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- OBJECTIVE:To determine the relations of IL 1 mRNA and protein expressive law in ischemical myocardium and reperfusion injury and observe the effect of N acetylcysteine(NAC) on ischemia tissues. 目的:研究IL-1mRNA及蛋白在缺血心肌的表达规律及与再灌注损伤之间的关系,并观察N-乙酰半胱氨酸(N-acetylcysteine,NAC)对缺血组织的影响。
- Ischemical myocardium 缺血心肌
- Here is a microabscess in the myocardium. 图示心肌微脓疡。
- Effects of Desflurane in Senescent Rat Myocardium. 地氟醚对于大鼠心肌衰老的作用。
- Mesenchyma of myocardium was edematous. 光镜、电镜观察心肌病理性变化。
- Table2. Contents of Mb, myocardium protein and LDH activity(± s). 表2.;实验各组冠状动脉灌洗液中肌红蛋白、肌蛋白含量和乳酸脱氢酶活性
- Degenerative changes of the myocardium occur in many diseases. 心肌的退化性变化发生于许多疾病。
- DLIP and RIP has the same protection to immature myocardium as MIP. 非心脏 IP对未成熟心肌具有明显的保护作用 ,与 MIP相同 ,可诱发同等效应的心肌保护作用。
- It felt very flabby, and the myocardium was poorly contractile. 摸上去非常软，心肌收缩力下降。
- Conclusion Captopril is able to preserve ischemic myocardium. 结论卡托普利对缺血心肌具有保护作用。
- Noncompaction of myocardium is a special type of myocardiopathy. 心肌致密化不全是一种特殊类型的心肌病。
- Non-infarcted myocardium is present at the far left. 左侧是没有发生梗死的心肌。
- Its hyperosmosis pressure could alleviate the myocardium endema. 在心内直视手术过程中，相继采用的保护心肌的具体方法有：常温、室颤、冠状动脉持续灌注法，主要用于冠状动脉架桥术，此法缺点：室颤时心内膜下血运仍不足，结果仍导致高能磷酸盐储备下降，乳酸积聚，心肌收缩力下降；
- A potential role for PINCH proteins in myocardium remains unknown. 心肌中PINCH蛋白潜在的作用尚不清楚。
- Adenosine-Induced Preconditioning of Human Myocardium? （腺苷-诱致人心肌的预适应？）
- Danshen may prevent the myocardium from damage with anoxia. 结论复方丹参对小鼠心肌缺氧损伤有保护作用。
- The abnormality mitral stenosis was in myocardium, not in the valve. 二尖瓣狭窄的病变是在心肌而不是在瓣膜。
- Not only has VEGF a high expression in ischemical eye disease,but also significantly elevate in some nuischemical eye disease. VEGF在 PVR中呈上调性表达。 VEGF不仅在缺血性眼部疾病中呈高表达 ,而且在某些非缺血性眼部疾病中表达升高。
- Ulinastatin reduces the risk of renal dysfunction and injury during CPB by attenuating renal ischemical reperfusion injury(IRI). 乌司他丁对高原体外循环犬肾功能有保护作用,主要与减轻肾脏缺血再灌注损伤(Ischemical reperfusion injury,IRI)有关。
- In the physiopathologic process of ischemical reperfusion injury, mitoKATP channel has become a novel target of research on neuroprotection. 在脑的缺血再灌注损伤的病理生理过程中,ATP敏感性钾通道已经成为人们研究抗损伤的一个靶点。
