Pretreatment with simvastatin reduces lung injury related to intestinal ischemia-reperfusion in rats

被引:76
作者
Pirat, A
Zeyneloglu, P
Aldemir, D
Yücel, M
Özen, Z
Candan, S
Arslan, G
机构
[1] Baskent Univ, Fac Med, Dept Anesthesiol, TR-06490 Ankara, Turkey
[2] Baskent Univ, Fac Med, Dept Biochem, TR-06490 Ankara, Turkey
[3] Baskent Univ, Fac Med, Dept Pathol, TR-06490 Ankara, Turkey
关键词
D O I
10.1213/01.ane.0000189554.41095.98
中图分类号
R614 [麻醉学];
学科分类号
100217 ;
摘要
In this rat model study we evaluated whether Pretreatment with simvastatin affects the severity of acute lung injury caused by intestinal ischemia-reperfusion (I/R). Twenty-four animals were randomly allocated to three equal groups (sham, control, simvastatin). The simvastatin group was pretreated with simvastatin 10 mg (.) kg(-1) (.) day(-1) for 3 days, whereas the other groups received placebo. The simvastatin and control groups underwent 60 min of superior mesenteric artery occlusion and 90 min of reperfusion. Compared with the simvastatin group, the control group exhibited significantly more severe intestinal I/R-induced acute lung injury, as indicated by lower PaO2 and oxygen saturation (P = 0.01 and P = 0.005, respectively) and higher mean values for neutrophil infiltration of the lungs (P = 0.003), total lung histopathologic injury score (P = 0.003), lung wet-to-dry weight ratio (P = 0.009), and lung-tissue malondialdehyde levels (P = 0.016). The control and simvastatin groups had similar serum levels and similar bronchoalveolar lavage fluid levels of cytokines (interleukin-1, interleukin-6, and tumor necrosis factor-alpha) and P-selectin at all measurements, except for a significantly higher level of bronchoalveolar lavage fluid P-selectin in the control group (P = 0.006). Pretreatment with simvastatin reduces the severity of acute lung injury induced by intestinal I/R in rats.
引用
收藏
页码:225 / 232
页数:8
相关论文
共 37 条
[1]   Neutrophils and acute lung injury [J].
Abraham, E .
CRITICAL CARE MEDICINE, 2003, 31 (04) :S195-S199
[2]   Treatment of ARDS [J].
Brower, RG ;
Ware, LB ;
Berthiaume, Y ;
Matthay, MA .
CHEST, 2001, 120 (04) :1347-1367
[3]  
Buege J A, 1978, Methods Enzymol, V52, P302
[4]   Interleukin-1 in ischemia-reperfusion acute lung injury [J].
Chang, DM ;
Hsu, K ;
Ding, YA ;
Chiang, CH .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1997, 156 (04) :1230-1234
[5]   New insights into the pharmacodynamic and pharmacokinetic properties of statins [J].
Corsini, A ;
Bellosta, S ;
Baetta, R ;
Fumagalli, R ;
Paoletti, R ;
Bernini, F .
PHARMACOLOGY & THERAPEUTICS, 1999, 84 (03) :413-428
[6]   Low-density lipoprotein-independent effects of statins [J].
Davignon, J ;
Laaksonen, R .
CURRENT OPINION IN LIPIDOLOGY, 1999, 10 (06) :543-559
[7]   HMG-CoA reductase inhibitors regulate inflammatory transcription factors in human endothelial and vascular smooth muscle cells [J].
Dichtl, W ;
Dulak, J ;
Frick, M ;
Alber, HF ;
Schwarzacher, SP ;
Ares, MPS ;
Nilsson, J ;
Pachinger, O ;
Weidinger, F .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2003, 23 (01) :58-63
[8]   In vivo anti-inflammatory effect of statins is mediated by nonsterol mevalonate products [J].
Diomede, L ;
Albani, D ;
Sottocorno, M ;
Donati, MB ;
Bianchi, M ;
Fruscella, P ;
Salmona, M .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2001, 21 (08) :1327-1332
[9]   Atorvastatin therapy in hypercholesterolemic patients suppresses cellular uptake of oxidized-LDL by differentiating monocytes [J].
Fuhrman, B ;
Koren, L ;
Volkova, N ;
Keidar, S ;
Hayek, T ;
Aviram, M .
ATHEROSCLEROSIS, 2002, 164 (01) :179-185
[10]   Statins and bone formation [J].
Garrett, IR ;
Gutierrez, G ;
Mundy, GR .
CURRENT PHARMACEUTICAL DESIGN, 2001, 7 (08) :715-736