Leukocyte capillary plugging in myocardial ischemia and reperfusion in the dog.

Leukocyte capillary plugging in myocardial ischemia and reperfusion in the dog.
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发表时间:
1983-04
期刊:
The American journal of pathology
影响因子:
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通讯作者:
R. Engler;G. Schmid-Schönbein;R. Pavelec
R. Engler;G. Schmid-Schönbein;R. Pavelec
中科院分区:
其他
文献类型:
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作者:
R. Engler;G. Schmid-Schönbein;R. Pavelec

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缺血数小时后,脑、肾、骨骼肌和心脏的血流恢复不完全。无复流现象的机制尚不清楚,血管周围水肿、血小板或红细胞栓塞和间质出血都有牵连。在本研究中提供的证据表明,白细胞截留在毛细血管可能有助于无复流。白细胞是大而硬的细胞,其天然粘附于血管内皮,并且已知其粘附特性在各种条件下改变。因此,11开胸犬进行了研究,左前降支冠状动脉闭塞后1-5小时。以乳酸林格氏液和碳混悬液作为毛细血管通畅性的标志物,在75 mm Hg动脉压下完成再灌注(9只狗)。在非缺血性组织中,98%的毛细血管含有碳,罕见的白细胞和少量红细胞,而闭塞动脉分布的组织是异质的:60%的毛细血管没有碳,高血细胞比容,每个未分支的毛细血管大约有一个白细胞; 40%表现出回流,没有白细胞。毛细血管无碳(无复流)和白细胞留在这些毛细血管中的频率之间的显着相关性表明,白细胞存在于阻塞的毛细血管。此外,在用乳酸盐洗脱后剩余的白细胞的频率是在没有洗脱的正常停止的心肌中的10倍。我们的研究结果表明,进行性白细胞毛细血管堵塞在心肌缺血有助于防止完全恢复毛细血管流量后再灌注。
After several hours of ischemia an incomplete return of blood flow has been reported in brain, kidney, skeletal muscle, and heart. The mechanisms responsible for the no-reflow phenomenon have been unclear, and perivascular edema, platelet or red cell plugs, and interstitial hemorrhage have been implicated. In the present study evidence is provided that leukocyte entrapment in capillaries might contribute to no reflow. Leukocytes are large and stiff cells, which adhere to vascular endothelium naturally and are known to alter in their adherence properties under a variety of conditions. Accordingly, 11 open-chest dogs were studied, 1-5 hours after left anterior descending coronary artery occlusion. Reperfusion (9 dogs) at 75 mm Hg arterial pressure was accomplished with Ringer's lactate and carbon suspension as a marker for capillary patency. In non-ischemic tissue, 98% of the capillaries contained carbon, rare leukocytes, and few erythrocytes, whereas tissue from the distribution of the occluded artery was heterogeneous: 60% of the capillaries had no carbon, high hematocrits, and approximately one leukocyte per unbranched capillary; 40% demonstrated reflow and no leukocytes. A significant correlation between capillaries without carbon (no reflow) and the frequency of leukocytes remaining in these capillaries indicated that leukocytes were present in obstructed capillaries. Furthermore, the frequency of leukocytes remaining after the washout with lactate was ten times greater than in normal arrested heart muscle without washout. Our results suggest that progressive leukocyte capillary plugging during myocardial ischemia contributes to preventing full restoration of capillary flow upon reperfusion.