Kolbitsch C, Hörmann C, Schmidauer C, Ortler M, Burtscher J, Benzer A
Department of Anesthesia, University of Innsbruck, Austria.
J Neurosurg Anesthesiol. 1997 Oct;9(4):313-5. doi: 10.1097/00008506-199710000-00004.
Investigations on the effects of opioids on cerebrovascular dynamics have repeatedly demonstrated mild to moderate increases in cerebral blood flow velocity in the middle cerebral artery (CBFVMCA), cerebral blood flow, and cerebrospinal fluid pressure in humans and animals. However, the influence of hypocapnia on these fentanyl effects has not been investigated. We compared mean CBFVMCA during normo- and hypocapnia before and after administration of fentanyl (2.5 micrograms/kg i.v.) in 20 awake humans. During normocapnia (end-tidal carbon dioxide [ETCO2] 40 mmHg) fentanyl significantly increased mean CBFVMCA (60 +/- 10 cm/s vs. 81 +/- 12 cm/s [mean +/- SD]; p < 0.01), whereas during hypocapnia (ETCO2 25 mmHg) mean CBFVMCA values were identical (40 +/- 7 cm/s vs. 40 +/- 7 cm/s) before and after fentanyl administration. These results confirm previous findings that administration of fentanyl increases CBFVMCA, but, more importantly, clearly indicate that hypocapnia reverses this potentially undesirable effect.
关于阿片类药物对脑血管动力学影响的研究反复表明,在人类和动物中,大脑中动脉的脑血流速度(CBFVMCA)、脑血流量以及脑脊液压力会出现轻度至中度升高。然而,低碳酸血症对这些芬太尼效应的影响尚未得到研究。我们比较了20名清醒人类静脉注射芬太尼(2.5微克/千克)前后在正常碳酸血症和低碳酸血症期间的平均CBFVMCA。在正常碳酸血症(呼气末二氧化碳[ETCO2] 40 mmHg)期间,芬太尼显著增加了平均CBFVMCA(60±10厘米/秒对81±12厘米/秒[平均值±标准差];p<0.01),而在低碳酸血症(ETCO2 25 mmHg)期间,芬太尼给药前后平均CBFVMCA值相同(40±7厘米/秒对40±7厘米/秒)。这些结果证实了先前的发现,即芬太尼给药会增加CBFVMCA,但更重要的是,明确表明低碳酸血症可逆转这种潜在的不良效应。