Figure 4
Figure 4. Vascular stasis as monitored in a DSFC model using hBERK1 mice subjected to H/R. Mice were treated with or without TSA for 3 days. After the third TSA dose, flowing venules were selected and studied. Animals were then subjected to H/R. After 1 hour and 4 hours of reoxygenation, the same venules were re-examined for blood flow. There were 5 mice and 251 venules in the TSA-treated group, and 4 mice and 85 venules in the vehicle group. At least 18 venules per mouse were evaluable. Expressed on a per-total venule basis, asterisk (*) shows P = .006 for both at 1 hour and 4 hours of reoxygenation. This demonstrates an antistasis effect of TSA, consistent with that of other hydroxamic acids we previously studied using a different intravital microscopy model.15 Error bars show SE.

Vascular stasis as monitored in a DSFC model using hBERK1 mice subjected to H/R. Mice were treated with or without TSA for 3 days. After the third TSA dose, flowing venules were selected and studied. Animals were then subjected to H/R. After 1 hour and 4 hours of reoxygenation, the same venules were re-examined for blood flow. There were 5 mice and 251 venules in the TSA-treated group, and 4 mice and 85 venules in the vehicle group. At least 18 venules per mouse were evaluable. Expressed on a per-total venule basis, asterisk (*) shows P = .006 for both at 1 hour and 4 hours of reoxygenation. This demonstrates an antistasis effect of TSA, consistent with that of other hydroxamic acids we previously studied using a different intravital microscopy model.15  Error bars show SE.

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