Fig. 4.
Fig. 4. Accumulation of fibrinogen and platelets during I/R in vivo. Alexa 488-conjugated human fibrinogen (17 mg/kg) was administered intravenously 30 minutes before the induction of ischemia (left column). Rhodamin-labeled platelets were visualized in identical arterioles and venules using a different filter set (right column; see Materials and Methods). In wild-type animals (A,B), fibrinogen is bound unevenly to the vascular wall of arterioles and venules in the postischemic microvasculature. Areas with large amounts of fibrinogen (A, large arrow) can be seen besides regions without detectable fibrinogen deposition (A, small arrow). The accumulation of large amounts of fibrinogen colocalizes with platelet adhesion (B, arrowhead). In mice lacking ICAM-1 (C,D), the I/R-induced accumulation of fibrinogen and platelets is attenuated. Monitor magnification, 450×.

Accumulation of fibrinogen and platelets during I/R in vivo. Alexa 488-conjugated human fibrinogen (17 mg/kg) was administered intravenously 30 minutes before the induction of ischemia (left column). Rhodamin-labeled platelets were visualized in identical arterioles and venules using a different filter set (right column; see Materials and Methods). In wild-type animals (A,B), fibrinogen is bound unevenly to the vascular wall of arterioles and venules in the postischemic microvasculature. Areas with large amounts of fibrinogen (A, large arrow) can be seen besides regions without detectable fibrinogen deposition (A, small arrow). The accumulation of large amounts of fibrinogen colocalizes with platelet adhesion (B, arrowhead). In mice lacking ICAM-1 (C,D), the I/R-induced accumulation of fibrinogen and platelets is attenuated. Monitor magnification, 450×.

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