CAJ | 학술논문

目的：研究慢性间歇性低压低氧( CIHH)对丹皮酚舒张大鼠离体胸主动脉环作用的影响，并探讨其可能的机制。方法♂ SD大鼠，随机分为CIHH组和常氧对照组。 CIHH大鼠给予28 d相当于海拔5000米高度，每天6 h的CIHH 处理；制备胸主动脉环，将动脉环置于浴槽内，恒温灌流、并记录其舒缩活动。结果 CIHH 对去甲肾上腺素( NE )和KCl引起的大鼠离体血管收缩活动无影响；CIHH增强了丹皮酚舒张大鼠离体胸主动脉环的作用；在CIHH组，丹皮酚舒张大鼠离体血管的作用可被心得安、格列苯脲和L-NAME部分阻断，丹皮酚抑制NE诱发的细胞内钙和外钙性收缩，而在正常氧组，未出现格列苯脲的阻断效应和对细胞内钙性收缩的抑制效应。吲哚美辛对丹皮酚舒张正常氧和 CIHH大鼠血管的效应均无阻断作用。结论 CIHH增强了丹皮酚舒张大鼠离体胸主动脉环的作用，推测其机制是增强了与正常氧相同的作用机制，还通过激活ATP敏感性K+通道和抑制内钙释放而发挥作用。
목적：연구만성간헐성저압저양( CIHH)대단피분서장대서리체흉주동맥배작용적영향，병탐토기가능적궤제。방법♂ SD대서，수궤분위CIHH조화상양대조조。 CIHH대서급여28 d상당우해발5000미고도，매천6 h적CIHH 처리；제비흉주동맥배，장동맥배치우욕조내，항온관류、병기록기서축활동。결과 CIHH 대거갑신상선소( NE )화KCl인기적대서리체혈관수축활동무영향；CIHH증강료단피분서장대서리체흉주동맥배적작용；재CIHH조，단피분서장대서리체혈관적작용가피심득안、격렬분뇨화L-NAME부분조단，단피분억제NE유발적세포내개화외개성수축，이재정상양조，미출현격렬분뇨적조단효응화대세포내개성수축적억제효응。신타미신대단피분서장정상양화 CIHH대서혈관적효응균무조단작용。결론 CIHH증강료단피분서장대서리체흉주동맥배적작용，추측기궤제시증강료여정상양상동적작용궤제，환통과격활ATP민감성K+통도화억제내개석방이발휘작용。
Aim To investigate the effect of chronic intermittent hypobaric hypoxia ( CIHH) on the paeonol induced vasomotion of isolated rat ’ s thoracic aorta rings and its underlying mechanisms. Methods Spra-gue-Dawlay ( SD ) rats were randomly divided into 2 groups: control group ( CON ) and CIHH treatment group ( CIHH) . CIHH rats were exposed to hypoxia in a hypobaric chamber simulating 5 000 m altitude, 6 hours daily for 28 days. CON rats lived in the same en-vironment as CIHH animals except hypoxia. Organ bath technique was used to observe the effect of pae-onol on isolated thoracic aorta rings of rats. Results There were no significant differences of noradrenaline ( NE )- and KCl-induced contraction in thoracic aorta rings among CIHH and CON rats;CIHH enhanced va-sodilative effects of paeonol on isolated thoracic aorta rings of rats; the vasodilative effects on CIHH rats could be partly decreased by β-receptor blocker prop-ranolol,ATP-sensitive potassium channel ( KATP ) bloc-ker glibenclamide and NO synthase inhibitor L-NAME. Paeonol significantly inhibited NE-induced intracellular and extracellular calcium-dependent contraction in CIHH rats. Paeonol didn ’ t inhibit NE-induced con-traction by intracellular calcium release and its inhibi-tory effect couldn ’ t be blocked by glibenclamide in CON. Vasodilative effects of paeonol couldn ’ t be re-versed by indomethacin, a cyclooxygenase inhibitor, in CIHH and CON rats. Conclusion CIHH significantly enhances vasodilative effects of paeonol on isolated tho-racic aorta rings of rats. Besides promoting the signa-ling pathway of paeonol in CON, CIHH significantly enhances vasodilative effects of paeonol via activating KATP and inhibiting Ca2+ release from sarcoplasmic re-ticulum.