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Influence of type 1 diabetes on basal and agonist‐induced permeability of the blood–brain barrier

机译：1型糖尿病对基底和激动剂引起的血脑屏障通透性的影响

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AbstractType 1 diabetes mellitus (T1D) impairs endothelial nitric oxide synthase (eNOS)-dependent responses of cerebral arterioles. However, the influence of T1D on another critical aspect of endothelial cell function in the cerebral microcirculation, i.e., regulation of permeability of the blood–brain barrier (BBB), remains largely unknown. Our goal was to examine basal and agonist-induced changes in permeability of the BBB in nondiabetic and type 1 diabetic (streptozotocin; 50 mg/kg IP) rats. On the day of the experiment (2–3 months after streptozotocin), a craniotomy was made over the parietal cortex in nondiabetic and diabetic rats. We measured the permeability of the BBB (FITC-dextran-10K) under basal conditions and during application of histamine. We also measured diameter of cerebral arterioles in response to histamine in the absence and presence of NG-monomethyl-L-arginine (L-NMMA). We found that basal permeability of the BBB was elevated in T1D and application of histamine did not produce a further increase in permeability. In contrast, basal permeability of the BBB was minimal in nondiabetics and histamine produced an increase in permeability. In addition, histamine-induced arteriolar dilation was less in diabetics than in nondiabetics, and vasodilation to histamine was inhibited by L-NMMA. Our findings suggest that T1D-induced endothelial dysfunction leads to an increase in basal permeability of the BBB, but decreases the ability of the endothelium of the BBB to respond to an important inflammatory mediator. Thus, T1D impairs two critical aspects of endothelial cell function in the cerebral microcirculation, i.e., basal and agonist-induced changes in permeability of the BBB and arteriolar dilation.
机译：摘要1型糖尿病（T1D）损害了脑小动脉的内皮一氧化氮合酶（eNOS）依赖性反应。然而，T1D对大脑微循环中内皮细胞功能的另一个关键方面的影响，即对血脑屏障（BBB）的通透性的调节，仍是未知之数。我们的目标是检查非糖尿病和1型糖尿病（链脲佐菌素; 50 mg / kg IP）大鼠中BBB通透性的基础和激动剂诱导变化。在实验当天（链脲佐菌素后2-3个月），在非糖尿病和糖尿病大鼠的顶叶皮质进行了开颅手术。我们在基础条件下和组胺应用过程中测量了血脑屏障的通透性（FITC-dextran-10K）。我们还测量了在不存在和存在NG-单甲基-L-精氨酸（L-NMMA）的情况下，响应组胺的脑小动脉直径。我们发现在T1D中血脑屏障的基础通透性增加，组胺的应用并没有进一步增加通透性。相反，在非糖尿病患者中，血脑屏障的基础通透性最小，组胺导致通透性增加。另外，糖尿病患者中组胺引起的小动脉扩张少于非糖尿病患者，并且L-NMMA抑制了向组胺的血管舒张。我们的发现表明，T1D诱导的内皮功能障碍导致BBB的基础通透性增加，但降低了BBB的内皮对重要炎症介质作出反应的能力。因此，T1D损害了大脑微循环中内皮细胞功能的两个关键方面，即基底和激动剂引起的血脑屏障通透性变化和小动脉扩张。

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