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短暂性脑缺血发作的动物模型:兔颈内动脉注射二磷酸腺苷的实验研究

Animal model of TIA: an experimental study with intracarotid ADP infusion in rabbits.

作者信息

Fieschi C, Battistini N, Volante F, Zanette E, Weber G, Passero S

出版信息

Stroke. 1975 Nov-Dec;6(6):617-21. doi: 10.1161/01.str.6.6.617.

Abstract

Adenosine diphosphate (8 mg per minute for five minutes) was infused into the carotid artery of 63 rabbits. The effects were twofold: systemic hypotension and platelet aggregation in the cerebral circulation. As a consequence of the last effect, platelet emboli were produced which occluded cerebral arteries in a number and size sufficient to cause cerebral ischemia. Areas of focal ischemia were observed through a cranial window, and documented with antipyrine autoradiography. Platelet thrombi were almost entirely transient, being fragmented and removed within a very short time of cessation of ADP infusion. Consequently, no permanent tissue damage ensued. This experimental model approaches the spontaneous transient ischemia attacks (TIAs) in man, demonstrating that these can be caused by pure platelet emboli. A high cholesterol diet administered for two months prior to ADP infusion did not enhance the effect of the procedure or make the platelet aggregation and the following ischemia longer in duration or more severe.

摘要

将二磷酸腺苷(每分钟8毫克,持续5分钟)注入63只兔子的颈动脉。其作用有两方面:全身性低血压和脑循环中的血小板聚集。由于后一种作用,产生了血小板栓子,其数量和大小足以阻塞脑动脉,从而导致脑缺血。通过颅骨视窗观察到局灶性缺血区域,并用安替比林放射自显影法记录下来。血小板血栓几乎完全是短暂的,在停止注入二磷酸腺苷后的很短时间内就会破碎并被清除。因此,没有造成永久性组织损伤。这个实验模型类似于人类的自发性短暂性脑缺血发作(TIA),表明这些发作可能由单纯的血小板栓子引起。在注入二磷酸腺苷前两个月给予高胆固醇饮食,并没有增强该操作的效果,也没有使血小板聚集以及随后的缺血持续时间更长或更严重。

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