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慢性无神经心肌中的细胞异常.慢性无神经心肌. 对移植心脏的影响
1Academic Unit of Cardiovascular Medicine, Charing Cross and Westminster, Medical School, London, UK.
Circulation
|November 1, 1989
概括
移植后心脏变质可能导致代谢问题. 慢性无神经化的狗心表现出改变的葡萄糖氧化和增加的氧气消耗,这表明心脏移植患者的潜在心肌代谢效率低下.
科学领域:
- 心脏病学 心脏病学
- 生理学 生理学 生理学
- 移植科学 移植科学
背景情况:
- 心脏移植的结果是慢性无神经,排斥和免疫抑制.
- 长期失去神经的狗心脏可以作为独立研究失去神经效应的模型.
- 在这些心脏中发现了带有血管活性肠 (VIP) 和神经Y (NPY) 的内在神经元.
研究的目的:
- 为了研究心脏中慢性变质的代谢后果.
- 评估心肌肌的氧气消耗,酶活动,和基质氧化在无神经心脏.
- 在心脏移植患者中预测潜在的代谢低效率.
主要方法:
- 分析心肌组织中神经递质度 (上腺素,多巴胺).
- 评估心房内尿素 (ANP) 释放和内尿素反应.
- 测量体外氧气消耗和Na-K,ATPase活性.
- 评估体内葡萄糖氧化和关键糖解酶活动 (例如,果酸酶).
- 确定各种心脏酶的最大体外活性.
主要成果:
- 诺拉丁上腺素水平显著下降,而多巴胺在无神经心脏中仍然接近正常.
- 对心房张张的尿反应是的,表明依赖于反射机制.
- 试验室研究显示,心肌氧消耗和Na-K,ATPase活性增加.
- 在体内,葡萄糖氧化被抑制,有证据表明酸果酶活性受损.
- 尽管有功能性变化,但关键酶蛋白度和最大活动在很大程度上是正常的.
结论:
- 慢性心脏缺血导致心肌代谢发生显著变化.
- 患有心脏移植的患者可能会因为缺血而经历心肌神经代谢效率低下.
- 需要进一步的研究来探索治疗策略,以减轻移植后代谢功能障碍.
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