Sawazaki S, Nakamura N, Hamazaki T, Yamazaki K, Urakaze M, Yano S
First Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Japan.
Am J Physiol. 1992 Jun;262(6 Pt 2):H1711-8. doi: 10.1152/ajpheart.1992.262.6.H1711.
During myocardial infarction leukotriene B4 (LTB4) is probably a major determining factor of tissue damage because it can amplify the inflammatory reaction by recruiting leukocytes and degranulating them. Oral administration of eicosapentaenoic acid (EPA) is known to reduce LTB4 production by polymorphonuclear leukocytes (PMNL). However, it takes several weeks for EPA to take effect. In this study, we formulated a trieicosapentaenoyl-glycerol emulsion and infused it into rabbits (0.8 g EPA/kg). In the ex vivo study, the inhibition of LTB4 production by PMNL from EPA-infused rabbits was maximal (32-60% of preinfusion values, P less than 0.01) 6 h after the infusion. There was also a tendency toward reduced LTB4 production 1, 24, and 168 h after the infusion. A lower dose (0.2 g EPA/kg) also reduced LTB4 production (45% of preinfusion values, P less than 0.02) 6 h after the infusion. There was no significant change in LTB4 production in control groups in which soybean oil emulsion was infused instead of EPA. EPA infusion might be useful for reduction of tissue damage in the acute phase of LTB4-related diseases such as acute myocardial infarction.
在心肌梗死期间,白三烯B4(LTB4)可能是组织损伤的主要决定因素,因为它可通过募集白细胞并使其脱颗粒来放大炎症反应。已知口服二十碳五烯酸(EPA)可减少多形核白细胞(PMNL)产生LTB4。然而,EPA生效需要数周时间。在本研究中,我们制备了三亚麻酸甘油酯乳剂并将其注入兔子体内(0.8 g EPA/kg)。在体外研究中,注入EPA的兔子的PMNL产生LTB4受到的抑制在注入后6小时达到最大(为注入前值的32 - 60%,P < 0.01)。在注入后1、24和168小时,LTB4的产生也有减少的趋势。较低剂量(0.2 g EPA/kg)在注入后6小时也可减少LTB4的产生(为注入前值的45%,P < 0.02)。注入大豆油乳剂而非EPA的对照组中,LTB4的产生没有显著变化。注入EPA可能有助于减少LTB4相关疾病如急性心肌梗死急性期的组织损伤。