Suppr超能文献

丙泊酚可减轻大鼠心脏在体缺血再灌注损伤。

Propofol attenuates ischaemia-reperfusion injury in the rat heart in vivo.

作者信息

Kobayashi I, Kokita N, Namiki A

机构信息

Asahikawa Red Cross Hospital, Department of Anesthesiology, Asahikawa, Hokkaido, Japan.

出版信息

Eur J Anaesthesiol. 2008 Feb;25(2):144-51. doi: 10.1017/S0265021507001342. Epub 2007 Aug 13.

Abstract

BACKGROUND

We have previously demonstrated, in the isolated rat heart, that propofol attenuates hydrogen peroxide-induced damage and ischaemia-reperfusion injury, and that the beneficial effect of propofol is correlated with reduction of the lipid peroxidation. This study was designed to evaluate whether propofol has a cardioprotective effect against ischaemia-reperfusion injury in a rat model in vivo.

METHODS

Adult rats were anaesthetized with pentobarbital 10 mg kg(-1) h(-1) alone (control group), pentobarbital 10 or 20 mg kg(-1) h(-1) + Intralipid as a vehicle (Pent-10, Pent-20 group), propofol 10 or 20 mg kg(-1) h(-1) (Prop-10, Prop-20 group) intravenously throughout the experiment. The left anterior descending coronary artery was occluded for 30 min followed by 120 min of reperfusion. Infarct size was determined at the end of reperfusion. The tissue concentration of malondialdehyde was measured at 30 min after reperfusion to evaluate lipid peroxidation.

RESULTS

The infarct sizes (% of area at risk) were significantly smaller in the Prop-10 (54 +/- 11%; P < 0.01 vs. control) and Prop-20 (39 +/- 8%; P < 0.01 vs. control) groups than in the control (68 +/- 9%), Pent-10 (69 +/- 13%) and Pent-20 (68 +/- 14%) groups (n = 12). In the Pent-10 and Pent-20 groups, ischaemia-reperfusion produced significant increases in the values for tissue malondialdehyde (0.72 +/- 0.24 micromol mg protein-1; P < 0.05 and 0.63 +/- 0.33 micromol mg protein-1; P < 0.05 vs. 0.46 +/- 0.22 micromol mg protein-1 in non-ischaemic hearts, n = 8). However, the values of malondialdehyde in the Prop-10 and -20 groups were suppressed by 41% and 63%, respectively, compared with the Pent-10 group (P < 0.01).

CONCLUSION

Our results suggest that propofol could be cardioprotective against ischaemia-reperfusion injury dose dependently in a rat model in vivo and that the beneficial action of propofol may be correlated with its antioxidant effect.

摘要

背景

我们之前在离体大鼠心脏中已证明,丙泊酚可减轻过氧化氢诱导的损伤和缺血再灌注损伤,且丙泊酚的有益作用与脂质过氧化反应的降低相关。本研究旨在评估丙泊酚在大鼠体内模型中对缺血再灌注损伤是否具有心脏保护作用。

方法

成年大鼠在整个实验过程中分别静脉注射以下药物:仅10 mg·kg⁻¹·h⁻¹的戊巴比妥(对照组);10或20 mg·kg⁻¹·h⁻¹的戊巴比妥 + 作为溶媒的脂肪乳剂(戊巴比妥10组、戊巴比妥20组);10或20 mg·kg⁻¹·h⁻¹的丙泊酚(丙泊酚10组、丙泊酚20组)。左冠状动脉前降支闭塞30分钟,随后再灌注120分钟。在再灌注结束时测定梗死面积。在再灌注30分钟后测量丙二醛的组织浓度以评估脂质过氧化反应。

结果

丙泊酚10组(54 ± 11%;与对照组相比P < 0.01)和丙泊酚20组(39 ± 8%;与对照组相比P < 0.01)的梗死面积(危险区域面积的百分比)显著小于对照组(68 ± 9%)、戊巴比妥10组(69 ± 13%)和戊巴比妥20组(68 ± 14%)(n = 12)。在戊巴比妥10组和戊巴比妥20组中,缺血再灌注使组织丙二醛值显著升高(0.72 ± 0.24 μmol·mg蛋白⁻¹;P < 0.05和0.63 ± 0.33 μmol·mg蛋白⁻¹;与非缺血心脏中的0.46 ± 之22 μmol·mg蛋白⁻¹相比P < 0.05,n = 8)。然而,与戊巴比妥10组相比,丙泊酚10组和丙泊酚20组的丙二醛值分别降低了41%和63%(P < 0.01)。

结论

我们的结果表明,在大鼠体内模型中丙泊酚对缺血再灌注损伤具有剂量依赖性的心脏保护作用,且丙泊酚的有益作用可能与其抗氧化作用相关。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验