CAJ | 학술논문

本文旨在探讨低渗和高渗内环境对心肌收缩性的影响及机制.取Sprague-Dawley(SD)大鼠左心室乳头状肌,在电刺激引起兴奋的条件下,分别记录在低渗、等渗和高渗灌流液中肌条的收缩力;同样条件下观察在低渗、等渗和高渗灌流液中加入渗透压敏感蛋白瞬时感受器电位离子通道家族香草素受体亚家族IV型(transient receptor potential vanilloid 4,TRPV4)的拮抗剂和激动剂后肌条收缩力的变化.结果显示:(1)与等渗(310 mOsm/L)时心肌收缩力相比,渗透压为290、270和230 mOsm/L时心肌收缩力分别增加11.5%、21.5%、25.O%(P<0.05);渗透压为350、370、390 mOsm/L时心肌收缩力分别降低16.0%、23.7%、55.2%(P<0.05).(2)在低渗液(270 mOsm/L)中加入TRPV4拮抗剂钌红(ruthenium red,RR),低渗对心肌收缩力的增强作用被抑制36%(P<0.01);在高渗液(390 mOsm/L)中加入RR,高渗对心肌收缩力的抑制作用增加56.1%(P<0.01).(3)在等渗液中(310 mOsm/L)加入TRPV4激动剂4-α-佛波醇-12,13-二癸酸(4-α-phorbol-12,13-didecanoate,4 α-PDD),心肌收缩力没有改变;在高渗液中(390 mOsm/L)加入4α-PDD,高渗对心肌收缩力的抑制作用增加27.1%(P<0.01).以上结果提示,TRPV4参与渗透压引起的心肌收缩力变化.
본문지재탐토저삼화고삼내배경대심기수축성적영향급궤제.취Sprague-Dawley(SD)대서좌심실유두상기,재전자격인기흥강적조건하,분별기록재저삼、등삼화고삼관류액중기조적수축력;동양조건하관찰재저삼、등삼화고삼관류액중가입삼투압민감단백순시감수기전위리자통도가족향초소수체아가족IV형(transient receptor potential vanilloid 4,TRPV4)적길항제화격동제후기조수축력적변화.결과현시:(1)여등삼(310 mOsm/L)시심기수축력상비,삼투압위290、270화230 mOsm/L시심기수축력분별증가11.5%、21.5%、25.O%(P<0.05);삼투압위350、370、390 mOsm/L시심기수축력분별강저16.0%、23.7%、55.2%(P<0.05).(2)재저삼액(270 mOsm/L)중가입TRPV4길항제조홍(ruthenium red,RR),저삼대심기수축력적증강작용피억제36%(P<0.01);재고삼액(390 mOsm/L)중가입RR,고삼대심기수축력적억제작용증가56.1%(P<0.01).(3)재등삼액중(310 mOsm/L)가입TRPV4격동제4-α-불파순-12,13-이계산(4-α-phorbol-12,13-didecanoate,4 α-PDD),심기수축력몰유개변;재고삼액중(390 mOsm/L)가입4α-PDD,고삼대심기수축력적억제작용증가27.1%(P<0.01).이상결과제시,TRPV4삼여삼투압인기적심기수축력변화.
The aim of the present study was to investigate the influence of osmotic pressure on myocardial contractility and thepossible mechanism. Electrical stimulation was used to excite papillary muscles of the left ventricle of Sprague-Dawley (SD) rats. Thecontractilities of myocardium in hyposmotic, isosmotic, and hyperosmotic perfusates were recorded~ The influences of agonist andantagonist of the transient receptor potential vanilloid 4 (TRPV4) on the contractility of myocardium under hyposmotic, isosmotic andhyperosmotic conditions were observed. The results were as follows: (1) Compared with that under isosmotic condition (310 mOsm/L),the myocardial contractility was increased by 11.5%, 21.5% and 25.0% (P<0.05) under hyposmotic conditions when the osmoticpressure was at 290, 270 and 230 mOsm/L, respectively; and was decreased by 16.0%, 23.7% and 55.2% (P<0.05) under hyperosmoticconditions when the osmotic pressure was at 350, 370 and 390 mOsm/L, respectively. (2) When ruthenium red (RR), an antagonist ofTRPV4, was added to the hyposmotic perfusate (270 mOsm/L), the positive inotropic effect of hyposmia was restrained by 36%(P<0.01); and when RR was added to the hyperosmotie perfusate (390 mOsm/L), the inhibitory effect of hyperosmia on myocardialcontractility was increased by 56.1% (P<0.01). (3) When 4-α-phorbol-12,13-didecanoate (4αt-PDD), an agonist of TRPV4, was addedto the isosmotic perfusate (310 mOsm/L), the myocardial contractility did not change; and when 4α-PDD was added to the hyperosmoticperfusate (390 mOsm/L), the inhibition of myocardial contractility by hyperosmia was increased by 27.1% (P<0.01). These resultsobtained indicate that TRPV4 is possibly involved in the osmotic pressure-induced inotropic effect.