Figure 1
Figure 1. Platelet thrombi induce leukocyte recruitment and intravascular migration following intestinal IR injury. Spontaneous thrombus formation and leukocyte interactions in the mesenteric vasculature were examined after IR injury by using histology and real-time DIC, epifluorescence, and confocal microscopy. (A) The percentage of microvascular vessels with either partially or fully occlusive thrombi was quantified by using Carstairs staining of histologic sections (mean ± standard error of the mean [SEM]; Control group: n = 3 mice and 24 sections with 380 vessels counted; IR group: n = 5 mice and 40 histologic sections with 893 vessels counted). (B-C) Representative histologic sections of the small bowel vasculature demonstrating (B) occlusive fibrin-rich thrombi (dark red) and thrombi containing both platelets (*) and (C) fibrin with numerous leukocytes within the thrombus body after IR injury. (D) Representative DIC and fluorescence images illustrating polarized leukocytes (Gr-1 Ab, green) within the spontaneous thrombus body (DIC, demarcated) in an IR-injured mesenteric vein. (E) Representative DIC image and corresponding three-dimensional reconstruction of spontaneous platelet rich thrombi (GPIbβ Ab, blue) within the bowel wall microvasculature associated with leukocyte accumulation (Gr-1 Ab, red) after IR injury. (F) Representative images depicting polarized and spread leukocytes (Gr-1 Ab, green) in the presence [ii) Platelets] but not absence [i) Endothelium] of adherent platelets on the endothelium after IR injury. (G) The number of polarized/spread leukocytes per square millimeter on the surface of endothelium or spontaneous platelet thrombi following IR injury. *P < .05;***P < .001.

Platelet thrombi induce leukocyte recruitment and intravascular migration following intestinal IR injury. Spontaneous thrombus formation and leukocyte interactions in the mesenteric vasculature were examined after IR injury by using histology and real-time DIC, epifluorescence, and confocal microscopy. (A) The percentage of microvascular vessels with either partially or fully occlusive thrombi was quantified by using Carstairs staining of histologic sections (mean ± standard error of the mean [SEM]; Control group: n = 3 mice and 24 sections with 380 vessels counted; IR group: n = 5 mice and 40 histologic sections with 893 vessels counted). (B-C) Representative histologic sections of the small bowel vasculature demonstrating (B) occlusive fibrin-rich thrombi (dark red) and thrombi containing both platelets (*) and (C) fibrin with numerous leukocytes within the thrombus body after IR injury. (D) Representative DIC and fluorescence images illustrating polarized leukocytes (Gr-1 Ab, green) within the spontaneous thrombus body (DIC, demarcated) in an IR-injured mesenteric vein. (E) Representative DIC image and corresponding three-dimensional reconstruction of spontaneous platelet rich thrombi (GPIbβ Ab, blue) within the bowel wall microvasculature associated with leukocyte accumulation (Gr-1 Ab, red) after IR injury. (F) Representative images depicting polarized and spread leukocytes (Gr-1 Ab, green) in the presence [ii) Platelets] but not absence [i) Endothelium] of adherent platelets on the endothelium after IR injury. (G) The number of polarized/spread leukocytes per square millimeter on the surface of endothelium or spontaneous platelet thrombi following IR injury. *P < .05;***P < .001.

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