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• W2800642554 abstract "ABSTRACT Traumatic brain injury-induced acute lung injury (TBI-ALI) is a serious complication of traumatic brain injury (TBI). Our previous clinical study found that high levels of blood glutamate after TBI were closely related to the occurrence and severity of TBI-ALI, while it remains unknown whether a high concentration of blood glutamate directly causes or aggravates TBI-ALI. We found that inhibition of the adenosine A 2A receptor (A 2A R) after brain injury alleviated the TBI-ALI; however, it is unknown whether lowering blood glutamate levels in combination with inhibiting the A 2A R would lead to better effects. Using mouse models of moderate and severe TBI, we found that intravenous administration of L-glutamate greatly increased the lung water content, lung-body index, level of inflammatory markers in bronchoalveolar lavage fluid and acute lung injury score and significantly decreased the PaO 2 /FiO 2 ratio. Moreover, the incidence of TBI-ALI and the mortality rate were significantly increased, and the combined administration of A 2A R activator and exogenous glutamate further exacerbated the above damaging effects. Conversely, lowering the blood glutamate level through peritoneal dialysis or intravenous administration of oxaloacetate notably improved the above parameters, and a further improvement was seen with concurrent A 2A R genetic inactivation. These data suggest that A 2A R activation aggravates the damaging effect of high blood glutamate concentrations on the lung and that combined treatment targeting both A 2A R and blood glutamate may be an effective way to prevent and treat TBI-ALI." @default.
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• W2800642554 date "2019-04-01" @default.
• W2800642554 modified "2023-09-23" @default.
• W2800642554 title "Reduction in Blood Glutamate Levels Combined With the Genetic Inactivation of A2AR Significantly Alleviate Traumatic Brain Injury-Induced Acute Lung Injury" @default.
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• W2800642554 doi "https://doi.org/10.1097/shk.0000000000001170" @default.
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