Abstract
Objective: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. Methods: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, ∼3 × 10−2M). Results: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 ∼50%. These hindlimbs were unresponsive to SNP, phosphorescence signal was undiminished by washout and SNP, and muscles became edematous. Conclusions: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. Microcirculation(2004) 11,317–326. doi:10.1080/10739680490437487