Ischemic preconditioning attenuates hypoperfusion after retinal ischemia in rats

Retinal blood flow (RBF) was measured in rats to test the hypotheses that hypoperfusion follows severe ischemia in the retina and that ischemic preconditioning (IPC) attenuates this change in blood flow.

Male Sprague-Dawley rats were anesthetized with halothane and mechanically ventilated by tracheostomy to maintain normocarbia and normoxia. Retinal ischemia was induced for 0, 5, 30, 60, 75, or 90 minutes. RBF was measured 60 and 150 minutes after the end of ischemia using the radioactive microsphere blood flow method, and electroretinography was performed during the first 120 minutes after ischemia to quantitate the extent of functional recovery. Additional groups received IPC (5 minutes of ischemia) 24 hours before 30, 60, or 75 minutes of ischemia.

Control (0 minutes' ischemia) RBF was 22+/-3 ml/100 g per minute (mean +/- SE). At 60 minutes after 5, 30, 60, 75, or 90 minutes of ischemia, RBF was 15+/-2 (NS), 11+/-1, 8+/-2, 8+/-1, and 10+/-1 ml/100 g per minute, respectively (significance, P<0.05 versus control). At 150 minutes after 5, 30, 60, 75, or 90 minutes of ischemia, RBF was 18+/-3 (NS), 13+/-1, 12+/-3, 12+/-2, and 11+/-1 ml/100 g per minute respectively (significance, p<0.05 versus control). With prior IPC, RBF after 30 and 60 minutes of ischemia was 21+/-1 and 19+/-3 ml/100 g per minute (both NS compared with control; P<0.05 compared with 30 or 60 minutes of ischemia without IPC). When ischemia was 75 minutes in duration, IPC did not prevent postischemic hypoperfusion. The extent of recovery of the electroretinogram b wave was inversely related to the length of ischemia.

Postischemic hypoperfusion is present in the rat retina 60 minutes after ischemia, does not resolve by 150 minutes after ischemia, and is attenuated by IPC when ischemia is 60 minutes or less in duration. Maintenance of postischemic perfusion in the retina may be one of the mechanisms involved in the neuroprotection afforded by IPC.