本文为观察瑞芬太尼对自发性高血压大鼠及Wistar-Kyoto大鼠离体脑基底动脉的作用,并探讨其作用机制。在急性分离的大鼠脑基底动脉上,应用压力肌动图技术,观察不同浓度RMF(10-10-10-5mol/L)对内皮非依赖的血管收缩剂苯肾上腺素预收缩的血管直径的变化,并作出比较。结果显示,RMF呈浓度依赖性舒张SHR及WKY大鼠脑基底动脉P〈0.05,n=5);在相同浓度下,与WKY大鼠相比,RMF对SHR脑基底动脉舒张作用较弱(P〈0.05,n=5);预灌流10-3mol/L的BKCa通道阻断剂四乙胺后,不同浓度的RMF对SHR及WKY大鼠脑基底动脉的舒张幅度减小,拟合曲线下移,且具有统计学差异(P〈0.05,n=6-7)。由此可知:RMF可能是通过激活BKCa通道呈浓度依赖性舒张大鼠脑基底动脉,且RMF对SHR脑基底动脉的舒张反应弱于WKY大鼠。
To observe the effects of remifentanil(RMF) on isolated cerebral basilar artery of spontaneously hypertensive rats(SHR) and Wistar- Kyoto(WKY) rats, and then to explore the mechanism. Pressure myograph system was used to observe and compare with the diameter changes of different concentrations of RMF(10- 10- 10- 5mol/L) on freshly isolated cerebral basilar artery, which was preshrunk by Phenylephrine(PE, endothelium independent vasoconstrictor). The results showed that cerebral basilar artery of SHR and WKY rats was relaxed by RMF in a concentration- dependent manner(P0.05, n=5). Compared to WKY rats, the diastolic effect of RMF on SHR was weaker at the same concentration(P0.05, n=5). Pre- perfused by 10- 3mol/L tetraethylammonium(TEA, BKCachannel blocker), the diastolic amplitudes of RMF on SHR and WKY rats decreased and the fitting curves shift down(P0.05, n=6- 7). These results suggest RMF plays a diastolic role in cerebral basilar artery in a dose- dependent manner, probably by activating BKCachannels, and SHR has a less diastolic reaction on RMF than WKY rats.