论文部分内容阅读
目的:研究辣椒素对离体家兔窦房结起搏细胞的电生理效应及其作用机制。方法:应用经典玻璃微电极方法。结果:辣椒素(10 μmol/L)使窦房结起搏细胞的零相最大上升速度(V_(max))由(2.4±0.5)V/s降至(1.7±0.2)V/s(P<0.05);舒张期除极速度(VDD)由(91±34)mV/s降至(70±30)mV/s(P<0.01);起搏放电频率(RPF)由(186±14)beat/min降至(162±10)beat/min(P<0.01);最大舒张电位(MDP)绝对值由(49±3)mV降至(44±2)mV(P<0.01);动作电位幅度(APA)由(55±4)mV降至(49±4)mV(P<0.05)。复极化90％时间(APD_(90))则由(149±21)ms延长至(167±27)ms(P<0.01)。应用辣椒素受体阻断剂钌红(10 μmol/L)对辣椒素的上述电生理效应无影响。提高灌流液中钙离子浓度(5 mmol/L)以及应用L型钙通道开放剂Bay-K-8644(0.5μmol/L)均可抑制辣椒素对起搏细胞的电生理效应。β-肾上腺素能受体激动剂异丙肾上腺素(20 nmol/L)可逆转辣椒素所引起的除极化时间延长和MDP的降低。结论:辣椒素对家兔窦房结细胞有负性变时作用,这些效应可能与其抑制钙离子内流及/或钾离子外流有关,而非由辣椒素受体介导。
Objective: To study the electrophysiological effects of capsaicin on pacemaker cells of sinoatrial node of isolated rabbit and its mechanism. Methods: The classical glass microelectrode method was used. Results: The maximum zero-phase velocity (V max) of the pacemaker cells in the sinoatrial node was decreased from (2.4 ± 0.5) V / s to (1.7 ± 0.2) V / s <0.05). The diastolic depolarization rate (VDD) decreased from 91 ± 34 mV / s to 70 ± 30 mV / s (P <0.01) (P <0.01). The absolute value of MDP decreased from (49 ± 3) mV to (44 ± 2) mV (P <0.01) The amplitude (APA) decreased from (55 ± 4) mV to (49 ± 4) mV (P <0.05). The duration of repolarization 90% (APD 90) prolonged from (149 ± 21) ms to (167 ± 27) ms (P 0.01). The application of capsaicin receptor blocker ruthenium red (10 μmol / L) had no effect on the electrophysiological effects of capsaicin. Increasing the calcium concentration in the perfusate (5 mmol / L) and the L-type calcium channel opener Bay-K-8644 (0.5 μmol / L) could inhibit the electrophysiological effect of capsaicin on the pacemaker cells. Beta-adrenoceptor agonist isoproterenol (20 nmol / L) reverses the prolonged depolarization and MDP reduction induced by capsaicin. CONCLUSION: Capsaicin has a negative potent effect on sinoatrial node cells in rabbits. These effects may be related to its inhibition of calcium influx and / or potassium efflux rather than capsaicin receptor.