Ahn S S, Gray-Allan P, Wood E R, Ghalili S S, Moore W S, Blaha C D
Section of Vascular Surgery, University of California, Los Angeles Center for the Health Sciences, USA.
J Vasc Surg. 1995 Aug;22(2):135-41. doi: 10.1016/s0741-5214(95)70107-9.
Intracranial norepinephrine release has been associated with post-carotid endarterectomy hypertension in human beings. To study this phenomenon under more controlled conditions, we studied the relationship of cerebral catecholamines and blood pressure in gerbils, whose cerebral circulation is similar to that in human beings.
Twelve anesthetized gerbils underwent iliac artery blood pressure monitoring and in vivo electrochemistry catecholamine monitoring with use of catecholamine-specific electrodes placed stereotactically into the cerebral striatum. Six gerbils underwent 10 minutes of bilateral carotid artery occlusion (ischemic), whereas six underwent carotid artery dissection without occlusion (control).
The control group demonstrated a continuous gradual decline in blood pressure and striatal catecholamine during the 150-minute observation period. In contrast the ischemic gerbils demonstrated a sharp catecholamine rise during ischemia, a marked catecholamine drop shortly after carotid artery unclamping, and then a secondary larger catecholamine release that peaks in 60 minutes and gradually returns to baseline in 120 minutes. The blood pressure closely followed the catecholamine levels, with a sharp 20 mm Hg rise in blood pressure above baseline during carotid artery occlusion, followed by a dramatic 10 mm Hg drop below baseline after carotid artery unclamping and then a gradual rise of the blood pressure 25 mm Hg above baseline, which peaks in 80 minutes, with a gradual decline to the same blood pressure as in the control subjects 120 minutes after ischemia.
We conclude that striatal catecholamine release correlates with peripheral blood pressure during transient cerebral ischemia and reperfusion. This phenomenon may explain the mechanism of post-carotid endarterectomy hypertension in human beings, and this gerbil model can be used to study its prevention and treatment.
颅内去甲肾上腺素释放与人类颈动脉内膜切除术后高血压有关。为了在更可控的条件下研究这一现象,我们研究了沙鼠脑内儿茶酚胺与血压的关系,沙鼠的脑循环与人类相似。
12只麻醉后的沙鼠接受髂动脉血压监测,并使用立体定向放置在脑纹状体中的儿茶酚胺特异性电极进行体内电化学儿茶酚胺监测。6只沙鼠接受10分钟的双侧颈动脉闭塞(缺血),而6只接受未闭塞的颈动脉解剖(对照)。
对照组在150分钟的观察期内血压和纹状体儿茶酚胺持续逐渐下降。相比之下,缺血沙鼠在缺血期间儿茶酚胺急剧上升,颈动脉夹闭后不久儿茶酚胺显著下降,然后是第二次更大的儿茶酚胺释放,在60分钟达到峰值,并在120分钟逐渐恢复到基线。血压密切跟随儿茶酚胺水平,颈动脉闭塞期间血压比基线急剧上升20 mmHg,颈动脉夹闭后血压比基线急剧下降10 mmHg,然后血压逐渐上升至比基线高25 mmHg,在80分钟达到峰值,缺血后120分钟逐渐下降至与对照组相同的血压。
我们得出结论,在短暂性脑缺血和再灌注期间,纹状体儿茶酚胺释放与外周血压相关。这一现象可能解释了人类颈动脉内膜切除术后高血压的机制,并且这种沙鼠模型可用于研究其预防和治疗。