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首页> 外文期刊>Brain research. Developmental brain research >Plasminogen activators contribute to age-dependent impairment of NMDA cerebrovasodilation after brain injury.
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Plasminogen activators contribute to age-dependent impairment of NMDA cerebrovasodilation after brain injury.

机译：纤溶酶原激活剂导致脑损伤后NMDA脑血管舒张的年龄依赖性损伤。

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Previous studies have observed that fluid percussion brain injury (FPI) impaired NMDA induced pial artery dilation in an age-dependent manner. This study was designed to investigate the contribution of plasminogen activators to impaired NMDA dilation after FPI in newborn and juvenile pigs equipped with a closed cranial window. In the newborn pig, NMDA (10(-8), 10(-6) M) induced pial artery dilation was reversed to vasoconstriction following FPI, but pretreatment with the plasminogen activator inhibitor PAI-1 derived hexapeptide (EEIIMD) (10(-7) M) prevented post injury vasoconstriction (9 +/- 1 and 16 +/- 1, vs. -6 +/- 2 and-11 +/- 3, vs. 5 +/- 1 and 9 +/- 1% for responses to NMDA 10(-8), 10(-6) M prior to FPI, after FPI, and after FPI in EEIIMD pretreated animals, respectively). In contrast, in the juvenile pig, NMDA dilation was only attenuated following FPI and EEIIMD pretreatment partially prevented such inhibition (9 +/- 1 and 16 +/- 1 vs. 2 +/- 1 and 4 +/- 1 vs. 5 +/- 1 and 7 +/- 1% for responsesto NMDA prior to FPI, after FPI, and after FPI in EEIIMD pretreated animals, respectively). Additionally, EEIIMD blunted age-dependent pial artery vasoconstriction following FPI. EEIIMD blocked dilation to the plasminogen activator agonists uPA and tPA while responses to SNP and papaverine were unchanged. Pretreatment with suPAR, which blocked dilation to uPA, elicited effects on pial artery diameter and NMDA vascular activity post FPI similar to that observed with EEIIMD. These data show that EEIIMD and suPAR partially prevented FPI induced alterations in NMDA dilation and reductions in pial artery diameter. EEIIMD and suPAR are efficacious and selective inhibitors of plasminogen activator induced dilation. These data suggest that plasminogen activators contribute to age-dependent impairment of NMDA induced dilation following FPI.
机译：以前的研究已经观察到，液压冲击性脑损伤（FPI）以年龄依赖性方式损害了NMDA诱导的颈动脉扩张。这项研究旨在调查纤溶酶原激活剂对FPI后新生猪和幼年猪的颅窗封闭的NMDA损伤的影响。在新生猪中，NMDA（10（-8），10（-6）M）诱导的颈动脉扩张在FPI后被逆转为血管收缩，但是用纤溶酶原激活物抑制剂PAI-1衍生的六肽（EEIIMD）预处理（10（- 7）M）预防了受伤后的血管收缩（9 +/- 1和16 +/- 1，比-6 +/- 2和11 +/- 3，比5 +/- 1和9 +/- 1分别为EEIIMD预处理动物在FPI之前，FPI之后和FPI之后对NMDA 10（-8），10（-6）M的响应的百分比（％）。相比之下，在幼猪中，NMDA扩张仅在FPI后减弱，而EEIIMD预处理部分阻止了这种抑制作用（9 +/- 1和16 +/- 1 vs. 2 +/- 1和4 +/- 1 vs. 5在EEIIMD预处理的动物中，在FPI之前，FPI之后和FPI之后，对NMDA的响应分别为+/- 1和7 +/- 1％。另外，在FPI之后，EEIIMD使年龄依赖性的颈动脉血管收缩变钝。 EEIIMD阻止了纤溶酶原激活剂激动剂uPA和tPA的扩张，而对SNP和罂粟碱的反应却没有改变。 suPAR预处理阻止了uPA的扩张，在FPI后引起了对颈动脉直径和NMDA血管活性的影响，类似于EEIIMD所观察到的。这些数据表明，EEIIMD和suPAR可以部分阻止FPI诱导的NMDA扩张改变和颈动脉直径的减小。 EEIIMD和suPAR是纤溶酶原激活剂诱导的扩张的有效和选择性抑制剂。这些数据表明纤溶酶原激活剂导致FPI后NMDA诱导的扩张的年龄依赖性损伤。

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