Extracellular potassium activity and cerebral blood flow during moderate hypoglycemia in anesthetized dogs.
Extracellular potassium activity and cerebral blood flow during moderate hypoglycemia in anesthetized dogs.
复制标题
麻醉犬中度低血糖期间的细胞外钾活性和脑血流量。
DOI：
10.1152/ajpheart.1993.264.6.h1774
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Traystman,RJ
中科院分区：
文献类型：
--
作者：
Sieber,FE;Wilson,DA;Hanley,DF;Traystman,RJ
中度低血糖（MH）可能与脑低碳酸血症性血管收缩减弱有关。与此同时，脑电图（EEG）变平。先前的报告表明，脑细胞外钾活性（[K+]o）增加与严重低血糖期间等电的发生相关，并且K+增加引起软脑膜血管舒张。使用MH模型，我们检验了[K+]o（约15 mM）增加与脑低碳酸血症血管收缩钝化相关的假设。在正常碳酸血症[动脉Pco 2（Paco 2）= 35 Torr）]和低碳酸血症（PaCO 2 = 15 Torr）期间测量MH（< 2 mM）和血糖正常的狗的脑血流量（CBF）、[K+]o和EEG。在MH期间，[K+]o的增加与EEG平坦化相关（从4.2 +/- 0.5至13.8 +/- 3.8 mM）。在正常血压和MH无[K+]o升高期间，发生低碳酸血症性血管收缩。MH引起的[K+]o升高与正常碳酸血症期间CBF增加和血管阻力降低（分别为对照组的146 +/- 5和42 +/- 2%）相关，当[K+]o在低碳酸血症期间升高时，脑低碳酸血症血管收缩减弱（正常碳酸血症对照组的93 +/- 16%）。这项研究表明，在MH期间增加[K+]o是必要的正常碳酸增加CBF和脑低碳酸血管收缩钝化。[K+]o的增加可能是MH期间脑血管阻力降低的机制。
Moderate hypoglycemia (MH) may be associated with blunting of cerebral hypocapnic vasoconstriction. Coincident with this change, electroencephalogram (EEG) flattening occurs. Previous reports show that brain extracellular potassium activity ([K+]o) increases in association with the onset of isoelectricity during severe hypoglycemia and that K+ increases cause pial vessel vasodilation. Using a model of MH, we tested the hypothesis that increases in [K+]o (approximately 15 mM) correlate with blunting of cerebral hypocapnic vasoconstriction. Cerebral blood flow (CBF), [K+]o, and EEG were measured during normocapnia [arterial Pco2 (Paco2) = 35 Torr)] and hypocapnia (PaCO2 = 15 Torr) in MH (< 2 mM) and normoglycemic dogs. During MH, increases in [K+]o occurred in association with EEG flattening (from 4.2 +/- 0.5 to 13.8 +/- 3.8 mM). During normoglycemia and MH without [K+]o elevations, hypocapnic vasoconstriction occurred. [K+]o elevations with MH were associated with increased CBF and decreased vascular resistance (146 +/- 5 and 42 +/- 2% of control, respectively) during normocapnia, and blunting of cerebral hypocapnic vasoconstriction (93 +/- 16% normocapnic control) when [K+]o increased during hypocapnia. This study shows that increases in [K+]o during MH are necessary for both normocapnic increases in CBF and blunting of cerebral hypocapnic vasoconstriction. Increases in [K+]o may represent a mechanism for decreases in cerebral vascular resistance during MH.