Fig. 1.
Fig. 1. Example of the effect of PFE on hemodynamic parameters in a PAF-treated mesocecum vasculature after SS RBC-induced obstruction. / A bolus of deoxygenated SS RBCs (Hct 30 in autologous plasma, 0.25 mL; HbO2 < 3%), delivered at an arterial pressure (Pa) of 60 mm Hg, caused a transient rise in Pa and venous outflow (Fv). After the passage of bolus, trapped SS RBCs resulted in only partial recovery of PRU compared with pre-SS baseline value (11.0 vs 8.6 mm Hg/mL per min/g). Next, the infusion of oxygenated Ringer–albumin solution (0.3 mL) caused a slight decrease in PRU from 11.0 to 10.3 mm Hg/mL per min/g. In contrast, a subsequent infusion of oxygenated PFE was followed by recovery PRU to the baseline (pre-SS) value. The PRU decrease was accompanied by complete dislodgement of trapped sickled RBCs from some partially obstructed vessels.

Example of the effect of PFE on hemodynamic parameters in a PAF-treated mesocecum vasculature after SS RBC-induced obstruction.

A bolus of deoxygenated SS RBCs (Hct 30 in autologous plasma, 0.25 mL; HbO2 < 3%), delivered at an arterial pressure (Pa) of 60 mm Hg, caused a transient rise in Pa and venous outflow (Fv). After the passage of bolus, trapped SS RBCs resulted in only partial recovery of PRU compared with pre-SS baseline value (11.0 vs 8.6 mm Hg/mL per min/g). Next, the infusion of oxygenated Ringer–albumin solution (0.3 mL) caused a slight decrease in PRU from 11.0 to 10.3 mm Hg/mL per min/g. In contrast, a subsequent infusion of oxygenated PFE was followed by recovery PRU to the baseline (pre-SS) value. The PRU decrease was accompanied by complete dislodgement of trapped sickled RBCs from some partially obstructed vessels.

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