Measurement of muscle microvascular oxygen pressures: compartmentalization of phosphorescent probe

To determine whether the phosphorescent probe Oxyphor R2 (a palladium porphyrin dendrimer) becomes extravasated within normotensive skeletal muscle, R2 perfusion and washout studies were performed using a perfused rat hindlimb preparation.

Phosphorescence signals were monitored in tibialis anterior muscles after 35 min of R2 blood perfusion and across a subsequent washout period that included vasodilation (sodium nitroprusside, SNP, approximately 3 x 10(-2) M).

Two responses were evident: Group 1 (n = 4)--Inflowing blood pressure and vascular conductance remained stable close to initial values and subsequently a marked vasodilation was evident with SNP (vascular conductance; R2 blood perfusion, 0.096 +/- 0.005; washout, pre-SNP, 0.085 +/- 0.005, post-SNP, 0.110 +/- 0.005 mL/min/mmHg, p <.05, for pre- vs. post-SNP). Baseline phosphorescence signals could be monitored up to 99 +/- 36 s post-SNP when the phosphorescence signal disappeared. For these muscles, palladium content was undetectable. Group 2 (n = 3)--Inflowing blood pressure increased 112% and vascular conductance fell approximately 50%. These hindlimbs were unresponsive to SNP, phosphorescence signal was undiminished by washout and SNP, and muscles became edematous.

These results suggest that in normotensive muscle (i.e., Group 1 above), extravasation of phosphorescent probe R2 over 35 min of perfusion is insufficient to yield a detectable phosphorescence signal in skeletal muscle.