Valen G, Vaage J
Department of Surgery, University of Tromsø, Norway.
Free Radic Res. 1996 Jan;24(1):31-38. doi: 10.3109/10715769609087997.
Adenosine is an endogenous cardioprotective substance. The present study examines whether exogenous adenosine attenuates cardiac injury induced by oxidative stress. Rat hearts (Langendorff model) were perfused with H2O2 (180 microM) for 10 min, then recovered for 60 min (n = 10). In other groups adenosine 55 microM, 11 0 microM, or 220 microM (n = 10 in each) was given in addition to H2O2 throughout perfusion. Control perfusion with Krebs Henseleit only (n = 7), adenosine 110 microM throughout perfusion (n = 7), and adenosine 110 microM as an intervention (n = 7) was performed. The hearts were paced at 320 beats/min. Left ventricular systolic (LVSP) and end-diastolic (LVEDP) pressures were measured together with coronary flow (CF), and left ventricular developed pressure (LVDP = LVSP - LVEDP) was calculated. H2O2 decreased LVSP from 105 +/- 8 to 60 +/- 5 mmHg (mean +/- SEM) after 10 min infusion (p < 0.008). Adenosine did not attenuate the decrease of LVSP. LVEDP increased from 0 to 59 +/- 10 mmHg (p < 0.004) and 62 +/- 11 mmHg 5 and 15 min after end of infusion of H2O2, respectively. Neither 55 microM nor 220 microM adenosine inhibited the H2O2-induced increase of LVEDP. Adenosine 110 microM attenuated the increase after 15 (15 +/- 4 mmHg, p < 0.004) and 25 min observation (26 +/- 7 mmHg, p < 0.012). Adenosine did not attenuate the reduction of LVDP. CF initially increased during infusion of H2O2, thereafter decreased. Hearts given adenosine had higher basal CF, and CF did not increase after H2O2. Control perfusion with adenosine, given throughout perfusion or as an intervention, increased CF and tended to increase LVSP. In summary, adenosine did not inhibit H2O2-induced depression of contractility or reduction of CF. One concentration of adenosine (110 microM) attenuated H2O2-induced impairment of relaxation. Exogenous adenosine does not have an important influence on functional injury caused by exogenous oxidants.
腺苷是一种内源性心脏保护物质。本研究旨在探讨外源性腺苷是否能减轻氧化应激诱导的心脏损伤。用H2O2（180微摩尔）灌注大鼠心脏（Langendorff模型）10分钟，然后恢复60分钟（n = 10）。在其他组中，在整个灌注过程中除了给予H2O2外，还分别给予55微摩尔、110微摩尔或220微摩尔的腺苷（每组n = 10）。仅用Krebs Henseleit进行对照灌注（n = 7），在整个灌注过程中给予110微摩尔的腺苷（n = 7），以及给予110微摩尔的腺苷作为干预措施（n = 7）。心脏以320次/分钟的频率起搏。测量左心室收缩压（LVSP）和舒张末期压（LVEDP）以及冠状动脉血流量（CF），并计算左心室压力差（LVDP = LVSP - LVEDP）。输注H2O2 10分钟后，LVSP从105±8降至60±5毫米汞柱（平均值±标准误）（p < 0.008）。腺苷并未减轻LVSP的下降。在H2O2输注结束后5分钟和15分钟，LVEDP分别从0升至59±10毫米汞柱（p < 0.004）和62±11毫米汞柱。55微摩尔和220微摩尔的腺苷均未抑制H2O2诱导的LVEDP升高。110微摩尔的腺苷在观察15分钟（15±4毫米汞柱，p < 0.004）和25分钟（26±7毫米汞柱，p < 0.012）后减轻了升高。腺苷并未减轻LVDP的降低。在输注H2O2期间CF最初升高，随后降低。给予腺苷的心脏基础CF较高，且在给予H2O2后CF未升高。用腺苷进行对照灌注，无论是在整个灌注过程中给予还是作为干预措施，均增加了CF并倾向于增加LVSP。总之，腺苷并未抑制H2O2诱导的收缩力降低或CF减少。一种浓度的腺苷（110微摩尔）减轻了H2O2诱导的舒张功能损害。外源性腺苷对由外源性氧化剂引起的功能损伤没有重要影响。
