Role of carotid body for neuronal protection in experimental subarachnoid haemorrhage

Objective: Carotid bodies are known as main arterialchemoregulatory units. Despite well known that carotidbodies have an important role in cerebral circulation andblood pH regulation, their roles has not been investigatedin subarachnoid haemorrhage. We investigated whetherthere is neuroprotective effect of neuron density of carotidbodies on the brain in subarachnoid haemorrhage.Methods: Twenty hybrid rabbits were studied. Four ofthem were used as reference group (n=4) and the remainingwas obliged to subarachnoid haemorrhage by injectingautologous blood into their cisterna magna (n=16)and sacrificed after one month. All carotid bodies andbrains examined histopathologically using by stereologicmethods. The relationship between the neuronal densityof carotid body and degenerated neuron density of thehippocampus were compared statistically.Results: Five rabbits with subarachnoid haemorrhagedead during the follow-up time (n=5). The average neuronaldensity of carotid body was 4500±500 cells/mm3and of hippocampus 170.000±17.000 cell/mm3 in normalrabbit family. The degenerated neuron density ofthe hippocampus was 20.000±3.000 cells/mm3 in rabbitswith have high neuron density of carotid body and was65.000±8.000 cells/mm3 in rabbits with low neuron densityof carotid body. The differences between the neuronaldensity of carotid body and the degenerated neuron numbersof the hippocampus were significant.Conclusion: The neuron density of carotid body mayplay an important role on the protection of brain in subarachnoidhaemorrhage.Key words: Subarachnoid haemorrhage, carotid body,hippocampus, neurodegeneration, cerebral ischemi

First report of the histopathological effect of electrocautery using on the urethral taste rosea during glans penis injury by incision in rabbits

Objective: Currently, electrocautery devices have frequently been used in penile surgical procedures. We hypothesized that electrocautery using during penile surgical procedures may harm the taste rosea and the dorsal nerve of the penis or clitoris. Methods: Eighteen young age male New Zealand rabbits were studied: five in the control (Group I, n=5), five in the penile surgery without using electrocautery (sham group, Group II, n=5), eight in the monopolar cautery (study group, Group III, n=8) groups under general anesthesia. The animals were followed for 3 weeks and sacrificed. Penile tissuedpudendal nerve root complexes and dorsal root ganglion of sacral 3 level were examined using stereological methods. The results were compared statistically. Results: The live and degenerated taste bud -like structures and degenerated neuron densities of pudendal ganglia (mean +/- standard deviation, n/mm3) were estimated as 198 +/- 24/mm3, 4 +/- 1/mm3, and 5 +/- 1/mm3 in Group I; 8 +/- 3/mm3, 174 +/- 21/mm3, and 24 +/- 7/mm3 in Group II; and 21 +/- 5/mm3, 137 +/- 14/mm3, and 95 +/- 12/mm3 in Group III, respectively. Neurodegeneration of taste buds and pudendal ganglia was significantly different between groups. Conclusion: Intact spinal cord and normal parasympathetic and thoracolumbar sympathetic networks are crucial for human sexual function. The present study indicates that the glans penis injury by using electrocautery may lead to pudendal ganglia degeneration. Iatrogenic damage to taste rosea and retrograde degeneration of the pudendal nerve may be the cause of sexual dysfunction responsible mechanism

Olfactory bulbectomy leads to prolonged induction phase of sevoflurane anesthesia in rats

The effect of olfactory bulb lesions on the induction time of sevoflurane has never been studied. We aimed to investigate this issue. In this study, we found that the volume of olfactory bulbs and the pore of the fila olfactoria were significantly lower with the fibrosis of olfactory bulbs in animals subjected to olfactory bulbectomy. Volatile anesthetics induction times were measured in all groups. Prolonged induction was observed in olfactory bulbectomy group. It was concluded that increased induction times of sevoflurane may be due to the olfactory bulb lesion

Bowel Pathologies Caused by the Use of Electrocautery Knife in Spinal Surgery with Facet Denervation: The First Experimental Study

