Ismail J A, McDonough K H
Department of Physiology, Louisiana State University Medical Center, New Orleans, Louisiana 70112, USA.
Am J Physiol. 1998 Jul;275(1):H8-14. doi: 10.1152/ajpheart.1998.275.1.H8.
Sepsis depresses myocardial function but prevents subsequent ischemia-reperfusion injury. Elevated coronary flow (CF) and endogenous adenosine may be important factors in the complete recovery of postischemic myocardial function observed in septic rat hearts. The purpose of this study was to determine the effects of manipulating CF and of antagonizing adenosine receptors on the postischemic recovery of left ventricular developed pressure (LVDP) in septic and control rat hearts. The relationship between CF and LVDP in septic rat hearts before ischemia was depressed compared with control. However, this relationship was unaltered by ischemia in septic hearts, whereas in control hearts it was severely depressed. Preventing the elevation of CF during reperfusion did not significantly affect the recovery of LVDP in septic rat hearts. Adenosine antagonism by 8-phenyltheophylline (0.1 and 1 nM) prevented the elevated CF during reperfusion, and the higher dose significantly depressed postischemic function. We conclude that elevated CF did not contribute to the recovery of postischemic LVDP in septic rat hearts but that endogenous adenosine may provide protection from ischemia.
脓毒症会抑制心肌功能，但可预防随后的缺血再灌注损伤。冠状动脉血流量（CF）升高和内源性腺苷可能是脓毒症大鼠心脏缺血后心肌功能完全恢复的重要因素。本研究的目的是确定调节CF以及拮抗腺苷受体对脓毒症和对照大鼠心脏缺血后左心室舒张末压（LVDP）恢复的影响。与对照相比，脓毒症大鼠心脏缺血前CF与LVDP之间的关系受到抑制。然而，脓毒症心脏缺血并未改变这种关系，而对照心脏中这种关系则严重受抑。在再灌注期间阻止CF升高对脓毒症大鼠心脏LVDP的恢复没有显著影响。8-苯基茶碱（0.1和1 nM）拮抗腺苷可阻止再灌注期间CF升高，且较高剂量显著抑制缺血后功能。我们得出结论，CF升高对脓毒症大鼠心脏缺血后LVDP的恢复没有贡献，但内源性腺苷可能提供对缺血的保护作用。
