Management of traumatic brain injury patients

Dash, Hari H.; Chavali, Siddharth

doi:10.4097/kjae.2018.71.1.12

Cited by 97 publications

(113 citation statements)

References 54 publications

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“…Finally, we examined the effect of the guanylate cyclase (GC) inhibitor methylene blue (3 × 10 -6 M) and the NO-sensitive GC inhibitor 1H- [1,2,4]oxadiazolo [4,3-a]quinoxalin-1-one (ODQ, 10 -5 M) on phenylephrine-induced contraction in endothelium-intact rat aortae pretreated at 33°C for 30 min. After isolated endothelium-intact rat aortae were treated at 33°C for 30 min in the presence or absence of methylene blue or ODQ, phenylephrine (10 -9 to 10 -5 M) was cumulatively added to the organ bath to produce phenylephrine concentration-response curves.…”

Section: Experimental Protocolsmentioning

confidence: 99%

“…Hypothermia may exert a neuroprotective effect in traumatic brain injury [1,2]. The alpha-adrenoceptor agonist phenylephrine can be used to improve cerebral perfusion pressure that has been compromised by hypothermia-induced hypotension, which is regarded as a side effect of hypothermia [1,2]. Mild hypothermia (34°C) attenuates phenylephrine-induced contraction by increasing nitric oxide (NO) production [3].…”

Section: Introductionmentioning

confidence: 99%

“…A: Effect of methylene blue (MB, A: N = 7) and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, B: N = 8) on phenylephrine-induced contraction in isolated endothelium-intact rat aortae pretreated at 33°C. The data represent the mean ± SD and are expressed as a percentage of the maximal contraction induced by isotonic 60 mM KCl.…”

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confidence: 99%

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Nitric oxide-mediated inhibition of phenylephrine-induced contraction in response to hypothermia is partially modulated by endothelial Rho-kinase

Lee

Kim

et al. 2020

Int. J. Med. Sci.

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This study examined the possible upstream cellular signaling pathway associated with nitric oxide (NO)-mediated inhibition of phenylephrine-induced contraction in isolated rat aortae in response to mild hypothermia, with a particular focus on endothelial Rho-kinase. We examined the effects of mild hypothermia (33°C), wortmannin, N ω -nitro-L-arginine methyl ester (L-NAME), Y-27632, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) and methylene blue, alone and combined, on phenylephrine-induced contraction in isolated rat aortae. Finally, we examined the effects of mild hypothermia, wortmannin, Y-27632 and L-NAME, alone and combined, on endothelial nitric oxide synthase (eNOS) and endothelial Rho-kinase membrane translocation induced by phenylephrine. Mild hypothermia attenuated phenylephrine-induced contraction only in endothelium-intact aortae. L-NAME, wortmannin, ODQ and methylene blue increased phenylephrine-induced contraction of endothelium-intact aortae pretreated at 33°C. Wortmannin did not significantly alter the L-NAME-induced enhancement of phenylephrine-induced maximal contraction of endotheliumintact aortae pretreated at 33°C. Wortmannin abolished the ability of Y-27632 to magnify the hypothermic inhibition of maximal phenylephrine-induced contraction. Wortmannin and L-NAME inhibited the enhancing effect of mild hypothermia on phenylephrine-induced eNOS phosphorylation. Y-27632 and L-NAME attenuated the enhancing effect of hypothermia on phenylephrine-induced endothelial Rho-kinase membrane translocation. The results suggest that hypothermia-induced, NO-dependent inhibition of phenylephrine-induced contraction is mediated by phosphoinositide 3-kinase and inhibited by endothelial Rho-kinase activation.

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Section: Experimental Protocolsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Nitric oxide-mediated inhibition of phenylephrine-induced contraction in response to hypothermia is partially modulated by endothelial Rho-kinase

Lee

Kim

et al. 2020

Int. J. Med. Sci.

