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Stroke. 1991;22:1276-1283

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Stroke, Vol 22, 1276-1283, Copyright © 1991 by American Heart Association


ARTICLES

Polymorphonuclear leukocytes occlude capillaries following middle cerebral artery occlusion and reperfusion in baboons

GJ del Zoppo, GW Schmid-Schonbein, E Mori, BR Copeland and CM Chang
Department of Molecular and Experimental Medicine, Scripps Clinic and Research Foundation, La Jolla, Calif 92037.

BACKGROUND AND PURPOSE: Microvascular perfusion defects may accompany sustained occlusion and subsequent reperfusion of the middle cerebral artery; however, the nature of such "no-reflow" defects remains unclear. METHODS: In the absence of antithrombotic pretreatment, we documented lenticulostriatal microvascular flow integrity following 3- hour middle cerebral artery occlusion and 1-hour reperfusion in a baboon occlusion/reperfusion model by two methods identifying 1) microvascular occlusion and 2) microvascular patency. RESULTS: Microvascular "no-reflow" involved capillaries (vessels of 4.0-7.5 microns diameter) of the lenticulostriatal territory. Capillary reflow included 27-39% of all capaillaries in two subjects, indicating a significant reduction of perfusion from normal (2p = 0.045). In identical experimental preparations, single polymorphonuclear leukocytes completely occluded 4.7% of microvessels of capillary diameter in randomly selected fields, partially occluded 3.5% of postcapillary venules, and occluded 40% (four of 10) of capillaries in linear reconstruction along a 110 microns length. Circumferential contact between polymorphonuclear leukocytes and the luminal endothelial cell membranes was documented, with an intrecellular gap of, at most, 160 nm. Fibrin was found with degranulated platelets when the latter were associated with granulocytes, but not with polymorphonuclear leukocytes alone. CONCLUSIONS: The finding of capillary-obstructing polymorphonuclear leukocytes in the microvascular bed following middle cerebral artery reperfusion in focal ischemia in this model satisfies an essential requirement for postulating their role in early microvascular injury and the "no-reflow" phenomenon.


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Ann. Thorac. Surg.Home page
B. K. Siesjo, Q. Zhao, K. Pahlmark, P. Siesjo, K.-i. Katsura, and J. Folbergrova
Glutamate, Calcium, and Free Radicals as Mediators of Ischemic Brain Damage
Ann. Thorac. Surg., May 1, 1995; 59(5): 1316 - 1320.
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StrokeHome page
J. H. Garcia, S. Wagner, K.-F. Liu, and X.-j. Hu
Neurological Deficit and Extent of Neuronal Necrosis Attributable to Middle Cerebral Artery Occlusion in Rats : Statistical Validation
Stroke, April 1, 1995; 26(4): 627 - 635.
[Abstract] [Full Text]


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StrokeHome page
Y. Yamasaki, N. Matsuura, H. Shozuhara, H. Onodera, Y. Itoyama, and K. Kogure
Interleukin-1 as a Pathogenetic Mediator of Ischemic Brain Damage in Rats
Stroke, April 1, 1995; 26(4): 676 - 681.
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StrokeHome page
Y. Yamasaki, Y. Matsuo, N. Matsuura, H. Onodera, Y. Itoyama, and K. Kogure
Transient Increase of Cytokine-Induced Neutrophil Chemoattractant, a Member of the Interleukin-8 Family, in Ischemic Brain Areas After Focal Ischemia in Rats
Stroke, February 1, 1995; 26(2): 318 - 323.
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Circ. Res.Home page
K. Shen, F. A. DeLano, B. W. Zweifach, and G. W. Schmid-Schonbein
Circulating Leukocyte Counts, Activation, and Degranulation in Dahl Hypertensive Rats
Circ. Res., February 1, 1995; 76(2): 276 - 283.
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ANGIOLOGYHome page
G. W. Schmid-Schonbein
The Damaging Potential of Leukocyte Activation in the Microcirculation
Angiology, January 1, 1993; 44(1): 45 - 56.
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