Does Serum Osmolarity Change as a Result of the Reflex Neuroprotective Mechanism of Cerebral Osmo-Regulation after Minor Head Trauma?

Balak, Naci; Işıksaçan, Nilgün; Türkoğlu, Recai

doi:10.3340/jkns.2009.45.3.151

Cited by 4 publications

(8 citation statements)

References 29 publications

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“…Unstimulated CX3CR1 GFP/+ cells continually distended and retracted their processes (top panel[s] of Figure 8a,b; Video S3). Reduction of extracellular osmolality to 285 mOsm (~5%, equivalent to tonicity changes in patients with mild traumatic brain injury; Balak, Isiksacan, & Turkoglu, 2009; Liotta et al, 2018) induced a slight perikaryal enlargement (bottom panel of Figure 8a) and shifted dendritic symmetry by thickening the second and third‐order branches (bottom panels of Figure 8a,b; Video S3). While the average process length showed no discernable difference from controls (Figure 8d), the number of secondary branches (protrusions extending from primary processes) was slightly but nonsignificantly reduced (25.9 ± 4.20) vis à vis isotonic (22.5 ± 2.01) conditions (Figure 8c; p = .07; two‐way ANOVA).…”

Section: Resultsmentioning

confidence: 99%

TRPV4 channels mediate the mechanoresponse in retinal microglia

Redmon

Yarishkin

Lakk

et al. 2021

Glia

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The physiological and neurological correlates of plummeting brain osmolality during edema, traumatic CNS injury, and severe ischemia are compounded by neuroinflammation. Using multiple approaches, we investigated how retinal microglia respond to challenges mediated by increases in strain, osmotic gradients, and agonists of the stretch‐activated cation channel TRPV4. Dissociated and intact microglia were TRPV4‐immunoreactive and responded to the selective agonist GSK1016790A and substrate stretch with altered motility and elevations in intracellular calcium ([Ca2+]i). Agonist‐ and hypotonicity‐induced swelling was associated with a nonselective outwardly rectifying cation current, increased [Ca2+]i, and retraction of higher‐order processes. The antagonist HC067047 reduced the extent of hypotonicity‐induced microglial swelling and inhibited the suppressive effects of GSK1016790A and hypotonicity on microglial branching. Microglial TRPV4 signaling required intermediary activation of phospholipase A2 (PLA2), cytochrome P450, and epoxyeicosatrienoic acid production (EETs). The expression pattern of vanilloid thermoTrp genes in retinal microglia was markedly different from retinal neurons, astrocytes, and cortical microglia. These results suggest that TRPV4 represents a primary retinal microglial sensor of osmochallenges under physiological and pathological conditions. Its activation, associated with PLA2, modulates calcium signaling and cell architecture. TRPV4 inhibition might be a useful strategy to suppress microglial overactivation in the swollen and edematous CNS.

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Section: Resultsmentioning

confidence: 99%

TRPV4 channels mediate the mechanoresponse in retinal microglia

Redmon

Yarishkin

Lakk

et al. 2021

Glia

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“…Zhang et al reported that an increased hematocrit level did not affect the neuroprotective or neurorestorative effects of EPO in rats after TBI, suggesting that the effect of EPO was independent of hematocrit 51) . Balak et al demonstrated that serum osmolarity decreased during the first 3 h after TBI 3) . We failed to show a significant role of hematocrit as an independent parameter, and quercetin had no effect on hematocrit.…”

Section: Discussionmentioning

confidence: 99%

Effects of Quercetin and Mannitol on Erythropoietin Levels in Rats Following Acute Severe Traumatic Brain Injury

