New Evidence for Causal Central Mechanism of Hyperglycemia in Subarachnoid Hemorrhage Secondary to Ischemic Degenerative Disruption of Circuitry Among Insular Cortex, Nodose Ganglion, and Pancreas: Experimental Study

Aydın, Mehmet Dumlu; Kanat, Ayhan; Kantarcı, Abdulmecit; Ayvaz, Muhammed Ali; Rakici, Halil; Yolaş, Coşkun; Kepoğlu, Ümit; Demirci, Elif

doi:10.1016/j.wneu.2017.06.176

Cited by 24 publications

(8 citation statements)

References 60 publications

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“…The balance between cell proliferation and cell death is crucial in all tissues, particularly in the nervous system. 19,42 In RD, we think that therapeutic strategies to halt patient cell death should include ways to defend the brain and eyes against the deleterious effect of OpA vasospasm, blood, and ICP secondary to SAH. If OpAs are prone to ischemic vasospasm in SAH, the low neuron density of PPGs cannot cause a sufficient vasodilatory response to dilatation of OpAs, decreased blood flow of choroidal arteries can cause subretinal fluid collection, and RD may be inevitable, which has not been mentioned in the literature.…”

Section: Specific Conclusive Hypothesis Of Our Resultsmentioning

confidence: 99%

Describing a New Mechanism of Retinal Detachment Secondary to Ophthalmic Artery Vasospasm Following Subarachnoid Hemorrhage: An Experimental Study

Fındık

Kanat

Aydın

et al. 2019

J Neurol Surg A Cent Eur Neurosurg

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Background The pterygopalatine ganglion (PPG) and ophthalmic arteries (OpAs) have important roles in ocular autoregulation and retinal and visual functions. The relationship between PPG neuron density, OpA vasospasm, and retinal detachment in subarachnoid hemorrhage (SAH) has never been studied. Methods This study was conducted on 25 rabbits. Five animals were in the control group (GI; n = 5), five in the sham group (GII; n = 5), and 15 in the study group (GIII; n = 15). After injection of 1 cc serum saline into the cisterna magna in the sham group, and autologous blood in the SAH group, the animals were followed for 3 weeks. All animals underwent a retinal examination five times a week for 3 weeks before and after the experiment. After the experiment, the neuron density of PPGs of the facial nerves, vasospasm index (VSI) of OpAs, and total basal surface values of the detached retinal parts (DRPs) were calculated. Results In the funduscopic examination, intravitreous hemorrhage ( Terson's syndrome) was detected in four animals in the SAH group. In the control groups, neuron density was 12,000 ± 1,240/mm3, VSI = 0.345 ± 0.076, and DRP = 0 to 1.5 mm2. Mean neuron density was 9,450 ± 940/mm3, VSI = 1.645 ± 0.940, and DRP = 6.23 ± 1.61 mm2 in the sham group (p < 0.05). Neuron density was 6,890 ± 932/mm3, VSI = 2.92 ± 0.97, and DRP = 9.43 ± 2.54 mm2 in SAH group. Conclusion Mean neuron density, VSI of OpAs, and DRP values differed statistically significant between the SAH group and other groups (p < 0.005). There is an inverse relationship between PPG neurons and DRP. However, a direct relationship was observed between the mean VSI and DRP values.

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Section: Specific Conclusive Hypothesis Of Our Resultsmentioning

confidence: 99%

Describing a New Mechanism of Retinal Detachment Secondary to Ophthalmic Artery Vasospasm Following Subarachnoid Hemorrhage: An Experimental Study

Fındık

Kanat

Aydın

et al. 2019

J Neurol Surg A Cent Eur Neurosurg

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“…Nodose ganglia‐linked ischemia may result in cardiac arrest with developing indirect sympathetic overactivity based on Takotsubo‐like cardiomyopathy . Insulo‐vago‐pancreatic circuitry ischemia may be responsible for hyperglisemia . There is a parallel link between CP degeneration and meningeal inflammation in SAH.…”

Section: Discussionmentioning

confidence: 99%

“…23 Insulo-vago-pancreatic circuitry ischemia may be responsible for hyperglisemia. 24 There is a parallel link between CP degeneration and meningeal inflammation in SAH. Aydin et al shown that CPs include a thermo-regulator cell-like structures which regulate brain temperature by changing CSF secretion from CPs.…”