Objective:Monopolar electrocautery (MEC) or bipolar electrocautery (BEC) are surgical instruments commonly used in spinal surgery. Our study aimed to determine the bowel end pathologies induced by sacral parasympathetic network degeneration due to the use of MEC or BEC in spinal surgery.Method:Twenty male hybrid rabbits were used in the study, including 5 in the control group, 7 in the BEC group, and 8 in the MEC group. We used the thoracic vertebra 11-lumbar vertebra 2 (T11-L2) spinal laminectomy for the operation technique. After one week, the animals’ abdominal organs were examined on computerized tomography, and then the animals were sacrificed. The descending colon and Onuf’s nucleus/S4 spinal ganglia were histopathologically examined. The colonic degeneration scores were numbered as follows: Normal (0P), vasospasm (1P), endothelial injury (2P), thrombus (3P), colonic wall injury (4P), inflammation (5P), colonic mucosal degeneration (6P), Auerbach myenteric ganglion degeneration (7P), and necrosis (8P). The groups were scored according to 36 points, and the results were compared with the number of degenerated pudendal ganglion neurons.Results:The mean numbers of normal neurons/degenerated neurons were 22.610±962/5±2, 21.617±890/103±21, and 16.692±641/345±62 in the control, BEC, and MEC groups, respectively. The colonic degeneration score was 31 points in the MEC group. Our results were statistically significant (p<0.05 for all).Conclusion:In this study, we have found that high-voltage electrical devices such as MEC/BEC may cause bowel pathologies due to their harmful effects on the Adamkiewicz artery/sacral parasympathetic network and should not be used in spinal surgery unless necessary

Paradoxic relations between basilar artery reconfiguration and superior cervical ganglia ischemia after bilateral common carotid artery ligation

Background: The relationship between superior cervical ganglia (SCG) ischemia due to bilateral common carotid artery ligation (BCCAL) and basilar artery (BA) reconfiguration was investigated. Methods: Twenty-three rabbits were randomly divided into 3 groups: group III rabbits underwent BCCAL (n = 13), group II rabbits were sham-operated controls (n = 5), and group I rabbits did not undergo surgery (n = 5). Degenerated neuron densities (DND) within the SCG were correlated with the BA vasodilatation index (VDI). Results: Mean live and DND in SCG of group I rabbits were 11.235 ± 982/μm3 and 11 ± 3/μm3, respectively, with a mean heart rate of 294 ± 21 beats/min. Mean SCG DND and heart rates were 213 ± 42/μm3 and 242 ± 17 beats/min for the sham group (group II) rabbits and 1743 ± 285/μm3 and 199 ± 19 beats/min for the study group (group III) rabbits, respectively. The BA VDI values in the sham group (group II) (1.32 ± 0.10) and the study group (group III) (0.976 ± 0.112) significantly differed from those in the control group (group I) (1.65 ± 0.12; P < 0.005) versus the sham group (group II) (P < 0.0001) versus the BCCAL applied group (group III) and between group II and group III (P < 0.005). Conclusions: A meaningful and paradoxic correlation was detected between the BA VDI values and degenerated neuron density of SCG after BCCAL. Although a low degenerated neuron density within SCG may provoke excessive sympathetic activity and prevent excessive BA dilatation with steno-occlusive carotid artery diseases, a high degenerated neuron density may cause dangerous vasodilatation of BA

First histopathological bridging of the distance between Onufʼs nucleus and substantia nigra after olfactory bulbectomy—new ideas about the urinary dysfunction in cerebral neurodegenerative disease: an experimental study

Objectives: Olfactory bulbectomy (OBX) in experimental studies induces neurochemical, neurodegenerative changes in various parts of the body. But no information is available about how OBX affects the spinal cord in rats. Our study aims to investigate this question. Methods: Twenty-eight male rats were used. The rats were divided into three groups: six as the control, six as the SHAM, and 16 as the study group in which OBX was performed. The animals were followed for 10 weeks. After decapitation of the animals, olfactory bulb (OB) volumes, the olfactory glomerulus (OG), and the neuron density of the ON (Onuf nucleus) per cubic centimeter at the L4-S4 level were examined histopathologically and analyzed stereologically. Results: The mean OB volume, remaining normal OG density, and degenerated neuron density (DND) of the ON was measured as 4.32 ± 0.21/mm3, 1842 ± 114/mm3, and 4 ± 1 /mm3 in the control (group I); 3.3 ± 0.14/mm3, 1321 ± 114/mm3, and 43 ± 8/mm3 in the SHAM (group II); and 1.672 ± 0.12/mm3, 852 ± 93/mm3, and 154 ± 11/mm3 in the study group (group III). There was a statistically significant difference between the SHAM and the study group (P <.05). Conclusions: In this study, histopathological bridging between ON-related lower urinary tract symptoms (LUTS) and OBX was shown the first time. According to the findings, LUTS may be reversed by the protection of the affected spinal cord through the correction of olfaction impairment in neurodegenerative disease. © 2020 John Wiley & Sons Australia, Ltd

