An improved three-vessel occlusion model of global cerebral ischemia in rats

- A new 3VO model of global cerebral ischemia in rats is invented.
- A. carotis communis sin., tr. brachiocephalicus and a. subclavia sinistra occlusion, excluding pneumothorax.
- The development of stable neurological deficits is demonstrated during the post-ischemic period.
- Global cerebral ischemia induces a decreasing of the numerical density of neurons in hippocampal zone CA1.

We developed an improved three-vessel occlusion model of global cerebral ischemia in rats. This method consists in cessation of cerebral blood flow by accessing a. carotis communis sinistra through the ventral surface of the neck as well as tr. brachiocephalicus and a. subclavia sinistra through the first intercostal space, bypassing the pleural cavity and excluding pneumothorax. After the occlusion of the vessels that resulted in interruption of their blood flow, according to laser-Doppler flowmetry, there was a sharp decline in local cerebral blood flow in the visual cortex to 4 ± 1% of the initial level. After restoring the level of local cerebral blood flow at the 5th minute, 10th minute, 20th minute and 24th hour of reperfusion, the levels of local cerebral blood flow were 51 ± 7%, 41 ± 5%, 35 ± 8% and 54 ± 9% of the initial level, respectively. Histo-quantitative analysis of changes in neurons of the hippocampus of rats showed that after ischemic injury, the numerical density of neurons in hippocampal zone CA1 in the observed 1 mm2 region decreased by 29%, 22%, and 35%, respectively, compared to sham-operated animals (p < 0.05). By the first day after global cerebral ischemia, the experimental group had shown a mean neurological deficit score equal to 7.5 ± 1.0 and 7.9 ± 0.7 points, followed by a decrease up to score 6.5 ± 1.1 and 5.9 ± 0.7 on the third day, 4.6 ± 0.8 and 4.7 ± 0.5 on the fifth day (on chloral hydrate and propofol anesthesia correspondently).

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