Soberman M S, Sink J D, Forest G C, Hatcher C R
Joseph B. Whitehead Department of Surgery, Emory University School of Medicine, Atlanta, Georgia 30322.
J Surg Res. 1989 Sep;47(3):255-9. doi: 10.1016/0022-4804(89)90117-0.
The increased susceptibility of hypertrophied myocardium to ischemic injury is well known. Hypertrophied hearts possess lower preischemic high energy phosphate stores and develop ischemic contracture following a shorter ischemic interval than normal hearts. The purpose of this study was to determine the ability of preischemic, arrested perfusion of the hypertrophied rat heart with oxygenated, glucose-containing perfluorocarbon cardioplegia (FC-43) to restore myocardial ATP stores to normal and prolong the duration of global ischemia prior to contracture initiation. Hearts from normal (NL) rats and hypertrophied hearts from spontaneously hypertensive rats (SHR) were subjected to 2 or 15 min of preischemic, arrested perfusion with FC-43 utilizing a modified Langendorff preparation. ATP was determined via HPLC and time to initiation of ischemic contracture was measured. Two minutes of FC-43 perfusion restored ATP in the SHR group to normal levels (P = NS compared to normal controls) and prolonged the time to initiation of ischemic contracture by 107%. Perfluorocarbons, with their unique oxygen-carrying properties, may be an ideal vehicle for intervention designed to enhance the tolerance of hypertrophied hearts to ischemia.
肥厚心肌对缺血损伤的易感性增加是众所周知的。肥厚心脏的缺血前高能磷酸储存较低,与正常心脏相比,在较短的缺血间隔后就会发生缺血性挛缩。本研究的目的是确定用含氧、含葡萄糖的全氟碳心脏停搏液(FC-43)对肥厚大鼠心脏进行缺血前停搏灌注,使心肌ATP储存恢复正常并在挛缩开始前延长全心缺血持续时间的能力。利用改良的Langendorff装置,对正常(NL)大鼠的心脏和自发性高血压大鼠(SHR)的肥厚心脏进行2或15分钟的缺血前FC-43停搏灌注。通过高效液相色谱法测定ATP,并测量缺血性挛缩开始的时间。FC-43灌注2分钟可使SHR组的ATP恢复到正常水平(与正常对照组相比P=无显著性差异),并使缺血性挛缩开始的时间延长107%。全氟碳具有独特的携氧特性,可能是旨在提高肥厚心脏对缺血耐受性的理想干预载体。