Response to Stevens et al. Glucose Dynamics of Cortical Spreading Depolarization in Acute Brain Injury: A Systematic Review (DOI: 10.1089/neu.2018.6175).
Response to Stevens et al. Glucose Dynamics of Cortical Spreading Depolarization in Acute Brain Injury: A Systematic Review (DOI: 10.1089/neu.2018.6175).
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对史蒂文斯等人的回应
DOI:
10.1089/neu.2019.6599
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发表时间:
2020
影响因子:
4.2
通讯作者:
Hurst T
中科院分区:
文献类型:
--
作者:
Hurst T
In the second of these articles3 we (1) found a highly significant relationship between number of depolarizations and mean plasma glucose (p< 0.001)(Fig. 1 [reproduced with permission] in which we treated incidence of SDs as the dependent variable), and (2) suggested in the Introduction2 the possibility of a “vicious circle” in which depletion of cerebral cortical tissue glucose by depolarization would challenge cortical energy state and destabilize neuronal membranes, hence predisposing to further depolarizations. The implications of the parameters of the relationship are (1) that glucose utilization rate is maximal (so as to have become limited by plasma availability) and (2) that depolarizations might be expected to cease if plasma glucose were to remain in the region of 8.8 mmol/L (160 mg/100 mL), raising the possibility of a similar treatment approach in the clinic. Given the various factors now believed to influence SD frequency, such as arterial hypotension, body temperature, and, we would suggest, local tissue oxygen tension, the idea of SD incidence being dependent on plasma–or, much better, brain tissue glucose–can only be tested when these other influences are held stable while plasma glucose is also steady, which is no easy task.