Upsher M E, Joselevitz-Goldman J, Weiss H R
Dept. of Physiology and Biophysics, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway 08854.
Res Exp Med (Berl). 1988;188(5):377-90. doi: 10.1007/BF01851206.
This study was designed to assess the effects of reperfusion on regional O2 supply and O2 consumption of ischemic areas of the myocardium in 15 anesthetized open-chested dogs. The left anterior descending coronary artery (LAD) was occluded for 6 h (n = 8), 2 h (n = 5), 2-h occlusion followed by 4-h period of reperfusion (n = 7), and 10-min occlusion followed by 90-min period of reperfusion (n = 3). Small artery and vein O2 saturations obtained microspectrophotometrically were combined with regional flow measurements using radioactive microspheres to determine regional myocardial O2 consumption. Coronary occlusion for 2 or 6 h significantly reduced mean flow to 15 +/- 8 and 13 +/- 14 ml/min/100 g (mean +/- SD), respectively, in the affected LAD areas as compared to 128 +/- 26 and 113 +/- 46 ml/min/100 g in the non-ischemic areas. In the 4-h reperfusion group, reperfusion increased the average flow (60 +/- 42 ml/min/100 g). O2 extraction was greater in the ischemic area than in the unaffected area after both occlusion and 4-h reperfusion. In the affected area, O2 consumption was reduced by 84% after 6-h occlusion. Reperfusion for 4 h increased O2 consumption toward normal values. Coronary artery occlusion produced an increase in the number of arteries and veins with reduced O2 saturations and this was not affected by reperfusion. Short-term occlusion had no significant O2 supply effects after 90 min of reperfusion. It can be concluded that even though there was an increased O2 consumption as a consequence of reperfusion, O2 consumption still appeared to be flow-limited as indicated by the microregions of low O2 supply and/or high O2 extraction.
本研究旨在评估再灌注对15只麻醉开胸犬心肌缺血区域局部氧供应和氧消耗的影响。左冠状动脉前降支(LAD)闭塞6小时(n = 8)、2小时(n = 5),2小时闭塞后再灌注4小时(n = 7),以及10分钟闭塞后再灌注90分钟(n = 3)。用显微分光光度法获得的小动脉和静脉氧饱和度与使用放射性微球的局部血流测量相结合,以确定局部心肌氧消耗。与非缺血区域的128±26和113±46 ml/min/100 g相比,LAD受累区域冠状动脉闭塞2小时或6小时分别使平均血流显著降低至15±8和13±14 ml/min/100 g。在4小时再灌注组中,再灌注增加了平均血流(60±42 ml/min/100 g)。闭塞和4小时再灌注后,缺血区域的氧摄取均高于未受累区域。在受累区域,6小时闭塞后氧消耗降低了84%。再灌注4小时使氧消耗增加至正常值。冠状动脉闭塞导致氧饱和度降低的动脉和静脉数量增加,且这不受再灌注影响。90分钟再灌注后,短期闭塞对氧供应无显著影响。可以得出结论,尽管再灌注导致氧消耗增加,但如低氧供应和/或高氧摄取的微区域所示,氧消耗似乎仍受血流限制。