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“…Traumatic brain injury (TBI) is one of the most complex and common types of brain injuries . TBI research has been centered on the CNS, and little is known about the peripheral alterations that may compromise brain pathology.…”

Section: Introductionmentioning

confidence: 99%

“…Traumatic brain injury (TBI) is one of the most complex and common types of brain injuries. [1] TBI research has been centered on the CNS, [2] and little is known about the peripheral alterations that may compromise brain pathology. In particular, the lack of The ORCID identification number(s) for the author(s) of this article can be found under https://doi.org/10.1002/mnfr.201801054 DOI: 10.1002/mnfr.201801054 knowledge about the systemic sequel of TBI is a big concern for the understanding and management of metabolic dysfunction that intuitively involves body metabolism.…”

Section: Introductionmentioning

confidence: 99%

Brain Trauma Disrupts Hepatic Lipid Metabolism: Blame It on Fructose?

Rege

Royes

Tsai

et al. 2019

Molecular Nutrition Food Res

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Scope The action of brain disorders on peripheral metabolism is poorly understood. The impact of traumatic brain injury (TBI) on peripheral organ function and how TBI effects can be influenced by the metabolic perturbation elicited by fructose ingestion are studied. Methods and Results It is found that TBI affects glucose metabolism and signaling proteins for insulin and growth hormone in the liver; these effects are exacerbated by fructose ingestion. Fructose, principally metabolized in the liver, potentiates the action of TBI on hepatic lipid droplet accumulation. Studies in isolated cultured hepatocytes identify GH and fructose as factors for the synthesis of lipids. The liver has a major role in the synthesis of lipids used for brain function and repair. TBI results in differentially expressed genes in the hypothalamus, primarily associated with lipid metabolism, providing cues to understand central control of peripheral alterations. Fructose‐fed TBI animals have elevated levels of markers of inflammation, lipid peroxidation, and cell energy metabolism, suggesting the pro‐inflammatory impact of TBI and fructose in the liver. Conclusion Results reveal the impact of TBI on systemic metabolism and the aggravating action of fructose. The hypothalamic‐pituitary‐growth axis seems to play a major role in the regulation of the peripheral TBI pathology.

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Cell and Tissue Instructive Materials for Central Nervous System Repair

Rocha

Silva

Barata‐Antunes

et al. 2020

Adv Funct Materials

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Neurodegenerative disorders and traumatic events affecting the central nervous system (CNS) represent one of the main health problems nowadays. The level of disability and impairment of these patients is very high, both at physiological and psychological level, drastically altering a person's lifestyle. The fact that CNS tissue has a limited capacity of regeneration has hampered the development of possible therapies to these conditions. The specificity of each disease also increases the complexity of creating strategies capable of inducing significant recovery. Therefore, the search for a solution for these problems most likely demands a combinatorial approach that integrates knowledge from different fields. Tissue engineering and regenerative medicine (TERM) concepts merge areas such as biology, chemistry, physics, or biomaterials science, and it is a strong candidate for CNS applications. In particular, the development of cell and tissue instructive materials (CTIMs) can bring new opportunities for the treatment of these conditions. In this review, the authors summarize and discuss the most recent advances in the development of CTIMs for CNS applications, focusing on traumatic conditions such as spinal cord injuy, traumatic brain injuy, but also stroke, and other neurodegenerative diseases such as Alzheimer's and Parkinson's disease as well as multiple sclerosis.

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Management of traumatic brain injury patients

Cited by 97 publications

References 54 publications

Nitric oxide-mediated inhibition of phenylephrine-induced contraction in response to hypothermia is partially modulated by endothelial Rho-kinase

Nitric oxide-mediated inhibition of phenylephrine-induced contraction in response to hypothermia is partially modulated by endothelial Rho-kinase

Brain Trauma Disrupts Hepatic Lipid Metabolism: Blame It on Fructose?

Cell and Tissue Instructive Materials for Central Nervous System Repair

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