Effect of Gamma-Hydroxybutyric Acid on Lipid Peroxidation and Tissue Lactate Level in Experimental Head Trauma

Yosunkaya, Alper; Ak, Ahmet; Barışkaner, Hülagü; Üstün, Mehmet Erkan; Tuncer, Sema; Gürbîlek, Mehmet

doi:10.1097/01.ta.0000058119.60074.25

Cited by 15 publications

(6 citation statements)

References 40 publications

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“…In zwei weiteren Untersuchungen am neurotraumatologischen Modell des Kaninchens aus dem Jahre 2004 konnte durch die Gabe von GHB eine Reduktion des Abfalls der Na + ,K + -ATPase sowie eine Reduktion der Gewebekonzentration von Laktat und der Lipidperoxidation nachgewiesen werden [39][40]. …”

Section: Ghb Als Sedativum Auf Der Intensivstationunclassified

Gamma-hydroxy butyric acid: Neurotransmitter, sedative and party drug

Meyer

Kleinschmidt

Gottschling

et al. 2005

Wien Med Wochenschr

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Gamma-hydroxybutyric acid (GHB) as a natural component of the mammalian brain was first introduced in clinical anaesthesic practice more than 40 years ago. The drug was nearly forced from clinical practice because of its prolonged and variable duration of action. The results of recent clinical studies indicate a re-evaluation of GHB in various clinical fields. In the intensive care unit, GHB may be a favourable alternative to established drugs. The results of various clinical studies also suggest that GHB is efficacious in the treatment of alcohol withdrawal syndrome, and narcolepsy. GHB has been used successfully for short-term sedation in children. In addition, GHB has emerged as a street drug ("liquid ecstasy"). Overdose may lead to respiratory depression, coma, and even death. Chronic abuse itself may lead to severe withdrawal syndrome. The purpose of this article is to outline the neurophysiological, pharmacodynamic and pharmacokinetic characteristics of GHB, and to summarize the potential fields of use and misuse of GHB in clinical medicine and toxicology.

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Section: Ghb Als Sedativum Auf Der Intensivstationunclassified

Gamma-hydroxy butyric acid: Neurotransmitter, sedative and party drug

Meyer

Kleinschmidt

Gottschling

et al. 2005

Wien Med Wochenschr

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“…A number of smaller animal and human studies suggest GHB and its precursor gamma‐butyrolactone may have a neuroprotective effect by reducing cerebral metabolic requirements, suppressing changes in Na + ‐K + ATPase and suppressing lipid peroxidation 10–12 . Drug doses used in experimental work are within the ranges used recreationally.…”

Section: Discussionmentioning

confidence: 99%

“…A number of smaller animal and human studies suggest GHB and its precursor gamma-butyrolactone may have a neuroprotective effect by reducing cerebral metabolic requirements, suppressing changes in Na + -K + ATPase and suppressing lipid peroxidation. [10][11][12] Drug doses used in experimental work are within the ranges used recreationally. It is therefore possible that in overdose a degree of cerebral protection is afforded by GHB, contributing to the good outcomes seen in those surviving respiratory arrest.…”

Section: Discussionmentioning

confidence: 99%

Survival of massive γ‐hydroxybutyrate/ 1,4‐butanediol overdose

Strickland

Felgate

Caldicott

2005

Emerg Medicine Australasia

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“…The third pathway -Warburg pentose-cycle or pentose phosphate pathway (hexose monophosphate shunt) -represents direct oxidation in cytosol and provides more energy but is slower compared to glycolysis. The switch from the first to the third energy production pathway may be done by using sodium oxybutirate and gamma-hydroxybutyrate, serotonin (mexamin), barbiturates, venotropic drugs and phenotiasin [86,[92][93][94][95][96]. The switch of cellular energy metabolism from the third to the first pathway may be forced by insulin, application of which in combination with glucose and potassium may be beneficial under the situation when immediate energy production is required [97].…”

Section: Paas That Switch the Pathways Of Cellular Energy Metabolismmentioning

confidence: 99%

Remediation of Cellular Hypoxic Damage by Pharmacological Agents

Minko¹,

Wang²,

Pozharov³

2005

CPD

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Many known pathological conditions lead to decreases in oxygen supply to various cells. When secondary cellular hypoxia becomes severe, it causes additional cellular damage, aggravating the primary disorder and leading to cell death. Therefore, remediation of secondary hypoxic damage should significantly increase the efficacy of the treatment of primary disease and prevent extensive cellular damage. Analysis of the literature and our experimental data show that the main mechanisms of secondary hypoxic cellular damage include lactate acidosis (lactic acidosis), the boost in free radical processes and the activation of apoptosis and necrosis. These factors result in damage to cellular membranes which in turn further limits oxygen supply leading to augmented hypoxic cellular damage. Therefore, to effectively break this vicious cycle of cellular hypoxia, antihypoxic therapy should simultaneously: (1) mitigate existing cellular hypoxic damage; (2) increase cellular ability to utilize available oxygen; (3) amplify the power of cellular antioxidant defense and (4) prevent hypoxic activation of apoptosis and necrosis. It is clear that such complex task cannot be fulfilled by a single pharmacological agent. Therefore, a complex multi component antihypoxic drug delivery system should be designed to address all the four desiderata indicated above. This review will examine existing pharmaceutical antihypoxic preparations and evaluate the new methods for the pharmacological remediation of cellular hypoxic damage and propose future directions for the design of the needed drug delivery systems.

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Effect of Gamma-Hydroxybutyric Acid on Lipid Peroxidation and Tissue Lactate Level in Experimental Head Trauma

Abstract: These results demonstrate that head trauma leads to an increase in brain tissue lactate and MDA levels, and GHB effectively suppresses the increase of lactate and MDA.

Cited by 15 publications

References 40 publications

Gamma-hydroxy butyric acid: Neurotransmitter, sedative and party drug

Gamma-hydroxy butyric acid: Neurotransmitter, sedative and party drug

Survival of massive γ‐hydroxybutyrate/ 1,4‐butanediol overdose

Remediation of Cellular Hypoxic Damage by Pharmacological Agents

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