Hazardous Hyperglisemic Effect of Facial Ischemia Following Subarachnoid Hemorrhage: An Experimental Study
Hyperglycemia has been tried to explain by different mechanisms, but glucose-sensing tongue taste buds-geniculate ganglia-facial nerve-vagal nerve-pancreas web relation has not been adequately investigated.
We aimed to investigate if there is any relationship between the described taste buds network degeneration and blood glucose levels following subarachnoid hemorrhage (SAH).
This study was conducted on 32 rabbits. Blood glucose levels were measured at the beginning, mid-phase, and the end of the experiment. Animals were divided into the groups of control (n = 5), physiologic serum saline (SHAM; n = 5), and subarachnoid hemorrhage with 0.5 cc homolog blood injection into cisterna magna (study; n = 22) three times a week and were sacrificed under general anesthesia after two weeks. The blood glucose level of 113 ± 20 mg/dL was accepted as normal (G-I; n = 11), lower than 80 mg/dl as hypoglycemic (G-II; n = 6), and higher than 149 mg/dl as hyperglycemic (G-III; n = 5). Their neuron densities of geniculate ganglia were examined by stereological methods. The statistical analysis was done between glucose levels/degenerated taste bud/neurons using Kruskal-Wallis and Mann-Whitney U tests. We accepted P > 0.005 as non-significance.
The mean normal blood glucose level was 115 ± 9 mg/dl before surgery. The pre-sacrificed glucose level was 113 ± 8 mg/dL and the neuron density of the geniculate ganglia was 7.421 ± 530/mm3. The degenerated neuron density of geniculate ganglia was 13 ± 4/mm3 in controls 21 ± 7/mm3 in SHAM, 27 ± 7/mm3 in G-I, 21 ± 5/mm3 in G-II, and 112 ± 18/mm3 in G-III groups. The P values of glucose levels-degenerated neuron density of geniculate ganglia between control/G-III was: P < 0.00001; SHAM/G-III: P < 0.0005; GI/GII: P < 0.005.
Glucose sensing tongue taste buds-geniculate ganglia-facial nerve-vagal nerve-pancreas circuitry should be an unexplained web for the regulation of blood glucose level.
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