Effect of proximal arterial perfusion pressure on function, spinal cord blood flow, and histopathologic changes after increasing intervals of aortic occlusion in the rat
Effect of proximal arterial perfusion pressure on function, spinal cord blood flow, and histopathologic changes after increasing intervals of aortic occlusion in the rat
复制标题
DOI：
10.1161/01.str.27.10.1850
复制
发表时间：
1996-10-01
期刊：
影响因子：
8.3
通讯作者：
Marsala, M
中科院分区：
文献类型：
--
作者：
Taira, Y;Marsala, M
背景和目的胸主动脉交叉夹紧会导致脊髓缺血和显着的全身性高血压。使用短暂性脊髓缺血的大鼠模型，我们检查了控制近端主动脉血压对脊髓血流 (SCBF)、神经功能障碍以及主动脉闭塞间隔增加后脊髓组织病理学变化的影响。 方法 通过将 2F Fogarty 导管放入大鼠胸主动脉，使其膨胀来诱导主动脉闭塞 用氟烷（1.5%）麻醉。尾动脉插管以监测远端动脉压（DAP）。为了测量 SCBF，将激光探针植入 L-2 椎骨的硬膜外腔。为了控制近端动脉压 (PAP)，左颈动脉插入 20 号聚四氟乙烯导管，以便在主动脉闭塞期间从外周血库抽血和输血。在一项调查研究中，以 6、10、15、30 或 40 分钟的间隔在单个动物中诱发脊髓缺血，并将 PAP 控制在 40、60、80 和 110 至 120 毫米汞柱。在第二个系列中，在 PAP 控制在 40 mm Hg 的情况下，在动物组中诱导缺血 0、6、8、10 和 12 分钟。缺血后，动物存活2至3天。在此恢复期间，对神经功能进行评估，然后对脊髓进行定量组织病理学检查。 结果 在正常情况下，交叉夹紧会产生急性近端高血压（125 至 135 mm Hg），DAP 下降至 15 至 22 mm Hg，SCBF 下降至基线值的 7% 至 11%。通过使用外部储液器，可以消除近端高血压并将 PAP 维持在目标压力。在这些研究中，在缺血间隔和 PAP 值的以下组合下，观察到再灌注 24 至 48 小时后影响灰质中心部分的典型触觉异常疼痛、痉挛性截瘫和坏死变化综合征：>10 分钟/40 mm Hg；>10 分钟/40 mm Hg； >12 分钟/60 毫米汞柱； >16 分钟/80 毫米汞柱；且 >30 分钟/不受控制。降低 PAP 导致残余 SCBF 相应减少。在 PAP 为 40 mm Hg、闭塞间隔为 6、8、10 和 12 分钟时进行的系统研究表明，10 分钟和 12 分钟缺血后，100% 的大鼠截瘫，并且这些大鼠表现出相应的脊柱组织病理学迹象。 结论 本研究表明，全身性缺血性低血压 (40 mm Hg) 显着增强短暂性主动脉粥样硬化后的神经功能障碍。 闭塞。观察到的作用机制可能包括主动脉闭塞期间侧支血流的消除和/或再灌注期间随之而来的灌注不足的增强。这些数据表明，应监测和/或控制闭塞期间的 PAP，因为它是确定脊髓缺血模型结果的关键变量。
Background and Purpose Cross-clamping of the thoracic aorta results in spinal cord ischemia and prominent systemic hy hypertension. Using a rat model of transient spinal cord ischemia, we examined the effects of manipulation of proximal aortic blood pressure on spinal cord blood flow (SCBF), neurological dysfunction, and changes in spinal histopathology after increasing intervals of aortic occlusion.Methods Aortic occlusion was induced by the inflation of a 2F Fogarty catheter placed into the thoracic aorta in rats anesthetized with halothane (1.5%). A tail artery was cannulated to monitor distal arterial pressure (DAP). To measure SCBF, a laser probe was implanted into the epidural space of the L-2 vertebra. To manipulate proximal arterial pressure (PAP), the left carotid artery was cannulated with a 20-gauge polytetrafluoroethylene catheter to permit blood withdrawal and infusion from a peripheral reservoir during aortic occlusion. In a survey study, spinal cord ischemia was induced in single animals at intervals of 6, 10, 15, 30, or 40 minutes with PAP controlled at 40, 60, 80, and 110 to 120 mm Hg. In a second series, ischemia was induced in groups of animals for 0, 6, 8, 10, and 12 minutes with PAP controlled at 40 mm Hg. After ischemia the animals survived for 2 to 3 days. During this recovery period, neurological functions were evaluated, followed by quantitative histopathology of the spinal cord.Results Under normal conditions, cross-clamping yields an acute proximal hypertension (125 to 135 mm Hg), a fall of DAP to 15 to 22 mm Hg, and a decrease in SCBF to 7% to 11% of baseline values. With the use of the external reservoir, proximal hypertension could be abolished and the PAP maintained at target pressures. In these studies a typical syndrome of tactile allodynia, spastic paraplegia, and necrotic changes affecting the central part of the gray matter after 24 to 48 hours of reperfusion was observed at the following combinations of ischemic intervals and PAP values: >10 minutes/40 mm Hg; >12 minutes/60 mm Hg; >16 minutes/80 mm Hg; and >30 minutes/uncontrolled. Lowering PAP resulted in a corresponding decrease in residual SCBF. Systematic studies at a PAP of 40 mm Hg at occlusion intervals of 6, 8, 10, and 12 minutes revealed that 100% of rats were paraplegic after 10- and 12-minute ischemia, and these rats showed corresponding signs of spinal histopathology.Conclusions The present study shows that systemic intraischemic hypotension (40 mm Hg) significantly potentiates neurological dysfunction after transient aortic occlusion. The mechanism of the observed effect may include elimination of collateral flow during aortic occlusion and/or consequent potentiation of hypoperfusion during reperfusion. These data indicate that PAP during occlusion should be monitored and/or controlled because it is a critical variable in the determination of outcome in this model of spinal cord ischemia.