中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2011年
8期
1229-1231
,共3页
山楂叶总黄酮%胸主动脉环%一氧化氮
山楂葉總黃酮%胸主動脈環%一氧化氮
산사협총황동%흉주동맥배%일양화담
Hawthorn leaf flavonoids%Thoracic aorta rings%NO
目的 观察山楂叶总黄酮(HLF)对大鼠胸主动脉血管环的作用,并探讨其作用机制.方法 采用大鼠胸主动脉环张力测定法,观察HLF对高浓度KCl(6×10-2mol/L)和去甲肾上腺素(NE,1×10-6mol/L)预收缩的离体大鼠胸主动脉血管环作用;并观察左旋硝基精氨酸甲酯(L-NAME,1×10-5mol/L)和吲哚美辛(1×10-4mol/L)对其作用的影响.结果 HLF(5×10～50×10-3g/L)对高浓度氯化钾(KCl,6×10-2mol/L)预收缩的内皮完整或去内皮的血管环均无明显作用(P＞0.05);对去甲肾上腺素(NE,1×10-6mol/L)预收缩的血管环产生内皮依赖性的舒张作用(P＜0.01);HLF对NE预收缩血管的舒张作用能被L-NAME(1×10-5 mol/L)显著阻断(P＜0.01),而不能被吲哚美辛(1×10-4mol/L)阻断(P＞0.05).结论 HLF对胸主动脉血管有舒张作用,其机制可能是通过抑制受体操纵的钙通道(ROC)的激活而直接抑制细胞外钙内流降低细胞内Ca2+浓度而起作用的;HLF的内皮依赖性舒张作用可能与血管内皮一氧化氮(NO)合成有关.
目的 觀察山楂葉總黃酮(HLF)對大鼠胸主動脈血管環的作用,併探討其作用機製.方法 採用大鼠胸主動脈環張力測定法,觀察HLF對高濃度KCl(6×10-2mol/L)和去甲腎上腺素(NE,1×10-6mol/L)預收縮的離體大鼠胸主動脈血管環作用;併觀察左鏇硝基精氨痠甲酯(L-NAME,1×10-5mol/L)和吲哚美辛(1×10-4mol/L)對其作用的影響.結果 HLF(5×10～50×10-3g/L)對高濃度氯化鉀(KCl,6×10-2mol/L)預收縮的內皮完整或去內皮的血管環均無明顯作用(P＞0.05);對去甲腎上腺素(NE,1×10-6mol/L)預收縮的血管環產生內皮依賴性的舒張作用(P＜0.01);HLF對NE預收縮血管的舒張作用能被L-NAME(1×10-5 mol/L)顯著阻斷(P＜0.01),而不能被吲哚美辛(1×10-4mol/L)阻斷(P＞0.05).結論 HLF對胸主動脈血管有舒張作用,其機製可能是通過抑製受體操縱的鈣通道(ROC)的激活而直接抑製細胞外鈣內流降低細胞內Ca2+濃度而起作用的;HLF的內皮依賴性舒張作用可能與血管內皮一氧化氮(NO)閤成有關.
목적 관찰산사협총황동(HLF)대대서흉주동맥혈관배적작용,병탐토기작용궤제.방법 채용대서흉주동맥배장력측정법,관찰HLF대고농도KCl(6×10-2mol/L)화거갑신상선소(NE,1×10-6mol/L)예수축적리체대서흉주동맥혈관배작용;병관찰좌선초기정안산갑지(L-NAME,1×10-5mol/L)화신타미신(1×10-4mol/L)대기작용적영향.결과 HLF(5×10～50×10-3g/L)대고농도록화갑(KCl,6×10-2mol/L)예수축적내피완정혹거내피적혈관배균무명현작용(P＞0.05);대거갑신상선소(NE,1×10-6mol/L)예수축적혈관배산생내피의뢰성적서장작용(P＜0.01);HLF대NE예수축혈관적서장작용능피L-NAME(1×10-5 mol/L)현저조단(P＜0.01),이불능피신타미신(1×10-4mol/L)조단(P＞0.05).결론 HLF대흉주동맥혈관유서장작용,기궤제가능시통과억제수체조종적개통도(ROC)적격활이직접억제세포외개내류강저세포내Ca2+농도이기작용적;HLF적내피의뢰성서장작용가능여혈관내피일양화담(NO)합성유관.
Objective To investigate the effects and mechanisms of hawthorn leaf flavonoids (HLF) on isolated thoracic aorta in rats. Methods The tension of rat thoracic aorta tings was measured.The effects of HLF on the thoracic aorta preconstricted by potassium chloride ( KCl, 6 × 10-2 mol/L) and norepinephrine (NE, 1 × 10-6 mol/L), as well as the effects of L-nitro arginine methyl ester (L-NAME,1 × 10-5 mol/L) and indomethacin ( 1 × 10-4 mol/L) on the relaxation response of HLF were observed.Results HLF completely relaxed the constriction induced by NE ( 1 × 10 -6 mol/L) in endothelium-intact thoracic aorta ( P ＜ 0. 01 ), but had no effect on those preconstricted aorta rings by a high concentration of KCl (6 × 10-2 mol/L) in endothelium-intact and endothelium-denuded rat aorta (P ＞ 0. 05). The relaxation response of HLF was significantly inhibited by L-NAME (P ＜ 0. 01 ), but not by indomethacin (P ＞0. 05). Conclusion The vasorelaxation induced by HLF in rat aorta rings may involve the reduction of Ca2+ influx through the calcium channels operated by receptor (ROC). The endothelium-dependent relaxation of HLF may be related to the generation of nitric oxide (NO).
