要.
- 心肌细胞中的超收缩可以扩散,可能会加剧心肌梗塞.
- 了解超收缩扩散的机制是制定保护策略的关键.
研究的目的:
- 调查通过间隙结的化学相互作用是否会导致细胞对细胞的超收缩进展.
- 确定这种现象是否会导致心肌梗塞的扩散程度.
- 评估隙连接调制在限制心脏病发作大小方面的潜力.
主要方法:
- 研究了成年大鼠心肌细胞中隔离的超收缩的细胞对细胞传播,使用微注射和黄.
- 利用间隙连接解器heptanol来评估其对超收缩传播的影响.
- 在低氧/低氧化和冠状动脉封闭/再输血模型期间,给隔离的透老鼠心脏和现场猪心脏注射赫塔诺尔.
- 评估了心脏病发作的大小,心脏功能和损伤的生物化学标志物.
主要成果:
- 由Ca2+微注射传递到相邻心肌细胞引起的超收缩,由黄传播证实.
- 肝醇显著抑制了心肌细胞对中的超收缩传播.
- 在注射过的老鼠心脏中,依赖于剂量的坦醇减少了氧悖论损伤,改善了压力恢复,并减少了LDH释放和亡.
- 在猪心脏中,冠状管内赫普坦醇限制了心肌收缩,减少了54%的心脏病发作大小,并改变了心脏病发作形态.
结论:
- 超收缩是通过间隙连接通过相邻的肌细胞之间传播的.
- 肝醇有效地干扰了这种传播,在再注射过程中显著降低了心肌缩.
- 差距连接导电性的药理控制为限制心脏病发作大小提供了一个新的治疗策略.
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