Vazospazmın indüklediği iskemiye bağlı spinal araknoidit ve spinal sinir köklerinin aksonal dejenerasyonu: Deneysel çalışma

Objective: Various 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.Amaç: Araknoidit gelişiminde çeşitli nedenler suçlanmaktadır, subaraknoid kanama (SAK) da bu süreçte önemli bir öğe olabilir. Bu deneysel çalışmada (tavşan SAK modelinde) SAK'ın histopatolojik bulgular üzerine etkisini, radiküler arterlerin hacimsel değişikliklerini ve C4 spinal sinir kök aksonlarının dansitesini araştırdık. Materyal ve Metot: Bu çalışmada 18 tavşan kullanıldı. Tavşanlar rastgele üç gruba ayrıldı: subaraknoid kanama (SAK; n = 10), serum fizyolojik (SF; n = 4) ve kontrol (n = 4). SAK, kulak veninden alınan 0.5 ml kanın sisterna magnaya verilmesiyle oluşturuldu. C4 servikal spinal sinir kökleri histopatolojik olarak incelendi. Sonuçlar: Makroskopik olarak, meningeal kalınlaşma ve yapışıklıklar, kızılımsı spinal kord ve kökler saptandı. Histopatolojik olarak sinir köklerinde, leptomeningeal yapışıklıklar, radiküler arterlerde intimal lezyonlar ve aksonal hasar saptandı. SAK grubunda, radiküler arter ortalama hacmi araknoidit gelişen hayvanlarda düşük olarak bulundu. SAK grubunda, C4 kökünün ortalama canlı akson dansitesinde azalma ve aksonal harabiyet gözlendi. Yorum: Çalışmamızın sonuçlarına göre SAK, spinal araknoiditde önemli bir etyolojik etken olabilir

Protective felix culpa effect of superior sympathetic cervical ganglion degenerations on prevention of basilar artery spasm after subarachnoid hemorrhage: A preliminary experimental study

BACKGROUND: Posterior cerebral blood flow is regulated by the basilar arteries (BAs). Vasospasm of BAs can occur after subarachnoid hemorrhage (SAH). Superior cervical sympathetic ganglia (SCG) fibers have a vasoconstrictor effect on the BA. We aimed to investigate the relationship between the degenerated neuron density of the SCG and the severity of BA vasospasm after experimental SAH. METHODS: Twenty-four rabbits were used. Five were used as the control group, and 5 were used as the sham group. Experimental SAHs were performed in the remaining 14 animals (study group) by injecting homologous blood into the cisterna magna. After 3 weeks of injection, neuron densities of SCG and the severity of BA vasospasm index values (VSI) were examined histopathologically and compared statistically. RESULTS: The mean VSI was 0.669 +/- 0.1129 in the control group, 0.981 +/- 0.159 in the sham group, and 1.512 +/- 0.298 in the study group. The mean degenerated neuronal density of SCG was 436 +/- 79/mm(3) in severe vasospasm (n = 3), 841 +/- 101/mm(3) in moderate vasospasm (n = 4), and 1.921 +/- 849/mm(3) in the less vasospasm detected animals (n = 6). CONCLUSIONS: This study shows an inverse relationship between the degenerated neuronal density in the SCG and VSI values. This finding indicates a diminished sympathetic input from the SCG, resulting in a beneficial effect the felix culpa) by dilating the lumen diameter of the BA, so SCG degeneration after SAH protects the BA spasm

The effect of choroidal artery vasospasm on choroid plexus ınjury in subarachnoid hemorrhage: experimental study

