Hypertonic Lactate to Improve Cerebral Perfusion and Glucose Availability After Acute Brain Injury*

Carteron, Laurent; Solari, Daria; Patet, Camille; Quintard, Hervé; Miroz, John‐Paul; Bloch, Jocelyne; Daniel, Roy Thomas; Hirt, Lorenz; Eckert, Philippe; Magistretti, Pierre J.; Oddo, Mauro

doi:10.1097/ccm.0000000000003274

Cited by 56 publications

(58 citation statements)

References 46 publications

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“…One of these studies even indicated that TBI patients whose serum lactate > 5 mmol/L were likely to have a better survival than those with relatively low lactate level [24]. Furthermore, exogenous supplement of lactate by infusing hypertonic sodium lactate has been veri ed bene cial for survival and neurologic outcome and cognitive recovery in TBI animal models and patients [26][27][28][29][30][31][32]. In our study, serum lactate was higher in nonsurvivors than survivors, and was useful in predicting mortality in moderate to severe TBI patients with AUC of 0.733.…”

Section: Discussionmentioning

confidence: 99%

“…The bene cial effects of hypertonic sodium lactate on injured brain has been de nitely recognized including improving cerebral perfusion and brain glucose availability, reversing impaired brain metabolism and oxygenation, etc. [26][27][28]. In addition to the function of neuroenergetic material, lactate is actually a crucial signaling molecule which could modulate the production of pentose phosphate, an important molecule to prevent oxidative stress injury in brain [40][41][42][43].…”

Section: Discussionmentioning

confidence: 99%

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Lactate Albumin Ratio is Associated with Mortality in Patients with Moderate to Severe Traumatic Brain Injury

Wang¹,

He²,

Ou³

et al. 2020

Preprint

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Abstract Background: Traumatic brain injury (TBI) is a serious public health issue all over the world. This study was designed to evaluate the prognostic value of lactate to albumin ratio (LAR) on moderate to severe traumatic brain injury.Methods: Clinical data of 273 moderate to severe TBI patients hospitalized in West China Hospital between May 2015 and January 2018 were collected. Multivariate logistic regression analyses were used to explore risk factors and construct prognostic model of in-hospital mortality in this cohort. Nomogram was drawn to visualize the prognostic model. Receiver operating characteristic (ROC) curve and calibration curve were respectively drawn to evaluate discriminative ability and stability of this model.Results: Non-survivors had higher LAR than survivors (1.0870 vs 0.5286, p<0.001). Results of multivariate logistic regression analysis showed that GCS (OR=0.818, p=0.008), blood glucose (OR=1.232, p<0.001), LAR (OR=1.883, p=0.012), and red blood cell distribution (RDW)-SD (OR=1.179, p=0.004) were independent risk factors of in-hospital mortality in included patients. These four factors were utilized to construct prognostic model. The area under the ROC curve (AUC) value of single lactate and LAR were 0.733 (95%Cl; 0.673-0.794) and 0.780 (95%Cl; 0.725-0.835), respectively. The AUC value of the prognostic model was 0.868 (95%Cl; 0.826-0.909), which was higher than that of LAR (Z=2.5143, p<0.05).Conclusions: LAR is a readily available prognostic marker of moderate to severe TBI patients. Prognostic model incorporating LAR is beneficial for clinicians to evaluate possible progression and make treatment decisions in these patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Lactate Albumin Ratio is Associated with Mortality in Patients with Moderate to Severe Traumatic Brain Injury

Wang¹,

He²,

Ou³

et al. 2020

Preprint

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“…This observation has led to the early identification of patients at higher risk that deserve more aggressive treatment. Furthermore, CMD has allowed the improvement of our understanding of novel mechanisms involved in brain metabolism and future treatment approaches (Quintard et al, 2016;Patet et al, 2016;Carteron et al, 2017Carteron et al, , 2018Bernini et al, 2018;Oddo and Hutchinson, 2018).…”

Section: Brain Metabolism and Multimodal Monitoring The Role Of Cerebmentioning

confidence: 99%

“…In this setting, the supply of glucose to the injured brain, the main energy substrate, may become limited, leading to reductions in cerebral extracellular glucose below critical thresholds. Emerging evidence has demonstrated that the brain can use substrates other than glucose to sustain increased activity, including lactate Quintard et al, 2016;Patet et al, 2016;Carteron et al, 2018;Magistretti and Allaman, 2018).…”

Section: Brain Metabolic Patterns and Optimization Of Substrate Supplymentioning

confidence: 99%

“…Lactate is then transferred to neurons, providing additional energy substrate while also acting as a signaling molecule for other processes. This knowledge has led not only to a better understanding of the cerebral metabolic impairment in TBI but also to therapeutic options that offer lactate supplementation to ameliorate brain dysfunction Quintard et al, 2016;Carteron et al, 2018). The administration of hypertonic lactate solutions demonstrated beneficial effects in patients with TBI.…”

Section: New Insights On Neuroenergetics and Energy Fuel Supplymentioning

confidence: 99%

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Nutrition Therapy, Glucose Control, and Brain Metabolism in Traumatic Brain Injury: A Multimodal Monitoring Approach

Kurtz

Rocha²

2020

Front. Neurosci.

