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Background Autonomous innervations of the lungs are maintained by cervical sympathetic and vagal nerves. Sympathetic overactivity-induced neurogenic pulmonary edema (NPE) is known as a serious complication of subarachnoid hemorrhage, but the rational neuronal mechanism of that overactivity has not yet been clarified fully. The aim of this study was to examine whether there is a relationship between vagal nerve ischemia related sympathetic overactivity and neurogenic pulmonary edema in subarachnoid hemorrhage. Methods This study was conducted on 27 rabbits. A control group was formed of 5 animals, a sham group of 7 to which saline was administered, and a study group of 15 animals that were injected with homologous arterial blood into the cisterna magna. Electrocardiography and respiratory rhythm parameters were monitored for 3 weeks and the animals were then decapitated. Statistical analysis was made of the numbers of degenerated axons in the pulmonary branches of the vagal nerves, the neuron density of stellate ganglions and the vasospasm index of the pulmonary arteries. Results In the control group, the normal respiration rate was 34 ± 6 bpm, total axon number was 1600 ± 270/mm 2 , degenerated axon number was 10 ± 3/mm 2 , and vasospasm index was 1.34 ± 0.25. The sham group values were 30 ± 3 bpm, 163 ± 47/mm 2 , and 1.95 ± 0.45 and the study group values were 45 ± 8 bpm, 530 ± 92/mm 2 , and 2.76 ± 0.83. The mean stellate ganglion neuron density was evaluated as 8.112 ± 1.230/mm 3 in all animals, as 7.420 ± 4.10/mm 3 in animals with slight NPE, and as 12.512 ± 1.236/mm 3 in animals that developed severe NPE. Conclusion High neuron density of stellate ganglion may have important roots in sympathetic overactivity-related NPE development in subarachnoid hemorrhage.

Objective The Adamkiewicz artery (AKA) supplies pudendal nerve roots and conus medullaris. The aim of this study was to elucidate if there is any relationship between neurodegenerative changes of the Onuf nucleus (ON)–pudendal nerve ganglia complex secondary to vasospasm of the AKA after spinal subarachnoid hemorrhage (SAH). Methods This study was conducted on 22 rabbits, which were randomly divided into 3 groups: control (n = 5), sham (n = 5), and spinal SAH (n = 12). Experimental spinal SAH was induced at the L2 level. After 2 weeks, the ON–pudendal nerve ganglia complex and AKA were examined histopathologically. Bladder volume values were estimated, and results were analyzed statistically. Results Two animals died within the first week of experiment. Histopathologically, severe vasospasm of the AKA and neuronal degeneration and neuronal apoptosis were observed in the ON–pudendal nerve ganglia complex in 5 animals of the SAH group. The mean volume of the imaginary AKA, mean bladder volumes, and degenerated neuron densities of ON and pudendal nerve ganglia were estimated. We found that vasospasm of the AKA led to numerous neuron degenerations in ON and pudendal ganglia and consequently urinary retention (P Conclusions ON–pudendal nerve ganglia complex degeneration secondary to vasospasm of the AKA may be a cause of urinary retention after spinal SAH.

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 Acute hydrocephalus (ventricular enlargement within 72 hours) is a common complication in patients with aneurysmal subarachnoid hemorrhage (SAH). Cerebrospinal fluid (CSF) secretion may be increased in the early phases of SAH, but it has not been proved definitively. We studied the histologic features of choroid plexus (CP) in the early and late phases of SAH. Methods This study was conducted on 20 rabbits, with 5 rabbits in the control group, 5 rabbits in the sham group, and 10 rabbits in the SAH group. In the SAH group, five of the animals were decapitated after 2 days of cisternal blood injections, and the other five animals were decapitated after 14 days of injections. The CP of lateral ventricles were obtained from coronary sections of brains at the level of the temporal horns of the lateral ventricles. Sections were stained with hematoxylin and eosin and Masson trichrome for SAH-related damage and examined stereologically to discern water-filled vesicles, which were counted. Sections were compared statistically. Results The mean numbers of water vesicles were different after SAH between the early decapitated group (group III) and the late decapitated group (group IV). The mean numbers of water vesicles were 2.80 (±0.05) in the control group (group I), 2.76 (±0.02) in the sham group (group II), 14.68 (±0.06) in the early decapitated group (group III), and 4.78 (±0.13) in the late decapitated group (group IV). Total number of fluid-filled vesicles of CP was also assessed stereologically; the total numbers were 840 (±16) in group I, 828 (±7) in group II, 4404 (±19) in group III, and 1434 (±41) in group IV. The numbers of water-filled cisterns were significantly increased in the early phases of SAH ( P Conclusions In SAH with aneurysm rupture, increased CSF secretion seems to be triggered by hemorrhage in the early phase, but it is not possible in the late phase because of CP degeneration. In the early phase of hemorrhage, CSF secretion may be stimulated by the irritant receptor glossopharyngeal and vagal nerve endings, which innervate the healthy CP epithelium and arteries. Our findings may be accepted as being causative. It is likewise possible that CSF blockage per se leads to hydrocephalus, and the morphologic changes are sequelae that occur later in the course of disease. This is the first study to show the water vesicles of CP as a causative factor in the development of acute hydrocephalus after SAH.

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.