AMAÇ: Bu çalışmada, subaraknoid kanamada (SAK) koroid arter vazospazmının koroid pleksusta (KP) iskemik hasar yapıp yapmadığını inceledik. YÖNTEM ve GEREÇLER: Bu çalışma 30 tavşan üzerinde yapıldı. Sekizi kontrol grubu, 14’ü SAK grubu, 8 tavşan da SHAM grubu olarak kullanıldı. Koroidal arterlerin tam koroid pleksusa girdiği noktadaki kesitlerinin çapı ve volümü mikrometrik mikroskop kullanılarak ölçüldü. Koroid pleksus hücre ve villuslarının iskemik morfolojik değişiklikleri hafiften ağıra doğru şu şekilde tanımlandı: hücresel küçülme (1puan), sitoplazmik yoğunlaşma (2 puan), angulasyon (3 puan) ve villus yıkımı (4 puan). Mevcut histopatolojik bulguların 1 ile 4 arasındaki dejenerasyon kriterlerinin toplamı dejenerasyon skoru olarak tanımlandı. Sonuçlar istatistiksel olarak değerlendirildi. BULGULAR: Üç grubun koroidal arter çapı ve volümü ile dejenerasyon skoru değerleri şu şekilde bulundu. Kontrol grubunda ortalama koroidal arter çapı 120±30?m, volümü 1,080±0,650 mm3 ve dejenerasyon skoru 0 ve 1 arasında idi. SHAM grubunda ortalama koroidal arter çapı 110±20?m, volümü 0,907±0,330 mm3 ve dejenerasyon skoru 1 ve 4 arasında idi. SAK grubunda ortalama koroidal arter çapı 80±15?m, volümü 0,480±0,175 mm3 ve dejenerasyon skoru 3 ve 0 arasında idi. Sonuçta vazospazm derecesi ile KP dejenerasyonu arasında anlamlı ilişki bulundu. SONUÇ: SAK olgularında koroidal arterlerin vazospazmı değişik derecelerde koroid pleksus hasarı oluşturabilir. Beynin immün, endokrin, detoksifikasyon, termoregulasyon ve sekretuar fonksiyonlarında önemli rolü olan koroid pleksusların hasar görmesi SAK’daki kötü prognozun önemli bir sebebi olabilir

New histophatological finding about data destroying amyloid black holes in hippocampus following olfactory bulb lesion like as the universe

Background: Many infinite theories have been suggested to explain memory loss in neurodegenerative diseases. However, there are clear data that iron-containing neurofibrillary networks can cause neuron death and erase the memory of neurons, just likeObjectives: Ths study aimed to investigate the electromagnetic properties of iron-loaded neurofibrillary networks formed in the hippocampus as a result of damage to the olfactory nerves, just like black holes in space, as well as whether they cause neuron death Methods: All rats were tested with star maze performance before, 3 weeks, and 3 months after surgery. The data used in the study were obtained from the subjects in the experimental groups who had been followed up for 3 months with control (GI; n = 5), SHAM (GII; n = 5) with only frontal burr hole, and study (GIII; n =15) animals with olfactory bulb lesion. All rats were tested with star maze performance before, 3 weeks, and 3 months after surgery. The olfactory bulbs and hippocampus of subjects were examined by stereological methods. Olfactory bulb volumes, degenerated neuron densities of the hippocampus, and numbers of hippocampal black holes were estimated quantitatively, and results were statistically analyzed by a 1-way analysis of variance (ANOVA). The properties of black holes in the brains and the universe were compared theoretically.Results: The mean olfactory bulb volumes, degenerated neuron density, and black holes of the hippocampus were estimated as 4.43 +/- 0.22 mm3, 42 +/- 9 mm3, and 3 +/- 1 mm3 in GI, 4.01 +/- 0.19 mm3, 257 +/- 78 mm3, and 11 +/- 3 mm3 in GII, and 2.4 +/- 0.8 mm3, 1675 +/- 119 mm3, and 34 +/- 7 mm3 in GIII. All animals were tested with star maze performance before, 3 weeks, and 3 months after surgery. Latency, distance, speed, and path efficiency values of all animals were detected. The more diminished olfactory bulb volume (P < 0.00001) causes more apoptotic neurons and black holes in the hippocampus (P < 0.0001) and more memory loss in olfactory bulbConclusions: Hippocampal black holes, which are similar to black holes in terms of their formation processes, may be responsible for neuronal losses and memory erasures in the brain by acting like black holes in space. These amyloid plaques, which cause neuron death and memory loss, will be called data-deleting amyloid black holes (DADA-Black Holes) in the paper