L-arginine and superoxide dismutase prevent or reverse cerebral hypoperfusion after fluid-percussion traumatic brain injury
L-arginine and superoxide dismutase prevent or reverse cerebral hypoperfusion after fluid-percussion traumatic brain injury
复制标题
DOI：
10.1089/neu.1997.14.223
复制
发表时间：
1997-04-01
影响因子：
4.2
通讯作者：
Prough, DS
中科院分区：
文献类型：
--
作者：
DeWitt, DS;Smith, TG;Prough, DS
为了确定用l -精氨酸或超氧化物歧化酶（SOD）治疗是否能有效减少创伤性脑损伤（TBI）后的脑灌注不足，我们用激光多普勒血流仪（LDF）测量了中度（2.2 atm）液体冲击（FP） TBI前后大鼠的脑血流量（CBF）。用异氟醚麻醉大鼠，然后用风冷钻头削薄颅骨，为中线FP TBI和LDF做准备。然后将大鼠随机分为假性损伤、假性损伤+ l -精氨酸（100 mg/kg，假性脑损伤后5分钟）、TBI + 0.9% NaCl、TBI + l -精氨酸（100 mg/kg，脑损伤后5分钟）、TBI + SOD（脑损伤前24000 U/kg +脑损伤后15分钟1600单位/kg/min）或TBI + SOD和l -精氨酸。第二组大鼠给予脑外伤加生理盐水、L-精氨酸或d -精氨酸（100 mg/kg，脑外伤后5分钟）。在治疗和TBI或假性损伤后，使用LDF连续测量CBF 2小时，CBF以TBI后2小时损伤前基线的百分比表示。用生理盐水或d -精氨酸治疗的大鼠表现出持续整个监测期间的CBF显著减少。单独使用l -精氨酸或与SOD联合使用的大鼠在TBI后CBF没有下降。脑外伤后15分钟内，sod治疗组的CBF显著下降，但在45分钟后恢复到基线水平。这些研究表明，脑外伤后给予l -精氨酸而非d -精氨酸可预防创伤后灌注不足，并且SOD预处理可在短时间灌注不足后恢复CBF。
To determine whether treatment with L-arginine or superoxide dismutase (SOD) would prove effective in reducing cerebral hypoperfusion after traumatic brain injury (TBI), we measured cerebral blood flow (CBF) using laser Doppler flowmetry (LDF) in rats treated before or after moderate (2.2 atm) fluid-percussion (FP) TBI. Rats were anesthetized with isoflurane and prepared for midline FP TBI and then for LDF by thinning the calvaria using an air-cooled drill. Rats were then randomly assigned to receive sham injury, sham injury plus L-arginine (100 mg/kg, 5 min after sham TBI), TBI plus 0.9 % NaCl, TBI plus L-arginine (100 mg/kg, 5 min post-TBI), TBI plus SOD (24,000 U/kg pre-TBI + 1600 units/kg/min for 15 min after TBI), or TBI plus SOD and L-arginine. A second group of rats received TBI plus saline, L-, or D-arginine (100 mg/kg, 5 min after-TBI). After treatment and TBI or sham injury, CBF was measured continuously using LDF for 2 h and CBF was expressed as a percent of the preinjury baseline for 2 h after TBI. Rats treated with saline or D-arginine exhibited significant reductions in CBF that persisted throughout the monitoring period. Rats treated with L-arginine alone or in combination with SOD exhibited no decreases in CBF after TBI. CBF in the SOD-treated group decreased significantly within 15 min after TBI but returned to baseline levels by 45 min after TBI. These studies indicate that L-arginine but not D-arginine administered after TBI prevents posttraumatic hypoperfusion and that pretreatment with SOD will restore CBF after a brief period of hypoperfusion.