Influence of CD73 on PMN accumulation during hypoxia in vivo: partial rescue with exogenous 5′-nucleotidase. (A) cd73-null (▪) or wild-type littermate (□) mice were subjected to either normoxia (room air) or normobaric hypoxia (8% O₂ and 92% N₂) for 4 hours, and the indicated organs (colon, Co; lung, Lu; liver, Li; or kidney, Ki) were assessed for PMN accumulation by myeloperoxidase activity (^*P < .025 compared with normoxia; #P < .025 compared with wild-type). (B) Representative low-power (top, × 100 total magnification) and high-power (bottom, × 400 total magnification) lung section from cd73-null animal subjected to hypoxia. Note inflammatory infiltration in the perivascular region of large vessels. (C) cd73-null (▪) or wild-type littermate (□) mice were administered purified 5′-nucleotidase (500 U/kg intraperitoneally [ip]), subjected to either normoxia (room air) or normobaric hypoxia (8% O₂ and 92% N₂) for 4 hours, and the indicated organs (colon, Co; lung, Lu; liver, Li; or kidney, Ki) were assessed for PMN accumulation by myeloperoxidase activity (^*P < .025 compared with normoxia). Data are presented as mean ± SEM.