Fig. 1.
Fig. 1. Representative micrographs of 150-kd FITC-dextran distribution in skull BM of a nonirradiated mouse and an animal 48 hours after irradiation. / (A) In normal BM, the high–molecular-weight plasma marker stays confined to the lumen of BM venules and sinusoids (*). There is no extravasation into extravascular BM cavities (+). (B) Irradiation-induced damage to BM endothelium causes a massive breakdown of endothelial barrier function, leading to the extravasation of FITC-dextran into BM cavities but not into adjacent solid bone tissue. Because of quenching of fluorescence by hemoglobin-rich erythrocytes, larger microvessels now appear darker than the surrounding extravascular compartment. Recordings in both animals were taken under identical conditions using a × 40 objective.

Representative micrographs of 150-kd FITC-dextran distribution in skull BM of a nonirradiated mouse and an animal 48 hours after irradiation.

(A) In normal BM, the high–molecular-weight plasma marker stays confined to the lumen of BM venules and sinusoids (*). There is no extravasation into extravascular BM cavities (+). (B) Irradiation-induced damage to BM endothelium causes a massive breakdown of endothelial barrier function, leading to the extravasation of FITC-dextran into BM cavities but not into adjacent solid bone tissue. Because of quenching of fluorescence by hemoglobin-rich erythrocytes, larger microvessels now appear darker than the surrounding extravascular compartment. Recordings in both animals were taken under identical conditions using a × 40 objective.

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