Ding Yuchuan, Li Jie, Rafols Josè A, Phillis John W, Diaz Fernando G
Department of Neurological Surgery, Wayne State University School of Medicine, Detroit, Mich 48201, USA.
Stroke. 2002 Oct;33(10):2492-8. doi: 10.1161/01.str.0000028237.15541.cc.
In ischemic stroke, the ischemic crisis activates a cascade of events that are potentiated by reperfusion, eventually leading to cell death. The chief aim in this study was to investigate whether our new experimental model for stroke therapy, flushing the ischemic territory with saline before reperfusion, could minimize this damage by (1) reducing the inflammatory reaction and (2) improving regional microcirculation.
Stroke in Sprague-Dawley rats (n=39) was induced by a 2-hour middle cerebral artery occlusion with the use of a novel intraluminal hollow filament. Before 48-hour reperfusion, 20 of the ischemic rats received 7 mL isotonic saline at 23 degrees C or 37 degrees C infused into the ischemic area through the filament. Regional cerebral blood flow in cortex supplied by the right middle cerebral artery was measured by laser-Doppler flowmetry during ischemia and reperfusion. Leukocyte infiltration, microvascular plugging, and infarct volume were compared with the use of hematoxylin and eosin staining. Expression of intercellular adhesion molecule 1 (ICAM-1) was determined by immunocytochemistry. Neurological deficits were evaluated.
After the prereperfusion infusion of saline, significantly (P<0.001) improved cerebral blood flow (105+/-12% of baseline) was obtained up to 48 hours after reperfusion, compared with 45+/-7% at 24 hours and 25+/-3% at 48 hours after reperfusion without local saline infusion. Significant (P<0.001) reductions in leukocyte infiltration (61%), vascular plugging (45%), infarct volume (approximately 65%), and neurological deficits were also produced. ICAM-1 expression in the infarct region was significantly (P<0.05) minimized by 37%.
The reduced brain infarct and neurological deficits may be attributed to adequate reperfusion and ameliorated inflammation induced by local prereperfusion infusion.
在缺血性卒中中，缺血危机激活一系列事件，再灌注会使其加剧，最终导致细胞死亡。本研究的主要目的是探究我们新的卒中治疗实验模型，即在再灌注前用生理盐水冲洗缺血区域，是否能通过以下方式将这种损伤降至最低：（1）减轻炎症反应；（2）改善局部微循环。
使用新型腔内空心纤维，对39只Sprague-Dawley大鼠进行2小时大脑中动脉闭塞诱导卒中。在48小时再灌注前，20只缺血大鼠通过纤维向缺血区域注入7毫升23℃或37℃的等渗盐水。在缺血和再灌注期间，通过激光多普勒血流仪测量右侧大脑中动脉供应的皮质区域脑血流量。使用苏木精和伊红染色比较白细胞浸润、微血管阻塞和梗死体积。通过免疫细胞化学测定细胞间黏附分子1（ICAM-1）的表达。评估神经功能缺损。
再灌注前输注盐水后，与未进行局部盐水输注的大鼠相比，再灌注后48小时脑血流量显著改善（达到基线的105±12%），而再灌注后24小时为45±7%，48小时为25±3%。白细胞浸润（61%）、血管阻塞（约45%）、梗死体积（约65%）和神经功能缺损也显著（P<0.001）减少。梗死区域ICAM-1的表达显著（P<0.05）降低了37%。
脑梗死和神经功能缺损的减少可能归因于局部再灌注前输注所诱导的充分再灌注和炎症改善。