Kalemcı

Aydın

Kızmazoğlu

et al. 2017

J Korean Neurosurg Soc

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ObjectiveThe aim of this study to investigate the normal values of erythropoietin (EPO) and neuroprotective effects of quercetin and mannitol on EPO and hematocrit levels after acute severe traumatic brain injury (TBI) in rat model.MethodsA weight-drop impact acceleration model of TBI was used on 40 male Wistar rats. The animals were divided into sham (group I), TBI (group II), TBI+quercetin (50 mg/kg intravenously) (group III), and TBI+mannitol (1 mg/kg intravenously) (group IV) groups. The malondialdehyde, glutathione peroxidase, catalase, EPO, and hematocrit levels were measured 1 and 4 hour after injury. Two-way repeated measures analysis of variance and Tukey’s test were used for statistical analysis.ResultsThe malondialdehyde levels decreased significantly after administration of quercetin and mannitol compared with those in group II. Catalase and glutathione peroxidase levels increased significantly in groups III and IV. Serum EPO levels decreased significantly after mannitol but not after quercetin administration. Serum hematocrit levels did not change significantly after quercetin and mannitol administration 1 hour after trauma. However, mannitol administration decreased serum hematocrit levels significantly after 4 hour.ConclusionThis study suggests that quercetin may be a good alternative treatment for TBI, as it did not decrease the EPO levels.

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“…The human brain is a blend of a dynamic network of neurons and hormones. 1 Traumatic Brain Injury (TBI) throughout the world is a major cause of mortality and morbidity and a major concern among the young age population. 2 Significant cerebral disturbances occur after TBI with alteration in cerebral hemodynamics leading to chemical, metabolic and immunological changes in besides parenchymal and vascular damages.…”

Section: Introductionmentioning

confidence: 99%

“…2 Significant cerebral disturbances occur after TBI with alteration in cerebral hemodynamics leading to chemical, metabolic and immunological changes in besides parenchymal and vascular damages. 1 Injury or dysfunction of hypothalamus and pituitary handles alteration in serum osmolarity in patients with Traumatic Brain Injury. 3 Disturbance of cellular osmoregulation in the brain results in enormity of intracellular sodium and water which is important in maintaining a constant milieu in the Central Nervous System (CNS).…”

Section: Introductionmentioning

confidence: 99%

“…As per Balak et al, significant changes were found in serum osmolarity after minor head trauma in comparison to patients with trauma to other parts of the body. 1 Agha et al studied 50 patients with severe or moderate Traumatic Brain Injury, out of which 11 (22%) developed hypernatremia. 4 In a study conducted by Maggiore U et al, 51% of patients with severe head injury developed Osmolarity was calculated using the formula, Osmolarity = 2Na+ 2K + urea +RBS.…”

Section: Introductionmentioning

confidence: 99%

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Effect of Serum Osmolarity on Prognosis of Traumatic Brain Injury

Banskota

Malla

2022

J. Nepalgunj Med. College

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Introduction: Road traffic accident has been a significant cause of mortality in today's fast paced world. Metabolic and intracranial parameters have affected the outcome of traumatic brain injury. Countless analysis on biomechanical injury and tissue damage has substantiated additional treatment strategies. Laboratory values have been less investigated to predict the outcome of brain injury. Aims: This study was done to find out the association between the serum osmolarity with severity of head injury and the outcome in traumatic brain injury. Methods: This study was conducted at Department of Neurosurgery, Nepalgunj Medical college, Kohalpur, Banke from July 2020 to June 2021. 106 patients were included in the study. Clinical profile of the patients and calculated plasma osmolarity were monitored daily. Results: 106 patients were enrolled with mean age of 39±18.6 and male study population being on the higher side. 62(58.49%) patients with Traumatic Brain Injury accounted for road traffic accident with mild head injury as the commonest presentation. In about 40.57% of the patients osmolarity ranged between 285 to 295 milliosmole/ litre with mean osmolarity of 290.99±10.60. There was no significant association between severity of head injury and serum osmolarity (p value=0.45). Conclusion: There is no association between the severity of head injury with serum osmolarity.

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Does Serum Osmolarity Change as a Result of the Reflex Neuroprotective Mechanism of Cerebral Osmo-Regulation after Minor Head Trauma?

Cited by 4 publications

References 29 publications

TRPV4 channels mediate the mechanoresponse in retinal microglia

TRPV4 channels mediate the mechanoresponse in retinal microglia

Effects of Quercetin and Mannitol on Erythropoietin Levels in Rats Following Acute Severe Traumatic Brain Injury

Effect of Serum Osmolarity on Prognosis of Traumatic Brain Injury

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