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The goal of neurocritical care in patients with traumatic brain injury (TBI) is to prevent secondary brain damage. Pathophysiological mechanisms lead to loss of body mass, negative nitrogen balance, dysglycemia, and cerebral metabolic dysfunction. All of these complications have been shown to impact outcomes. Therapeutic options are available that prevent or mitigate their negative impact. Nutrition therapy, glucose control, and multimodality monitoring with cerebral microdialysis (CMD) can be applied as an integrated approach to optimize systemic immune and organ function as well as adequate substrate delivery to the brain. CMD allows real-time bedside monitoring of aspects of brain energy metabolism, by measuring specific metabolites in the extracellular fluid of brain tissue. Sequential monitoring of brain glucose and lactate/pyruvate ratio may reveal pathologic processes that lead to imbalances in supply and demand. Early recognition of these patterns may help individualize cerebral perfusion targets and systemic glucose control following TBI. In this direction, recent consensus statements have provided guidelines and recommendations for CMD applications in neurocritical care. In this review, we summarize data from clinical research on patients with severe TBI focused on a multimodal approach to evaluate aspects of nutrition therapy, such as timing and route; aspects of systemic glucose management, such as intensive vs. moderate control; and finally, aspects of cerebral metabolism. Research and clinical applications of CMD to better understand the interplay between substrate supply, glycemic variations, insulin therapy, and their effects on the brain metabolic profile were also reviewed. Novel mechanistic hypotheses in the interpretation of brain biomarkers were also discussed. Finally, we offer an integrated approach that includes nutritional and brain metabolic monitoring to manage severe TBI patients.

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Metabolic Rewiring of Kynurenine Pathway during Hepatic Ischemia–Reperfusion Injury Exacerbates Liver Damage by Impairing NAD Homeostasis

Zhang

Tang

et al. 2022

Advanced Science

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Hepatic ischemia–reperfusion (IR) injury remains a common issue lacking effective strategy and validated pharmacological targets. Here, using an unbiased metabolomics screen, this study finds that following murine hepatic IR, liver 3‐hydroxyanthranilic acid (3‐HAA) and quinolinic acid (QA) decline while kynurenine and kynurenic acid (KYNA) increase. Kynurenine aminotransferases 2, functioning at the key branching point of the kynurenine pathway (KP), is markedly upregulated in hepatocytes during ischemia, shifting the kynurenine metabolic route from 3‐HAA and QA to KYNA synthesis. Defects in QA synthesis impair de novo nicotinamide adenine dinucleotide (NAD) biosynthesis, rendering the hepatocytes relying on the salvage pathway for maintenance of NAD and cellular antioxidant defense. Blocking the salvage pathway following IR by the nicotinamide phosphoribosyltransferase inhibitor FK866 exacerbates liver oxidative damage and enhanced IR susceptibility, which can be rescued by the lipid peroxidation inhibitor Liproxstatin‐1. Notably, nicotinamide mononucleotide administration once following IR effectively boosts NAD and attenuated IR‐induced oxidative stress, inflammation, and cell death in the murine model. Collectively, the findings reveal that metabolic rewiring of the KP partitions it away from NAD synthesis in hepatic IR pathophysiology, and provide proof of concept that NAD augmentation is a promising therapeutic measure for IR‐induced liver injury.

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Hypertonic Lactate to Improve Cerebral Perfusion and Glucose Availability After Acute Brain Injury*

Cited by 56 publications

References 46 publications

Lactate Albumin Ratio is Associated with Mortality in Patients with Moderate to Severe Traumatic Brain Injury

Lactate Albumin Ratio is Associated with Mortality in Patients with Moderate to Severe Traumatic Brain Injury

Nutrition Therapy, Glucose Control, and Brain Metabolism in Traumatic Brain Injury: A Multimodal Monitoring Approach

Metabolic Rewiring of Kynurenine Pathway during Hepatic Ischemia–Reperfusion Injury Exacerbates Liver Damage by Impairing NAD Homeostasis

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