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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/mm 3 in the control group, while it was 45 ± 7/mm 3 in the SHAM group and 1688 ± 191/mm 3 in the SAH group. The DND of the IC was 65 ± 12/mm 3 in the control group, 689 ± 112/mm 3 in the SHAM group, and 3709 ± 643/mm 3 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.

Objective The chemoreceptor network, consisting of the glossopharyngeal nerve and carotid body (GPN-CB), is essential for the regulation of blood pH. Its ischemic insuts following subarachnoid hemorrhage (SAH)which may contribute to develop acidosis has not been investigated. Materials and Methods Twent-three hybrid rabbits were used.They divided into three groups; Five (n=5) as control group, five (n=5) as SHAM group, the remaining 13 (n=13) as study group. 1cc serum saline, 1cc autolog arterial blood into the cisterna magna were injected; in SHAM and study group, respectively. Blood pH values of all annimals were recorded. After two weeks, animal were decapitated. The number of normal and degenerated neuron density ofCBs were counted by stereological methods,analysed statistically. Results Two of 13 rabbits died within the second week. The mean blood pH values were measured as 7.35±0.07 in control, 7.33±0.06 in SHAM, 7.29±0.05 in rabbits with slight acidisis (n=6) and 7.23±0.02 in in rabbits with prominent acidosis. In control groups, the average normal neuronal density of the CB was 6432±790/mm 3 and degenerated neuron density was 11±3/mm 3 while the degenerated neuronal density in CB was 35±8/mm 3 in SHAM group, 1034±112/mm 3 in slight acidis developed group (n=6; p 3 in the prominent acidosis developed animals (n=8; p 3 Conclusion Inverse relationship between neurodegeneration in the CB and PH values secondary to the disruption ofGPN-CBnetwork following SAH was foundwhich may contribute to develop acidosis.

Background Hydrocephalus is a serious complication of subarachnoid hemorrhage (SAH). Obstruction of the cerebral aqueduct may cause hydrocephalus after SAH. Although various etiologic theories have been put forward, choroidal artery vasospasm–related ependymal desquamation and subependymal basal membrane rupture as mechanisms of aqueductal stenosis have not been suggested in the literature. Methods This study was conducted on 26 hybrid rabbits. Five rabbits were placed in a control group, 5 were placed in a sham group, and the remaining rabbits ( n = 16) were placed in the SAH group. In the first 2 weeks, 5 animals in the SAH group died. The other 21 animals were decapitated after the 4-week follow-up period. Choroidal artery changes resulting from vasospasm, aqueduct volume, ependymal cell density, and Evans index values of brain ventricles were obtained and compared statistically. Results Mean aqueduct volume was 1.137 mm 3 ± 0.096, normal ependymal cell density was 4560/mm 2 ± 745, and Evans index was 0.32 ± 0.05 in control animals ( n = 5); these values were 1.247 mm 3 ± 0.112, 3568/mm 2 ± 612, and 0.34 ± 0.15 in sham animals ( n = 5); 1.676 mm 3 ± 0.123, 2923/mm 2 ± 591, and 0.43 ± 0.09 in animals without aqueductal stenosis ( n = 5); and 0.650 mm 3 ± 0.011, 1234/mm 2 ± 498, and 0.60 ± 0.18 in animals with severe aqueductal stenosis ( n = 6). The choroidal vasospasm index values were 1.160 ± 0.040 in the control group, 1.150 ± 0.175 in the sham group, 1.760 ± 0.125 in the nonstenotic group, and 2.262 ± 0.160 in the stenotic group. Aqueduct volumes, ependymal cell densities, Evans index, and choroidal artery vasospasm index values were statistically significantly different between groups ( P Conclusions Ependymal cell desquamation and subependymal basal membrane destruction related to choroidal artery vasospasm may lead to aqueductal stenosis and hydrocephalus after SAH.