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Öğe Important interaction between urethral taste bud-like structures and Onuf's nucleus following spinal subarachnoid hemorrhage: A hypothesis for the mechanism of dysorgasmia(Elsevier Espana Slu, 2022) Caglar, Ozgur; Aydin, Mehmet Dumlu; Aydin, Nazan; Ahiskalioglu, Ali; Kanat, Ayhan; Aslan, Remzi; Onder, ArifBackground: We previously postulated that orgasmic sensation may occur through recently discovered genital taste bud-like structures. The interaction between the pudendal nerve and Onuf's nucleus may be important for developing orgasmic information. The study aims to investigate whether ischemic damage to Onuf's nucleus-pudendal network following spinal subarachnoid hemorrhage (SAH) causes taste bud degeneration or not. Methods: The study was conducted on 22 fertile male rabbits who were divided into three groups: control (GI; n = 5), SHAM (GII; n = 5) and study (GIII; n = 12). Isotonic solution, .7 cm(3), for the SHAM, and .7 cm(3) homologous blood was injected into spinal subarachnoid spaces at S2 level of the study group. Two weeks later, Onuf's nucleus, pudendal ganglia and the taste bud-like structures of the penile urethra were examined histopathologically. Degenerated neuron densities of Onuf's nucleus, pudendal ganglia and atrophic taste bud-like structures were estimated per mm(3) and the results analyzed statistically. Results: The mean degenerated neuron densities of taste bud-like structures, Onuf's nucleusand pudendal ganglia were estimated as 2 +/- 1/mm(3), 5 +/- 1/mm(3), 6 +/- 2/mm(3) in GI; 12 +/- 4/mm(3), 35 +/- 9/mm(3), 188 +/- 31/mm(3), in GII and 41 +/- 8/mm(3), 215 +/- 37/mm(3), 1321 +/- 78/mm(3), in GIII. Spinal SAH induced neurodegeneration in Onuf's nucleus, pudendal ganglia and taste budatrophy was significantly different between GI/GII (p <.005); GII/GIII (p <.0005) and GI/GIII(p<.0001). Conclusion: Ischemic neuronal degenerations of Onuf's nucleus and pudendal ganglia following spinal SAH lead to genital taste bud-like structure atrophy. This mechanism may be responsible for sexual anhedonia and sterility in cases with spinal cord injury, which has not been documented so far. More studies are needed. (C) 2020 Asociacion Espanola de Andrologia, Medicina Sexual y Reproductiva. Published by Elsevier Espana, S.L.U. All rights reserved.Öğe The relationship between the neuron density of the trigeminal ganglion and the posterior communicating artery vasospasm in subarachnoid hemorrhage an experimental study(Neurosurgery Quarterly, 2012) Aydın, Mehmet Dumlu; Serarslan, Yurdal; Gündoğdu, Cemal; Aydın, Nazan; Aygül, Recep; Dündar, Dilcan Kotan; Hızır, Ulvi; Önder, Arif; Kanat, AyhanObjective: Cerebral arteries innervated by several systems contribute to the control of cerebral blood flow. Sensory fibers of the trigeminal nerve have a vasodilatory effect on the basilar artery. Subarachnoid hemorrhage (SAH) causes severe cerebral vasospasm by various neurochemical mechanisms. We examined possible relationships between the neuron density of the trigeminal ganglion and the severity of basilar artery vasospasm in SAH. Methods: In this study, 28 rabbits were used. The animals were randomly divided into 3 groups: SAH (n=18), serum physiologic (n=5) and control (n=5) groups. Experimental SAH was induced by injecting homologous blood into the cisterna magna. After 20 days, the basilar arteries and trigeminal ganglions were examined histopathologically. Basilar artery volumes and the neuron density of the ophthalmic divisions of the trigeminal ganglions were estimated stereologically, and the results were statistically analyzed. Results: The mean basilar artery volume was 4.15±0.19 mm3 and the mean neuronal density of the trigeminal ganglion was 6500±750/mm3 for the control group. These values were 4.05±0.29 mm3 and 6400±584/mm3 for the serum physiologic group, 3.80±0.35 mm3 and 4600±300/mm3 for living animals in the SAH group, and 2.26±0.29 mm3 and 2950±618/mm3 for dead animals in SAH group, respectively. A linear relationship was found between the neuronal density of the trigeminal ganglion and basilar artery volumes. Conclusions: The neuron density of the trigeminal ganglion may be an important factor in the regulation of basilar artery volume and for the continuation of cerebral blood flow. The low neuron density of the trigeminal ganglion may be involved in the pathogenesis of severe basilar artery vasospasm induced by SAH. The Role of Trigeminal Ganglion Neuron Density in the Prevention of Subarachnoid Hemorrhage-induced Basilar Artery Vasospasm: An Experimental Study. Available from: https://www.researchgate.net/publication/232176472_The_Role_of_Trigeminal_Ganglion_Neuron_Density_in_the_Prevention_of_Subarachnoid_Hemorrhage-induced_Basilar_Artery_Vasospasm_An_Experimental_Study [accessed Jul 7, 2017].Öğe Spinal arachnoiditis and axonal degeneration of the spinal nevre roots due to Ischemia induced by vasospasm an experimental study(Journal of Neurosurgical Sciences-Turkish, 2009) Önder, Arif; Serarslan, Yurdal; Aydın, Mehmet Dumlu; Kanat, Ayhan; Gürsan, Nesrin; Yolaş, CoşkunVarious reasons have been ascribed to arachnoiditis development, among which subarachnoid hemorrhage (SAH) may be an important factor in this process. In this experimental study, we investigated the effect of SAH on histopathological findings. The volumetric changes of the radicular arteries and the density of spinal nerve root axons of a SAH model on C4 roots in rabbits were measured. Materials and Methods: In this study, 18 rabbits were used. The animals were randomly divided into three groups: subarachnoid hemorrhage (SAH; n = 10), physiologic serum (SF; n = 4) and control (n = 4) groups. SAH was performed by injecting 0.5 cc of blood into cisterna magna taken from their auricular veins. Cervical spinal nerve roots at the C4 level were examined histopathologically. Results: Meningeal thickening and adhesions, reddish spinal cord and radices were detected macroscopically. Histopathologically, leptomeningeal adhesions, intimal lesions of radicular arteries and axonal injury were detected at the nerve radices. The mean radicular artery volume was found to be low on the arachnoiditis developing animals. The mean alive axon density of the C4 nerve root decreased and axonal degeneration was observed in the SAH group. Conclusion: Our study suggests that SAH may be an important etiologic factor in spinal arachnoiditis.