Section: Innervation Of Cpsmentioning

confidence: 99%

First definition of burned choroid plexus in acidic cerebrospinal fluid‐filled brain ventricles during subarachnoid hemorrhage: Experimental study

et al. 2020

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Blood and cerebrospinal fluid (CSF) acidosis is the most troubling complication in subarachnoid hemorrhage (SAH) if carotid body (CB) networks are disrupted. However, histopathological examination of the choroid plexus (CP) in acidic CSF has not been evaluated so far. In this study, we aimed to investigate the CP in acidic CSF following SAH. Twenty‐eight rabbits were used. Five rabbits were used to analyze CB network (control group; n = 5); seven rabbits were injected 1 mL of saline (Sham group; n = 7); and the rest 16 rabbits were given 1 mL of autologous arterial blood inject into the cisterna magna to create SAH (SAH group; n = 16). Blood and CSF pH values were recorded before/during/after the experimental procedures. Nuclear darkening, cellular shrinkage and pyknosis suggested the presence of apoptosis of epithelial cells of CP. The densities of normal and degenerated epithelial cells of CPs were estimated using stereological methods. The relationship between the pH values and degenerated epithelial cell densities of CPs were statistically compared by Mann–Whitney U‐test. The pH values of blood were estimated as 7.359 ± 0.039 in the control group, 7.318 ± 0.062 in the Sham group, 7.23 ± 0.013 in the SAH group. CSF pH values were 7.313 ± 0.028 in the control group, 7.296 ± 0.045 in the Sham group, and 7.224 ± 0.012 in the SAH group. Degenerated epithelial cell density of CP was 25 ± 7 in the control group, 226 ± 64 in the Sham group, and 2115 ± 635 in the SAH group. There was a considerable link between CSF pH values and degenerated epithelial cells of CP (P < 0.0001). This study shows that CB insult causes acidosis of CSF as well as cellular degeneration of CP during SAH. This is the first description of this in the literature.

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“…17 All taste information of tongue, mammary gland and genitalia reach to caudal regions of the solitary tract nucleus, limbic forebrain, reticular formation, 6 and insular cortex. 7 In the brain, primarily mediodorsal prefrontal cortex, 18 insular cortex, 19 lateral hypothalamus, amygdala and globus pallidus have also glucose-sensitive and glucose level monitoring neurons 20 to manage body glucose modulation. The sympathetic nervous system also mediates catabolic responses to glucose metabolism.…”

Section: Discussionmentioning

confidence: 99%

New description of vagal nerve commanted intrapancreatic taste buds and blood glucose level: An experimental analysis

et al. 2020

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Introduction: There have been thousands of neurochemical mechanism about blood glucose level regulation, but intrapancreatic taste buds and their roles in blood glucose level has not been described. We aimed to investigate if there are taste buds cored neural networks in the pancreas, and there is any relationship between blood glucose levels. Methods: This examination was done on 32 chosen rats with their glucose levels. Animals are divided into owned blood glucose levels. If mean glucose levels were equal to 105 ± 10 mg/dL accepted as euglycemic (G-I; n = 14), 142 ± 18 mg/dL values accepted as hyperglycemic (G-II; n = 9) and 89 ± 9 mg/dL accepted as hypoglycemic (G-III; n = 9). After the experiment, animals were sacrificed under general anesthesia. Their pancreatic tissues were examined histological methods and numbers of newly described taste bud networks analyzed by Stereological methods. Results compared with Mann-Whitney U test P < 0.005 considered as significant. Results: The mean normal blood glucose level (mg/dL) and taste bud network densities of per cm3 were: 105 ± 10 mg/dL; 156±21 in G-I; 142 ± 18 mg/dL and 95 ± 14 in G-II and 89 ± 9 mg/dL and 232 ± 34 in G-III. P values as follows: P < 0.001 of G-II/G-I; P < 0.005 of G-III/G-I and P < 0.0001 of G-III/G-II. We detected periarterial located taste buds like cell clusters and peripherally located ganglia connected with Langerhans cells via thin nerve fibers. There was an inverse relationship between the number of taste buds networks and blood glucose level. Conclusion: Newly described intrapancreatic taste buds may have an important role in the regulation of blood glucose level.

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New Evidence for Causal Central Mechanism of Hyperglycemia in Subarachnoid Hemorrhage Secondary to Ischemic Degenerative Disruption of Circuitry Among Insular Cortex, Nodose Ganglion, and Pancreas: Experimental Study

Cited by 24 publications

References 60 publications

Describing a New Mechanism of Retinal Detachment Secondary to Ophthalmic Artery Vasospasm Following Subarachnoid Hemorrhage: An Experimental Study

Describing a New Mechanism of Retinal Detachment Secondary to Ophthalmic Artery Vasospasm Following Subarachnoid Hemorrhage: An Experimental Study

First definition of burned choroid plexus in acidic cerebrospinal fluid‐filled brain ventricles during subarachnoid hemorrhage: Experimental study

New description of vagal nerve commanted intrapancreatic taste buds and blood glucose level: An experimental analysis

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