Browsing by Author "Aydin, Mehmet Dumlu"

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A New Described Mechanisms of Intestinal Glandular Atrophy Induced by Vagal Nerve/Auerbach Network Degeneration Following Subarachnoid Hemorrhage: the First Experimental Study
(Elsevier Sci Ltd, 2019) Cakir, Murtaza; Ahiskalioglu, Ali; Karadeniz, Erdem; Aydin, Mehmet Dumlu; Malcok, Umit Ali; Soyalp, Celaleddin; Yayik, Ahmet Murat
Stress ulcers is a trouble complication of subarachnoid hemorrhage (SAH). Although gastrointestinal ulcerations may be attributed to increased HCL secretion in SAH; the exact mechanism of that complication has not been investigated definitively. We studied if vagal network degeneration may cause intestinal atrophy following SAH. Study was conducted on 25 rabbits, with 5 control group (Group-A), 5 SHAM group (Group-B), and 15 SAH group via injection of autologue blood to cisterna magna. Seven animals followed for seven days (Early Decapitated-Group-C) and eight animals followed 21 days (Late Decapitated-Group-D). The vagal nodosal ganglia (NGs), Auerbach plexuses and goblet cells of duodenums were examined by current stereological methods and compared statistically. The mean numbers of degenerated axon density/mm(2) of gastric branches of vagal nerves was 8 +/- 2, 34 +/- 11, 189 +/- 49 and 322 +/- 81 in the Group A, B, C, and D respectively. The mean numbers of degenerated neuron density/mm(3) of NGs was 5 +/- 2, 54 +/- 7, 691 +/- 87 and 2930 +/- 410 in the Group A, B, C, and D respectively. The mean numbers of degenerated Auerbach neurons 2 +/- 1, 4 +/- 1, 12 +/- 3 and 27 +/- 5/mm(3) in the Group A, B, C, and D respectively. The mean numbers of degenerated goblet cells/mm(3) were 4.3 +/- 1.02, 11.5 +/- 0.26, 143 +/- 26 and 937 +/- 65 Group A, B, C, and D respectively. Statistical analysis showed that vagal network ischemia could cause intestinal bleeding and so atrophy in SAH progression. Statistical analyses of groups were; Group-D/Group-A < 0.001, Group-D/Group-B < 0.005, Group-C/Group-A < 0.005. Undiscovered effect of ischemic vagal network injuries should be regarded as a major cause of stress ulcerations following SAH which has not been mentioned in the literature. (C) 2018 Elsevier Ltd. All rights reserved.
New Determinants for Casual Peripheral Mechanism of Neurogenic Lung Edema in Subarachnoid Hemorrhage Due To Ischemic Degeneration of Vagal Nerve, Kidney and Lung Circuitry. Experimental Study
(Acta Cirurgica Brasileira, 2019) Soyalp, Celaleddin; Kocak, Mehmet Nuri; Ahiskalioglu, Ali; Aksoy, Mehmet; Atalay, Canan; Aydin, Mehmet Dumlu; Ozmen, Sevilay
Purpose: To evaluate whether there is a relationship between renal artery vasospasm related low glomerular density or degeneration and neurogenic lung edema (NLE) following subarachnoid hemorrhage. Methods: This study was conducted on 26 rabbits. A control group was formed of five animals, a SHAM group of 5 to which saline and a study group (n=16) injected with homologous blood into the sylvian cisterna. Numbers of degenerated axons of renal branches of vagal nerves, atrophic glomerulus numbers and NLE scores were recorded. Results: Important vagal degeneration, severe renal artery vasospasm, intrarenal hemorrhage and glomerular atrophy observed in high score NLE detected animals. The mean degenerated axon density of vagal nerves (n/mm(2)), atrophic glomerulus density (n/mm(3)) and NLE scores of control, SHAM and study groups were estimated as 2.40 +/- 1.82, 2.20 +/- 1.30, 1.80 +/- 1.10, 8.00 +/- 2.24, 8.80 +/- 2.39, 4.40 +/- 1.14 and 154.38 +/- 13.61, 34.69 +/- 2.68 and 12.19 +/- 1.97 consecutively. Degenerated vagal axon, atrophic glomerulus and NLE scores are higher in study group than other groups and the differences are statistically meaningful (p<0.001). Conclusion: Vagal complex degeneration based glomerular atrophy have important roles on NLE following SAH which has not been extensively mentioned in the literature.
