DECREASED MICROVASCULAR PERFUSION IN THE RABBIT EAR AFTER 6 HOURS OF ISCHEMIA

The cellular injury produced by reperfusion of ischemic tissue with ox ygen-rich blood has been studied in numerous tissues but has not been investigated extensively in thermoregulatory tissue. This study was de signed (a) to compare 4 and 6 hours of ischemia to document the eviden ce of impaired capillary perfusion after resumption of blood flow (rep erfusion injury) in a thermoregulatory end organ (the rabbit ear), and (b) to examine, with use of vital capillaroscopy (VC) and laser Doppl er flowmetry (LDF), the altered microvascular blood flow in the rabbit ear after ischemia and reperfusion. One ear from each of five rabbits underwent warm ischemia for 4 hours. VC showed no deficits of capilla ry perfusion in these ears after reperfusion; LDF measurements in both ears also demonstrated no significant difference between control and reperfusion blood flow. One ear from each of eight additional rabbits underwent 6 hours of warm ischemia. LDF values were significantly redu ced in the ischemic ear after reperfusion as compared with baseline me asurements for that ear and as compared with the control ear. VC showe d arrested perfusion and static plasma gaps within three to five capil laries per high-power field (an area of 300 x 500 mu m) in the ischemi c ear and good perfusion of all vessels in the contralateral control e ar. This evidence of reperfusion injury in a thermoregulatory end orga n may help to explain the poor functional result that often occurs aft er replantation of an amputated digit.