Bukoski R D, Wang S N, Bian K, DeWitt D S
Department of Internal Medicine, University of Texas Medical Branch, Galveston 77555-1065, USA.
Am J Physiol. 1997 Mar;272(3 Pt 2):H1406-11. doi: 10.1152/ajpheart.1997.272.3.H1406.
Previous studies have shown that traumatic brain injury (TBI) significantly reduces cerebral blood flow determined in vivo and reduces vascular reactivity in the pial circulation measured with cranial window preparations. We have now tested the hypothesis that TBI induces these changes by impairing intrinsic contractile activity of cerebral arteries. Anesthetized rats underwent moderate (2.2 atm) and severe (3.0 atm) midline fluid percussion TBI or sham injury following which posterior cerebral or middle cerebral arteries were isolated and isometric force generation was measured. Moderate (n = 5) and severe (n = 3) trauma had no effect on the magnitude of serotonin- or K+-induced force generation or sensitivity to serotonin in arteries isolated within 10 min of TBI. Functional disruption of the endothelium of posterior cerebral arteries isolated 10 min after moderate trauma or sham injury caused a reduction in the active tension response to serotonin that was similar in both groups. Blockade of cyclooxygenase with 5 microM indomethacin had no effect on serotonin-induced force generated by vessels with moderate trauma or in sham-treated rats. Acetylcholine induced an endothelium-dependent relaxation of posterior and middle cerebral arteries; the magnitude of the response was unaffected by moderate TBI. To determine whether prolonged in situ exposure of vessels to the traumatized cerebral milieu could reveal an alteration in intrinsic contractility, posterior cerebral arteries were isolated 30 min after TBI; again, no differences in the tension or relaxation responses were observed. It is concluded that midline fluid percussion TBI did not affect contraction or relaxation of proximal middle or posterior cerebral arteries in rats.
先前的研究表明，创伤性脑损伤（TBI）显著降低了体内测定的脑血流量，并降低了用颅骨开窗制剂测量的软脑膜循环中的血管反应性。我们现在检验了这样一个假设，即TBI通过损害脑动脉的内在收缩活性来诱导这些变化。对麻醉的大鼠进行中度（2.2个大气压）和重度（3.0个大气压）的中线液体冲击性TBI或假损伤，之后分离大脑后动脉或大脑中动脉并测量等长力的产生。中度（n = 5）和重度（n = 3）创伤对TBI后10分钟内分离的动脉中血清素或钾离子诱导的力产生幅度或对血清素的敏感性没有影响。中度创伤或假损伤后10分钟分离的大脑后动脉内皮的功能破坏导致两组对血清素的主动张力反应均降低。用5 microM吲哚美辛阻断环氧化酶对中度创伤血管或假手术处理大鼠中血清素诱导的力没有影响。乙酰胆碱诱导大脑后动脉和大脑中动脉的内皮依赖性舒张；该反应的幅度不受中度TBI的影响。为了确定血管在创伤性脑环境中的长时间原位暴露是否会揭示内在收缩性的改变，在TBI后30分钟分离大脑后动脉；同样，未观察到张力或舒张反应的差异。结论是中线液体冲击性TBI不影响大鼠大脑中动脉近端或大脑后动脉的收缩或舒张。
