灌注

NM regulates the function of RCIA by antioxygenic effection, and has the protective effect on RBC membrane during ischemia reperfusion brain damage.

NM通过抗氧化作用对RBC免疫粘附功能有调节作用，从而对沙土鼠缺血再灌注脑组织损伤时红细胞膜起到保护作用。

Prostaglandin E2,alpha-1 antitrypsin and 764-3, a extract from Dansheng, have significant protection for hypoxia-reoxygenation induced LSEC IRI.

前列腺素E2、a-1抗胰蛋白酶和单参的单体764-3都可以明显保护肝窦内皮细胞的缺血－再灌注损伤。

Objective To investigate the protective effect and its role of apigenin on hepatic ischemia reperfusion injury in rats.

目的 观察芹菜素对大鼠缺血再灌注肝脏损伤的防护作用。

The apigenin have a prominent protective effect on hepatic ischemia reperfusion injury in rats.

芹菜素对大鼠肝脏缺血再灌注损伤有一定的保护作用。

The apigenin have a prominent protective effect on hepatic ischemia reperfusion injury in rats.??

葛根素预处理对大鼠缺血再灌注肝脏损伤有一定的保护作用。？？

The infusion of DADLE, a δ-opioid receptor agonist, produced a dose-dependent increase of ARNA without affecting renal pelvic substance P release, urine flow rate, and urinary sodium excretion.

此外，从肾盂灌注类鸦片致效剂DADLE([D-Ala2， D-Leu5]-enkephalin)，则会有一浓度依存性的增加ARNA的活性，但却不会影响肾盂内物质P的释放及对侧肾脏尿液流速(urine flow rate， UV)和钠离子排泄率(urinary sodium excretion， UNaV)；而此ARNA的增加并不会因预先给予NK-1受体拮抗剂spantide I (0.1mg/ml， 20μl/min)而有所减少。

Objective:The appraisal liver vein pours into the embolism to unite arsenous acid treatment primary liver cancer this new therapy.

目的：评价肝动脉灌注栓塞联合亚砷酸治疗原发性肝癌这一新的疗法。

Liver vein pours into the embolism to unite the arsenous acid treatment primary liver cancer is one extremely is worth the application the method of treatment.......

肝动脉灌注栓塞联合亚砷酸治疗原发性肝癌是一非常值得应用的治疗方法。亚砷酸；原发性肝癌；治疗

32 examples liver cancer after liver vein pour into,the embolism in advance treat,after 7 day,joins the 500ml physiological saline with arsenous acid inoculation fluid 10mg,a vein drop note,4 ~5h drops every day,altogether uses medicine 7 day.

32例肝癌先行经肝动脉灌注、栓塞治疗，7天后，用亚砷酸注射液10mg加入500ml生理盐水，每日1次静脉滴注，4～5h滴完，共用药7天。

Using an LQT2 model in arterially perfnsed rabbit left ventricular wedge preparations,we find that in intact ventricular walI,EAD can be generated and a trigger to initiate the onset of Tdp can be produced.

结论通过冠状小动脉灌注兔左室心肌组织块LQT2模型，发现整体心室肌组织在QT延长的条件下，2相EAD是触发并引起Tdp的机制；TDR增加是产生EAD和形成折返的基础。

The split between the two groups can hardly be papered over.

这两个团体间的分歧难以掩饰。

This approach not only encourages a greater number of responses, but minimizes the likelihood of stale groupthink.

这种做法不仅鼓励了更多的反应，而且减少跟风的可能性。