Figure 3
Figure 3. Leukocyte recruitment by platelet thrombi in injured arteries. (A-D) C57Bl/6 mice were administered an anti–Gr-1 Ab and DiOC6 prior to needle injury of arteries. Subsequent leukocyte thrombus interactions were monitored by DIC and fluorescence microscopy. The number of (A) stably adherent leukocytes and (C) migrating leukocytes to the site of vascular needle injury were quantified in sham-operated C57Bl/6 mice (Control), and mice subjected to IR injury (IR) (mean ± SEM; Control group: n = 7 mice with 13 injuries; IR group: n = 8 mice with 14 injuries). (B) Representative DIC images of thrombi induced by needle injury in sham-operated mice (Control) or mice after IR injury (IR). Note the (B) significant leukocyte recruitment (pseudo-colored green) and (D) migration (Gr-1 Ab, green) to thrombi after IR injury. *P < .05; ***P < .001.

Leukocyte recruitment by platelet thrombi in injured arteries. (A-D) C57Bl/6 mice were administered an anti–Gr-1 Ab and DiOC6 prior to needle injury of arteries. Subsequent leukocyte thrombus interactions were monitored by DIC and fluorescence microscopy. The number of (A) stably adherent leukocytes and (C) migrating leukocytes to the site of vascular needle injury were quantified in sham-operated C57Bl/6 mice (Control), and mice subjected to IR injury (IR) (mean ± SEM; Control group: n = 7 mice with 13 injuries; IR group: n = 8 mice with 14 injuries). (B) Representative DIC images of thrombi induced by needle injury in sham-operated mice (Control) or mice after IR injury (IR). Note the (B) significant leukocyte recruitment (pseudo-colored green) and (D) migration (Gr-1 Ab, green) to thrombi after IR injury. *P < .05; ***P < .001.

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