New Evidence for Causal Central Mechanism of Hyperglycemia in Subarachnoid Hemorrhage Secondary to Ischemic Degenerative Disruption of Circuitry Among Insular Cortex, Nodose Ganglion, and Pancreas: Experimental Study.

INTRODUCTION

Although hyperglycemia is a serious complication of subarachnoid hemorrhage, its pathophysiologic mechanism based on neural circuitry has not been known.

MATERIALS AND

METHODS

Twenty-five rabbits were divided into 4 groups, with 5 in the control group. The SHAM and study groups received 1 mL saline and 1 mL autologous arterial blood into the sylvian cisterna, respectively. Blood glucose values (BGVs) of all animals were recorded 3 times weekly. After 2 weeks, animals were decapitated. BGVs, the number of normal and degenerated neuron densities (DNDs) of insular cortex (IC), and nodose ganglia, degenerated islands of Reil's surfaces values, were estimated by stereologically and analyzed statistically.

RESULTS

The mean blood glucose values were measured as 101 ± 10 mg/dL in the control group (n = 5), 114 ± 11 mg/dL in the SHAM group (n = 5), and 137 ± 12 mg/dL in the subarachnoid hemorrhage (SAH) group (n = 15). The DND of the nodose ganglion was 10 ± 3/mm3 in the control group, while it was 45 ± 7/mm3 in the SHAM group and 1688 ± 191/mm3 in the SAH group. The DND of the IC was 65 ± 12/mm3 in the control group, 689 ± 112/mm3 in the SHAM group, and 3709 ± 643/mm3 in the SAH group. In addition, the proportion of degenerated surface areas in the islet of Langerhans was 0.3% in the control group, 6% in the SHAM group, and 28% in the SAH group.

CONCLUSION

There is an important linear relationship among the blood glucose levels, DND of the IC, and nodose ganglia and degenerated surface areas of IL following experimentally induced sylvian SAH.