B. Friesenecker et al., CAPILLARY PERFUSION DURING ISCHEMIA-REPERFUSION IN SUBCUTANEOUS CONNECTIVE-TISSUE AND SKIN MUSCLE, American journal of physiology. Heart and circulatory physiology, 36(6), 1994, pp. 80002204-80002212
Ischemia-reperfusion injury was investigated in terms of functional ca
pillary density (FCD), capillary red blood cell velocity (cRBCv), and
arteriolar and venular diameter after 4-h ischemia in the unanesthetiz
ed hamster skin-fold preparation. Animals in group 1 were studied by t
ransillumination. Group 2 received a bolus injection of fluorescein is
othiocyanate (FITC)-dextran (mol wt 150,000) and was studied by transi
llumination (zone 1) and epi-illumination (zone 2). In group 1, FCD de
creased after ischemia (92% of baseline, 30 min), returning to control
up to 24 h. cRBCv increased after reperfusion, being 175% of baseline
at 24 h. Arterioles and venules dilated for 24 h after reperfusion. I
n group 2/zone 2, FCD progressively decreased to 11% of control, arter
iolar dilation was inhibited, and cRBCv increased 30 min and 2 h after
reperfusion. Tissue perfusion index (FCD x cRBCv) increased 158% in g
roup 1 at 24 h, did not change in group 2/zone 1, and was 9% of contro
l at 24 h in group 2/zone 2 (P less than or equal to 0.05). We conclud
e that increased perfusion is a normal reaction to ischemia-reperfusio
n injury in this model, and previously observed capillary no reflow is
due to FITC-dextran phototoxicity.