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目的探索猪的冠状动脉中,钙激活钾通道(Calcium-activated potassium channels,K_Ca)在内皮源性超极化因子(Endothelium-Derived Hyperpolarizing Factor,EDHF)介导的血管舒张中的作用。方法 K_Ca通常分为三类:大电导K_Ca(Large-Conductance K_Ca,BK_Ca),中电导K_Ca(Intermediate-Conductance K_Ca,IK_Ca)和小电导K_Ca(Small-Conductance K_Ca,SK_Ca),因此根据加入K_Ca阻滞剂的不同,将血管环分为对照组(不加入K_Ca阻滞剂),Charybodotoxin(BK_Ca和IK_Ca通道阻断剂)组,Apamin(SK_Ca通道阻断剂)组,Charybodotoxin+Apamin组,Iberiotoxin(BK_Ca通道阻断剂)组,每组血管环n=6。采用器官槽法,所有血管环平衡1h后,对照组加入7umol/L环加氧酶阻滞剂吲哚美辛(Indomethacin,Indo)和300 umol/L一氧化氮合酶阻滞剂N-硝基-L-精氨酸(N-nitro-L-arginine,L-NNA),实验组在加入Indo和L-NNA的基础上分别或联合应用BK_Ca、IK_Ca和SK_Ca的阻断剂,水浴30min后,记录由前列腺素F2α(Prostaglandin F2α,U46619)及缓激肽(Bradykinin,BK)引起的血管收缩和舒张反应。结果 Charybodotoxin组,Charybodotoxin+Apamin组和Iberiotoxin组中EDHF介导的内皮依赖性血管最大舒张百分比与对照组相比显著下降,且Charybodotoxin组的最大舒张百分比较Charybodotoxin+Apamin组更低,但Apamin组血管环最大舒张百分比与对照组相比无统计学意义。结论研究证明BK_Ca和SK_Ca通道均在EDHF介导的舒张功能中发挥一定作用,且以协同的方式作用于血管,IK_Ca通道也可能发挥了一定的作用。
Objective To explore the role of Calcium-activated potassium channels (K_Ca) in the vasodilation induced by Endothelium-Derived Hyperpolarizing Factor (EDHF) in porcine coronary arteries. Methods K_Ca is generally divided into three categories: Large-Conductance K_Ca (BK_Ca), Intermediate-Conductance K_Ca (IK_Ca) and Small-Conductance K_Ca (SK_Ca). Therefore, Vascular rings were divided into control group (without K_Ca blocker), Charybodotoxin (BK_Ca and IK_Ca channel blockers) group, Apamin (SK_Ca channel blocker) group, Charybodotoxin + Apamin group, Iberiotoxin Channel blocker) group, n = 6 in each group. In the control group, 7umol / L cyclooxygenase inhibitor Indomethacin (Indo) and 300umol / L nitric oxide synthase blocker N-nitro L-arginine (N-nitro-L-arginine, L-NNA). The experimental groups were treated with BK_Ca, IK_Ca and SK_Ca blockers respectively after adding Indo and L-NNA, Vasoconstrictive and vasodilatory responses to prostaglandin F2α (U46619) and bradykinin (BK) were recorded. Results The maximum percentage of EDHF-mediated endothelium-dependent vasodilation in Charybodotoxin, Charybodotoxin + Apamin and Iberiotoxin groups was significantly lower than that in control group, and the maximum relaxation percentage in Charybodotoxin group was lower than that in Charybodotoxin + Apamin group. However, The maximum percentage of diastolic relaxation was not statistically significant compared with the control group. Conclusions It has been demonstrated that both BK_Ca and SK_Ca channels play a role in EDHF-mediated diastolic function and act in a synergistic manner on blood vessels. IK_Ca channels may also play a role.