The Role of Cardiac Ganglia in the Prevention of Coronary Atherosclerosis: an Analytical Examination of Cholesterol-Fed Rabbits
(Galenos Publ House, 2020) Koza, Yavuzer; Aydin, Mehmet Dumlu; Bayram, Ednan; Sipal, Sare; Altas, Ender; Soyalp, Celaleddin; Koza, Enise Armagan
Background: The heart is innervated by the autonomic nervous system, which contributes to the control of the heart's rhythm and coronary circulation. It has been suggested that the cardiac fibers of the vagus nerve play important roles in controlling circulatory functions and in protecting against atherosclerotic pathologies in coronary arteries. Aims: To investigate the presence of atherosclerotic differences in the coronary arteries of cholesterol-fed rabbits by measuring the density of cardiac ganglia neurons. Study Design: Animal experiment. Methods: This study was conducted using 45 male rabbits. Over a period of 16 weeks, they were kept on an atherogenic diet of water ad libitum and high fat (8.6%) containing saturated fatty acids with 205 mg/kg of cholesterol (1%) per day. Then, their hearts were removed and examined by histopathological methods. Atherosclerotic plaques of the main coronary arteries were examined using the Cavalieri method. Atherosclerosis index values (AIVs) were estimated as the wall surface area/plaque surface area, and the results were analyzed with the Kruskal-Wallis and Mann-Whitney U tests. Results: While the average atherosclerosis index value was estimated to be <= 8% in 21 animals, the atherosclerosis index value was 9-20% in animals with minor plaque detection (n=11) and >= 20% in animals with major plaque detection (n=10). Increased atherosclerosis index values were more common in animals with low neuron densities than in animals with high neuron densities (p<0.017). Conclusion: The low neuron density of the cardiac ganglia in cholesterol-fed rabbits is associated with an increased atherosclerotic plaque incidence and volume.
Role of the Trigeminal System on Posterior Communicating Artery Remodelization After Bilateral Common Carotid Artery Ligation
(Sci Printers & Publ inc, 2013) Aygul, Recep; Aydin, Mehmet Dumlu; Kotan, Dilcan; Demir, Recep; Ulvi, Hizir; Karalar, Mustafa; Eseoglu, Metehan
OBJECTIVE: To examine whether or not there is a possible relationship between the neuron density of trigeminal ganglion (TGG) and the severity of posterior communicating artery (PComA) vasodilation values after permanent bilateral common carotid artery ligation (BCCAL). STUDY DESIGN: This study included 25 rabbits. Both the common carotid arteries of 20 rabbits were explored and denervated. Five animals served as controls. Permanent BCCAL was applied in 15 of the 20 rabbits, and the other 5 were used as the SHAM group without ligation. All animals were followed for 2 months and then sacrificed. Their brains and cranial nerves were extracted and fixed in 10% formalin solution. The relationship between PComA vasodilation values and TGG neuron densities were compared. RESULTS: Elongation, convolution and enlargement were detected in all the basilar arteries of all ligated animals and 2 from the SHAM group. On histopathogical examination vascular wall thinning, luminal enlargement, flattened inner elastic membrane, flattened vessel muscle cells, endothelial desquamation and intimal erosions were detected. An inverse relationship was discovered between the neuron density of TGG and the severity of PComA vasodilation index. CONCLUSION: BCCAL may lead to important beneficial and hazardous histomorphological changes at the posterior communicating artery. The high neuron density of TGG may provide a beneficial effect by facilitating PComA enlargement via its vasodilatory properties for the increase of decreased cerebral circulation, although this situation may be hazardous for certain subjects with congenital or acquired cerebrovascular pathologies.
Spinal Subarachnoid Hemorrhage Induced Intractable Miotic Pupil. a Reminder of Ciliospinal Sympathetic Center Lschemia Based Miosis: an Experimental Study
(Turkish Neurosurgical Soc, 2019) Aydin, Mehmet Dumlu; Kanat, Ayhan; Yolas, Coskun; Soyalp, Celalettin; Onen, Mehmet Resid; Yilmaz, Ilhan; Ramazanoglug, Leyla
Aim: To examine ischemic neurodegeneration of the ciliospinal center on permanent miosis following subarachnoid hemorrhage (SAH). MATERIAL and METHODS: Nineteen rabbits were examined in this study. The animals were divided into three groups, as control (GI, n=5), sham (GII, n=5) and study group (GIII, n=9). Pupil diameters were measured after giving 0.5 mL physiological saline for sham and autologous arterial blood for the study group into the cervico-thoracic subarachnoid space. After three weeks of follow up, the cervico-thoracic cord and bilateral superior cervical sympathetic ganglia were removed. The pupil diameter values were compared with degenerated neuron volumes of sympathetic ganglia and degenerated neuron densities of thoracic sympathetic nuclei which were studied by stereological methods. RESULTS: The mean pupil diameter was 5180 +/- 370 pm and the mean degenerated neuron density of the ciliospinal center was 4 +/- 1/mm(3) in animals of the control group (GI). These values were 9850 +/- 610 mu m, 10 +/- 3/mm(3) in sham (GII), and 7.010 +/- 440 mu m and 98 +/- 21/mm(3) in the study (GIII) groups. There was an inverse relationship between degenerated neuron density of the ciliospinal nuclei and pupil diameters. CONCLUSION: Although there is a widespread belief that the main cause of miosis is oculomotor nerve injury during SAH, we showed and reported for the first time that ciliospinal sympathetic center ischemia-induced neurodegeneration may have been responsible for permanent miosis following SAH.