Schröck H, Kuschinsky W
Department of Physiology, University of Bonn, Federal Republic of Germany.
Am J Physiol. 1989 Oct;257(4 Pt 2):H1220-7. doi: 10.1152/ajpheart.1989.257.4.H1220.
Chronic metabolic alkalosis was induced in rats by combining a low K+ diet with a 0.2 M NaHCO3 solution as drinking fluid for either 15 or 27 days. Local cerebral blood flow and local cerebral glucose utilization were measured in 31 different structures of the brain in conscious animals by means of the iodo-[14C]antipyrine and 2-[14C]deoxy-D-glucose method. The treatment induced moderate [15 days, base excess (BE) 16 mM] to severe (27 days, BE 25 mM) hypochloremic metabolic alkalosis and K+ depletion. During moderate metabolic alkalosis no change in cerebral glucose utilization and blood flow was detectable in most brain structures when compared with controls. Cerebrospinal fluid (CSF) K+ and H+ concentrations were significantly decreased. During severe hypochloremic alkalosis, cerebral blood flow was decreased by 19% and cerebral glucose utilization by 24% when compared with the control values. The decrease in cerebral blood flow during severe metabolic alkalosis is attributed mainly to the decreased cerebral metabolism and to a lesser extent to a further decrease of the CSF H+ concentration. CSF K+ concentration was not further decreased. The results show an unaltered cerebral blood flow and glucose utilization together with a decrease in CSF H+ and K+ concentrations at moderate metabolic alkalosis and a decrease in cerebral blood flow and glucose utilization together with a further decreased CSF H+ concentration at severe metabolic alkalosis.
通过将低钾饮食与0.2 M NaHCO₃溶液作为饮用水相结合，对大鼠诱导15天或27天，从而引发慢性代谢性碱中毒。采用碘代-[¹⁴C]安替比林和2-[¹⁴C]脱氧-D-葡萄糖法，在清醒动物的大脑31个不同结构中测量局部脑血流量和局部脑葡萄糖利用率。该处理诱导出中度（15天，碱剩余[BE]为16 mM）至重度（27天，BE为25 mM）的低氯性代谢性碱中毒和钾缺乏。在中度代谢性碱中毒期间，与对照组相比，大多数脑结构中的脑葡萄糖利用率和血流量未检测到变化。脑脊液（CSF）中的钾离子和氢离子浓度显著降低。在严重低氯性碱中毒期间，与对照值相比，脑血流量降低了19%，脑葡萄糖利用率降低了24%。严重代谢性碱中毒期间脑血流量的降低主要归因于脑代谢的降低，在较小程度上归因于脑脊液氢离子浓度的进一步降低。脑脊液钾离子浓度未进一步降低。结果表明，在中度代谢性碱中毒时，脑血流量和葡萄糖利用率未改变，同时脑脊液氢离子和钾离子浓度降低；在严重代谢性碱中毒时，脑血流量和葡萄糖利用率降低，同时脑脊液氢离子浓度进一步降低。
