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    Are unresponsive dilated pupils an indicator for brain death? an evaluation of Edinger Westphal nucleus in rabbits with brain death
    (2019) Ozmen, Ozgur; Aksoy, Mehmet; Aydin, Mehmet Dumlu; Atalay, Canan; Dostbil, Aysenur; Ince, Ilker; Sener, Ebru
    Aim: To investigate a relationship between unresponsive pupils and severity of neurodegeneration in Edinger Westphal nucleus (EWN) of animals diagnosed with brain death.Material and Methods: A total of 24 New Zealand white rabbits were used. The animals were divided into three groups, as control group (n=5), sham (n=5) and subarachnoid hemorrhage (SAH) group (n=14). Pupil diameters were measured after giving 2 mL of physiological saline for sham and 2 ml non‑heparinized autologous arterial blood for the study group into the cisterna magna. Brain death was diagnosed in 10 rabbits in the SAH group. Then all animals were sacrificed. The brains, oculomotor nerves of all animals were extracted and stored in 10% formalin solutions for histopathological examination.Results:TThe mean neuron numbers of Edinger Westphal nucleus was 253±43/mm3 in the control group; 244±12/mm3 in the sham group and 236±12/mm3 in dead unresponsive animals. Pupil diameters and degenerated neuron density of EWN in control, sham and SAH groups were found as follows, respectively: 8960±990µm-3±1/mm3; 10543±1.123µm-13±4/mm3 and 13540±1.356µm-63±11/mm3 (P0.005). There was a positive relationship between degenerated neuron density of the EWN and pupil diameters (P0.001). The mean nondegenerated neuron numbers were 170±32/mm3 in unresponsive pupils of examined animals.Conclusion: In the absence of electrocardiographic/electroencephalographic functions, unresponsive pupils could not indicate real brain death.
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    Dry Mouth Caused by Facial Nerve Ischemia due to Subarachnoid Hemorrhage: An Experimental Study
    (Elsevier Science Inc, 2021) Pasahan, Ramazan; Yardim, Ahmet; Karadag, Mehmet Kursat; Alpaslan, Aslihan; Aydin, Mehmet Dumlu
    OBJECTIVE: Parasympathetic network damage results in facial nerve damage, sublingual ganglion degeneration, sublingual gland dysfunction, and dry mouth. In this study, subarachnoid hemorrhage (SAH) was considered to be the cause of dry mouth. METHODS: We assessed 23 hybrid rabbits, including 5 control (group 1, Control). One milliliter of serum saline was injected into the cisterna magna of 5 animals (group 2). SAH was induced by injecting 1 mL of autologous blood into the cisterna magna of 13 animals (group 3). The animals were killed after 3 weeks of induction. The animals' sublingual ganglion and sublingual gland were excised for histopathological examination. The number of degenerated cells in the sublingual ganglion, secretory vesicles, and secretory granules in the sublingual gland that contain salivary components were estimated using Sequential Window Acquisition of All Theoretical Mass Spectra data analysis. The values were compared by the Mann-Whitney U-test. RESULTS: The numbers of secretory vesicles in the sublingual gland were 5.3 +/- 1.1 x 10(3) (group 1), 4.23 +/- 0.45 x 10(3) (group 2), and 1.56 +/- 0.22 x 10(3) (group 3); the numbers of secretory vesicles containing saliva in the sublingual gland were 324 +/- 12.18 (group 1), 263 +/- 36.23 (group 2), and 114 +/- 23.14 (group 3); and the numbers of degenerated cells in the sublingual ganglion were 11 +/- 3/mm(3) (group 1), 98.43 +/- 15.54/mm(3) (group 2), and 346 +/- 12.28/mm(3) (group 3) (P < 0.05). CONCLUSIONS: Clinical findings in infection and diseases such as Sjogren syndrome, aseptic meningitis, and SAH are similar. However, until now, SAH has not been demonstrated experimentally to cause dry mouth. Discovering that SAH might cause dry mouth might prevent unnecessary use of antibiotics and decrease morbidity due to the wrong or late diagnosis.
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    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, Arif
    Background: 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.