Propofol inhibits human neutrophil functions

Propofol inhibits human neutrophil functions
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DOI:
10.1097/00000539-199809000-00039
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发表时间:
1998-09-01
影响因子:
5.7
通讯作者:
Niwa, Y
Niwa, Y
中科院分区:
医学2区
文献类型:
--
作者:
Mikawa, K;Akamatsu, H;Niwa, Y

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中性粒细胞在宿主的抗菌防御机制和组织损伤的发病机制中起重要作用。据报道,丙泊酚会损害中性粒细胞产生活性氧。我们研究了丙泊酚(2,6-二异丙基苯酚),在临床相关的浓度和在10和100倍的浓度,对人体中性粒细胞功能的几个方面,使用体外系统的影响。丙泊酚以剂量依赖性方式显著抑制中性粒细胞的趋化性、吞噬作用和活性氧(ROS)(O-2(-)、H2 O2、OH)产生。在临床相关浓度下,丙泊酚抑制了这些中性粒细胞功能,但没有减少无细胞(黄嘌呤-黄嘌呤氧化酶)系统产生的ROS。N-甲酰-L-甲硫氨酰-L-亮氨酰-L-苯丙氨酸刺激的中性粒细胞胞内钙浓度升高被丙泊酚剂量依赖性地减弱。这种对中性粒细胞[Ca 2 +](i)的降低作用可能是丙泊酚抑制中性粒细胞功能的机制之一。中性粒细胞在抗菌宿主防御系统和组织损伤中起着关键作用。我们发现,在临床相关浓度,异丙酚损害中性粒细胞功能。进一步的研究可能会确定这种在体外观察到的损伤是否会导致临床免疫抑制。
Neutrophils play important roles in the antibacterial host defense mechanism and in the pathogenesis of tissue injury. Propofol has been reported to impair the production of reactive oxygen species from neutrophils. We examined the effect of propofol (2,6-diisopropylphenol), at clinically relevant concentrations and at 10 and 100 times this concentration, on several aspects of human neutrophil functions using an in vitro system. Propofol significantly inhibited chemotaxis, phagocytosis, and reactive oxygen species (ROS) (O-2(-), H2O2, OH) production of neutrophils in a dose-dependent manner. At clinically relevant concentrations, propofol suppressed these neutrophil functions, but it did not decrease ROS generation by the cell-free (xanthine-xanthine oxidase) system. Increase in intracellular calcium concentrations in neutrophils stimulated by N-formyl-L-methionyl-L-leucyl-L-phenylalanine was dose-dependently attenuated by propofol. This decreasing effect on [Ca2+](i) in neutrophils may represent one of the mechanisms responsible for the inhibition of neutrophil functions by propofol. implications: Neutrophils play a pivotal role in the antibacterial host defense system and tissue injury. We found that at clinically relevant concentrations, propofol impaired neutrophil functions. Further studies may determine whether this impairment,observed in vitro, leads to clinical immunological suppression.