Talmor D, Roytblat L, Artru A A, Yuri O, Koyfman L, Katchko L, Shapira Y
Division of Anesthesiology, Soroka Medical Center, Faculty of Health Science, Ben Gurion University of the Negev, Beer-Sheva, Israel.
Anesth Analg. 1998 Sep;87(3):574-8. doi: 10.1097/00000539-199809000-00014.
Phenylephrine-induced hypertension (increase of 30-35 mm Hg for 15 min) is reported to increase cerebral perfusion pressure and collateral flow to ischemic areas of the brain in a rat model of focal cerebral ischemia. In the present study, we examined whether phenylephrine-induced hypertension of similar magnitude and duration was beneficial in a rat model of closed head trauma (CHT). Forty-eight rats were randomized into four experimental conditions: CHT at time 0 min (yes/no), plus phenylephrine-induced hypertension (increase of 30-35 mm Hg for 15 min) at 65 min (yes/no). CHT was delivered using a weight-drop device (0.5 J). Outcome measures were neurological severity score (NSS) at 1, 4, and 24 h, and brain tissue specific gravity (microgravimetry) and injury volume (2,3,5-triphenyltetrazoium chloride) at 24 h. After CHT, NSS at 24 h (median +/- range) and brain tissue specific gravity (mean +/- SD, injured hemisphere) were 7+/-2 and 1.033+/-0.007 without phenylephrine and 8+/-2 and 1.035+/-0.005 with phenylephrine (P = 0.43), respectively. Tissue injury volume (mean +/- SD) was 335+/-92 mm3 without phenylephrine and 357+/-154 mm3 with phenylephrine (P > 0.62). The results of our study indicate that postinjury treatment with 15 min of phenylephrine-induced hypertension does not attenuate brain edema, reduce tissue injury volume, or improve neurological outcome after CHT in rats.
Phenylephrine-induced hypertension is reported to increase cerebral perfusion pressure and blood flow in a rat model of focal cerebral ischemia. In our study, phenylephrine-induced hypertension did not decrease brain edema or tissue injury volume or improve neurological outcome in a rat model of closed head trauma.
据报道,在局灶性脑缺血大鼠模型中,去氧肾上腺素诱发的高血压(15分钟内血压升高30 - 35毫米汞柱)可增加脑灌注压以及流向脑缺血区域的侧支血流。在本研究中,我们检测了类似幅度和持续时间的去氧肾上腺素诱发的高血压在闭合性颅脑损伤(CHT)大鼠模型中是否有益。48只大鼠被随机分为四种实验条件:在0分钟时进行CHT(是/否),加上在65分钟时去氧肾上腺素诱发的高血压(15分钟内血压升高30 - 35毫米汞柱,是/否)。使用重量下落装置(0.5焦耳)造成CHT。观察指标为1、4和24小时时的神经严重程度评分(NSS),以及24小时时的脑组织比重(微量比重测定法)和损伤体积(2,3,5 - 三苯基氯化四氮唑)。CHT后,在未使用去氧肾上腺素时,24小时时的NSS(中位数±范围)和脑组织比重(平均±标准差,损伤半球)分别为7±2和1.033±0.007,使用去氧肾上腺素时分别为8±2和1.035±0.005(P = 0.43)。未使用去氧肾上腺素时组织损伤体积(平均±标准差)为335±92立方毫米,使用去氧肾上腺素时为357±154立方毫米(P > 0.62)。我们的研究结果表明,损伤后用15分钟去氧肾上腺素诱发高血压进行治疗并不能减轻大鼠CHT后的脑水肿、减少组织损伤体积或改善神经功能结局。
据报道,在局灶性脑缺血大鼠模型中,去氧肾上腺素诱发的高血压可增加脑灌注压和血流量。在我们的研究中,去氧肾上腺素诱发的高血压并未降低闭合性颅脑损伤大鼠模型中的脑水肿或组织损伤体积,也未改善神经功能结局。