Xiao Feng, Arnold Thomas C, Zhang Shu, Brown Carlos, Alexander J Steven, Carden Donna L, Conrad Steven A
Department of Emergency Medicine, Louisiana State University Health Sciences Center, 1501 Kings Highway, Shreveport, LA 71130, USA.
Acad Emerg Med. 2004 Oct;11(10):1001-7. doi: 10.1197/j.aem.2004.05.026.
Brain edema occurs following clinical as well as experimental cardiac arrest (CA) and predicts a poor neurologic outcome. The objective of this study was to determine the expression of cerebral cortex aquaporin (AQP)-4, a member of a family of membrane water-channel proteins, in brain edema formation following normothermic or hypothermic CA.
Twenty-four rats were subjected to time-matched normothermic (N-Sham, 37.5 degrees C +/- 0.5 degrees C, n = 6) or hypothermic (H-Sham, 34 degrees C +/- 0.5 degrees C, n = 6) sham experiments and normothermic (N-CA, n = 6) or hypothermic (H-CA, n = 6) CA induced by asphyxiation for 8 minutes. Hypothermia was induced before CA. The animals were resuscitated with cardiopulmonary resuscitation, ventilation, and epinephrine administration. Brain edema was determined by brain wet-to-dry weight ratio at one hour of resuscitation. AQP4 immunoactivity in the cerebral cortex was determined using immunohistochemical staining and was semiquantified as an intensity of staining with an automated cell imaging system.
Mild hypothermia in the sham experiments did not alter cerebral cortex AQP4 immunoactivity (mean +/- SD) (55.0 +/- 3.7 in H-Sham vs. 53.3 +/- 1.7 in N-Sham, p > 0.05). N-CA resulted in a significant increase in AQP4 immunoactivity (61.8 +/- 4.5) compared with N-Sham (p = 0.01) and H-Sham (p = 0.03). H-CA attenuated AQP4 compared with N-CA (53.4 +/- 1.3, p = 0.01). Brain wet-to-dry weight ratios were 4.41 +/- 0.07 in N-Sham, 4.40 +/- 0.08 in H-Sham (p > 0.05 vs. N-Sham), 4.55 +/- 0.04 in N-CA (p = 0.004 vs. N-Sham; p = 0.005 vs. H-Sham), and 4.43 +/- 0.09 in H-CA (p = 0.02 vs. N-CA; p > 0.05 vs. N-Sham and H-Sham).
Cerebral cortical AQP4 expression is up-regulated after normothermic CA, which is attenuated by hypothermia induced before CA.
临床及实验性心脏骤停（CA）后会发生脑水肿，且预示着神经功能预后不良。本研究的目的是确定膜水通道蛋白家族成员脑皮质水通道蛋白（AQP）-4在常温或低温CA后脑水肿形成过程中的表达情况。
将24只大鼠进行时间匹配的常温（N-假手术组，37.5℃±0.5℃，n = 6）或低温（H-假手术组，34℃±0.5℃，n = 6）假手术实验，以及通过窒息8分钟诱导的常温（N-CA组，n = 6）或低温（H-CA组，n = 6）CA。在CA前诱导低温。动物通过心肺复苏、通气和给予肾上腺素进行复苏。在复苏1小时时通过脑湿重与干重之比来确定脑水肿情况。使用免疫组织化学染色确定脑皮质中AQP4的免疫活性，并通过自动细胞成像系统将其半定量为染色强度。
假手术实验中的轻度低温并未改变脑皮质AQP4免疫活性（均值±标准差）（H-假手术组为55.0±3.7，N-假手术组为53.3±1.7，p>0.05）。与N-假手术组（p = 0.01）和H-假手术组（p = 0.03）相比，N-CA导致AQP4免疫活性显著增加（61.8±4.5）。与N-CA相比，H-CA使AQP4减弱（53.4±1.3，p = 0.01）。脑湿重与干重之比在N-假手术组为4.41±0.07，H-假手术组为4.40±0.08（与N-假手术组相比p>0.05），N-CA组为4.55±0.04（与N-假手术组相比p = 0.004；与H-假手术组相比p = 0.005），H-CA组为4.43±0.09（与N-CA组相比p = 0.02；与N-假手术组和H-假手术组相比p>0.05）。
常温CA后脑皮质AQP4表达上调，而在CA前诱导的低温可使其减弱。
