A canine model of acute hindbrain ischemia and reperfusion

ANIMAL MODELS OF brain stem ischemia are needed for pathophysiological study and evaluation of treatment; few such models are available currently. A new canine model of hindbrain ischemia and reperfusion is introduced in this article. Through an anterior cervical approach, the basilar artery was surgically exposed in 18 dogs. The posterior communicating and superior cerebellar arteries were embolized with cyanoacrylate glue to isolate the posterior circulation from the anterior circulation. Reversible hindbrain ischemia was induced in 14 dogs by the temporary clipping of the vertebral and ventral spinal arteries for various periods (10–30 min), then the clips were removed and reperfusion was achieved for 5 hours. In all 14 dogs, the hindbrain ischemia was confirmed by the decreased perfusion pressure in the basilar artery (<10 mm Hg), the diminished regional cerebral blood flow as measured with a laser Doppler flowmeter at the medulla oblongata (<10 ml/100 g/min), the flattened brain stem auditory evoked potentials, and the increased leakage of Evans blue dye from tissue. These parameters did not change in the four control dogs. The changes in brain stem auditory evoked potentials were closely related to the length of ischemic interval; after 10 minutes of ischemia, reperfusion fully reversed the changes in brain stem auditory evoked potentials, but 20-minute and 30-minute ischemic intervals partially or totally depleted the brain stem auditory evoked potentials. Delayed postischemic hypoperfusion occurred in all five dogs that underwent the 30-minute ischemic interval. The early physiological changes in this model allowed us to estimate the severity of brain stem ischemia and the resulting damage. This model may be useful for studying the effectiveness of brain-protective strategies against brain stem ischemia, particularly in the cases of 20-minute and 30-minute ischemic intervals.