Effect of hypoglycemia on cerebral metabolism and carbon dioxide responsivity.
Effect of hypoglycemia on cerebral metabolism and carbon dioxide responsivity.
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低血糖对脑代谢和二氧化碳反应性的影响。
DOI：
10.1152/ajpheart.1989.256.3.h697
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Traystman,RJ
中科院分区：
文献类型：
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作者：
Sieber,FE;Derrer,SA;Saudek,CD;Traystman,RJ
本研究探讨了低血糖（HG）对脑代谢和脑血管对二氧化碳反应性的影响。在戊巴比妥麻醉的狗中使用放射性标记的微球测定脑血流量（CBF）。使用动脉和矢状窦血液样本中测量的相应浓度计算脑氧、葡萄糖、乳酸、丙酮酸、乙酰乙酸和β-羟基丁酸的摄取。在每个实验中记录EEG。用胰岛素诱导HG，使血糖低于30 mg/100 ml。在10只动物（3只对照，7只HG）中研究了高碳酸血症，方法是在正常血压（NG）和HG期间将动脉二氧化碳张力（PaCO 2）从对照（35 +/- 4;平均值+/- SE）增加到54 +/- 2 Torr。通过将NG和HG中的PaCO 2从对照组（39 +/- 1）降低至14 +/- 1 Torr，在11只动物（3只对照组，8只HG）中研究了低碳酸血症。在两组达到稳态PaCO 2后，在每个对照和改变的PaCO 2状态下进行测量。在高碳酸血症组中，葡萄糖从71 +/- 3降至28 +/- 3 mg/100 ml。在NG和HG中，CBF随高碳酸血症增加至对照组的175%。高碳酸血症组脑氧代谢率和脑电图无明显变化。在低碳酸血症组中，葡萄糖从71 +/- 3降至19 +/- 2 mg/100 ml。在NG中，CBF随着低碳酸血症降低至对照的62 +/- 5%，但在HG中保持在对照水平。这并不伴随着脑耗氧量的变化，然而，平坦的EEG发生在所有HG低碳酸血症动物。在任何组中测量的其他脑代谢物的摄取均未发生变化。这项研究表明，CBF高碳酸血症的反应保持完整的HG期间，然而，低碳酸血症引起严重的EEG干扰和损害脑血管收缩反应。
This study examined the effects of hypoglycemia (HG) on cerebral metabolism and cerebrovascular reactivity to carbon dioxide. Cerebral blood flow (CBF) was determined using radiolabeled microspheres in pentobarbital-anesthetized dogs. Cerebral oxygen, glucose, lactate, pyruvate, acetoacetate, and beta-hydroxybutyrate uptakes were calculated using the respective concentrations measured in arterial and sagittal sinus blood samples. EEG was recorded throughout each experiment. HG was induced with insulin to obtain a blood glucose less than 30 mg/100 ml. Hypercapnia was studied in 10 animals (3 control, 7 HG) by increasing arterial carbon dioxide tension (PaCO2) from control (35 +/- 4; mean +/- SE) to 54 +/- 2 Torr during normoglycemia (NG) and HG. Hypocapnia was studied in 11 animals (3 control, 8 HG) by decreasing PaCO2 from control (39 +/- 1) to 14 +/- 1 Torr in NG and HG. Measurements were taken after reaching steady-state PaCO2 in both groups at each control and altered PaCO2 state. In the hypercapnic group, glucose decreased from 71 +/- 3 to 28 +/- 3 mg/100 ml. CBF increased with hypercapnia to 175% of control in both NG and HG. Cerebral metabolic rate of oxygen and electroencephalogram (EEG) did not change in the hypercapnic group. In the hypocapnic group glucose decreased from 71 +/- 3 to 19 +/- 2 mg/100 ml. CBF decreased with hypocapnia to 62 +/- 5% of control in NG but remained at control in HG. This was not accompanied by changes in cerebral oxygen consumption; however, a flat EEG occurred in all HG hypocapnic animals. No change occurred in uptake of the other cerebral metabolites measured in any group. This study shows that the CBF hypercapnic response remains intact during HG; however, hypocapnia causes severe EEG disturbances and impairs the cerebral vasoconstriction response.