Krukenkamp I B, Silverman N A, Sorlie D, Pridjian A, Feinberg H, Levitsky S
Circulation. 1986 Nov;74(5 Pt 2):III125-9.
To define the pertubations in myocardial oxygen consumption (MVO2) previously noted after potassium-induced arrest, MVO2 was determined in 19 canine hearts during isovolumetric pressure-volume loading before and serially after 2 hr of cardioplegic ischemia at 20 degrees C. Starling curves were initially unchanged after cardioplegic arrest, but postischemic propranolol (0.2 mg/kg) depressed peak developed pressure 36 +/- 4% and heart rate 24 +/- 1% (p less than .01, for both). MVO2 indexed per beat and for left ventricular weight at defined ranges of peak developed pressure was augmented postischemically by 40% (p less than .05) and this increased oxygen utilization persisted after attenuation of coronary hyperemia, normalization of oxygen extraction, 1 hr of reperfusion, and effective beta-adrenergic-receptor blockade. These data suggest that increased MVO2 to generate physiologic pressures is a sensitive biological marker for cardioplegic efficacy that is independent of coronary flow and oxygen uptake and is not solely attributable to increased beta-adrenergic stimulation.
为了明确先前在钾诱导停搏后所观察到的心肌耗氧量（MVO2）的扰动情况，在20℃下对19只犬心脏进行了等容压力 - 容积负荷实验，在冷停搏缺血2小时之前及之后连续测定MVO2。冷停搏后Starling曲线最初未改变，但缺血后给予普萘洛尔（0.2mg/kg）使峰值收缩压降低36±4%，心率降低24±1%（两者p均小于0.01）。在特定的峰值收缩压范围内，每搏的MVO2指数以及相对于左心室重量的MVO2指数在缺血后增加了40%（p小于0.05），并且在冠状动脉充血减轻、氧摄取正常化、1小时再灌注以及有效的β - 肾上腺素能受体阻断后，这种增加的氧利用持续存在。这些数据表明，为产生生理压力而增加的MVO2是冷停搏效果的一个敏感生物学标志物，它独立于冠状动脉血流和氧摄取，且不仅仅归因于β - 肾上腺素能刺激的增加。
