Maldonado C, Qiu Y, Tang X L, Cohen M V, Auchampach J, Bolli R
Experimental Research Laboratory, University of Louisville, Kentucky 40292, USA.
Am J Physiol. 1997 Sep;273(3 Pt 2):H1324-32. doi: 10.1152/ajpheart.1997.273.3.H1324.
Conscious rabbits underwent six 4-min coronary occlusions interspersed with 4-min periods of reperfusion for 2 consecutive days (days 1 and 2 of stage I); 2 wk later, they underwent the same protocol (days 1 and 2 of stage II) except that they received either 8-(p-sulfophenyl)theophylline (SPT) on day 1 (group I, n = 5) or 2-chloro-N6-cyclopentyl-adenosine (CCPA) on the day before day 1 (group II, n = 6). In both groups I and II, on day 1 of stage I, systolic wall thickening (WTh) remained significantly depressed for several hours, indicating myocardial stunning; on day 2, however, the total deficit of WTh was approximately 50% less than on day 1 (P < 0.01), indicating the development of late preconditioning (PC) against myocardial stunning. Despite administration of SPT, in group I the deficit of WTh during stage II was 55% less on day 2 than on day 1 (P < 0.05). Similar results were obtained in three other rabbits treated with PD-115199 on day 1. In group II, pretreatment with CCPA during stage II failed to decrease the deficit of WTh on day 1. This study presents a new conscious rabbit model for studying myocardial stunning that is relatively inexpensive and technically less demanding than larger animal models. In this model, the development of late PC against myocardial stunning is not blocked by nonselective blockade of adenosine receptors with either SPT or PD-115199, nor is it induced by activation of adenosine A1 receptors with CCPA, indicating that adenosine receptors are not involved in the pathogenesis of this phenomenon.
清醒兔连续两天(I期第1天和第2天)接受6次4分钟的冠状动脉闭塞,期间穿插4分钟的再灌注期;2周后,它们接受相同方案(II期第1天和第2天),不同的是,第1天I组(n = 5)接受8 - (对 - 磺基苯基)茶碱(SPT),II组(n = 6)在第1天前一天接受2 - 氯 - N6 - 环戊基腺苷(CCPA)。在I组和II组中,I期第1天,收缩期室壁增厚(WTh)持续数小时显著降低,表明心肌顿抑;然而,第2天,WTh的总缺失比第1天减少约50%(P < 0.01),表明针对心肌顿抑的晚期预处理(PC)形成。尽管给予了SPT,I组在II期第2天WTh的缺失比第1天减少55%(P < 0.05)。另外3只在第1天用PD - 115199治疗的兔也得到了类似结果。在II组中,II期用CCPA预处理未能降低第1天WTh的缺失。本研究提出了一种用于研究心肌顿抑的新的清醒兔模型,该模型相对便宜,技术要求比大型动物模型低。在该模型中,用SPT或PD - 115199非选择性阻断腺苷受体并不阻断针对心肌顿抑的晚期PC的形成,用CCPA激活腺苷A1受体也不诱导其形成,这表明腺苷受体不参与该现象的发病机制。