Pannier J L, Weyne J, Demeester G, Leusen I
Stroke. 1978 Jul-Aug;9(4):354-9. doi: 10.1161/01.str.9.4.354.
Acute alterations in plasma bicarbonate concentration have minimal effects on intracerebral pH and cerebral blood flow, perhaps due to blood-brain barrier mechanisms. To test this hypothesis, the consequences of an acute rise in the plasma bicarbonate concentration were studied in anesthetized rats previously subjected to an acute pressure pulse in the carotid system with unilateral damage to the blood-brain barrier. In rats subjected to a "heavy" hypertensive insult, the hemisphere on the side of the lesion showed a lactic acidosis, edema, and a depression of cerebral blood flow. An increase in the plasma bicarbonate concentrations of 15--20 mEq/1 during 35 minutes provoked a marked rise in the total CO2 content of this hemisphere, and a further increase in the lactate concentration, but did not later the brain edema nor affect further the already very low cerebral blood flow. An increase in the lactate concentration and a decrease of cerebral blood flow in the "reference" hemisphere indicated that the lesion was not completely unilateral. In rats subjected to a "moderate" hypertensive insult the changes were less pronounced and statistically not significant for all the parameters. There results illustrate the importance of an intact blood-brain barrier for the maintenance of intracerebral pH in the face of acute alterations in plasma [HCO3]. The impaired cerebral blood flow after an acute hypertensive insult did not appear to be influenced by the intracerebral [HCO3].
血浆碳酸氢盐浓度的急性改变对脑内pH值和脑血流量的影响极小，这可能归因于血脑屏障机制。为验证这一假说，研究人员在先前经历过颈动脉系统急性压力脉冲且血脑屏障单侧受损的麻醉大鼠中，观察了血浆碳酸氢盐浓度急性升高的后果。在遭受“重度”高血压损伤的大鼠中，损伤侧半球出现乳酸酸中毒、水肿以及脑血流量降低。在35分钟内将血浆碳酸氢盐浓度提高15 - 20 mEq/1，导致该半球的总二氧化碳含量显著升高，乳酸浓度进一步增加，但并未减轻脑水肿，也未对本已很低的脑血流量产生进一步影响。“对照”半球中乳酸浓度升高和脑血流量降低，表明损伤并非完全单侧性。在遭受“中度”高血压损伤的大鼠中，所有参数的变化均不明显且无统计学意义。这些结果表明，在血浆[HCO3]急性改变时，完整的血脑屏障对于维持脑内pH值至关重要。急性高血压损伤后受损的脑血流量似乎不受脑内[HCO3]的影响。
