Focaccio A, Ambrosio G, Enea I, Russo R, Balestrieri P, Chiariello M, Volpe M
Department of Medicine, Federico II School of Medicine, Naples, Italy.
Am J Physiol. 1995 Jun;268(6 Pt 2):H2352-7. doi: 10.1152/ajpheart.1995.268.6.H2352.
The separate effects of hypoxia and ischemia on atrial natriuretic peptide (ANP) release were evaluated in Langendorff-perfused rabbit hearts. Heart rate, coronary flow, and atrial and ventricular volumes were kept constant. Hypoxia was induced for 20 min at room temperature in seven hearts and at 37 degrees C in a second group of seven hearts. A third group of eight hearts was subjected to global ischemia for 20 min by reducing coronary flow to 1 ml/min at room temperature. All hearts were reoxygenated/reperfused at 37 degrees C for 30 min. Hypoxia at 37 degrees C induced a significant increase in ANP release. In contrast, both room temperature hypoxia and ischemia were characterized by a significant decrease in ANP release, despite hemodynamic alterations similar to those recorded during hypoxia at 37 degrees C. Both reoxygenation and reperfusion induced a prompt reversal of the changes of ANP release observed during the period of oxygen deprivation. These data demonstrate that decreased oxygen availability and reduced coronary flow are not the primary factors affecting release of ANP during ischemia and that alterations of myocardial temperature may play a major role in this phenomenon.
在Langendorff灌注兔心脏中评估了缺氧和缺血对心房利钠肽（ANP）释放的单独影响。心率、冠状动脉流量以及心房和心室容积保持恒定。在室温下对七颗心脏诱导缺氧20分钟，对另一组七颗心脏在37℃诱导缺氧。通过在室温下将冠状动脉流量降至1 ml/min，对第三组八颗心脏进行20分钟的全心缺血。所有心脏均在37℃复氧/再灌注30分钟。37℃的缺氧诱导ANP释放显著增加。相比之下，尽管室温下的缺氧和缺血期间的血流动力学改变与37℃缺氧时记录的相似，但二者均表现为ANP释放显著减少。复氧和再灌注均导致在缺氧期间观察到的ANP释放变化迅速逆转。这些数据表明，氧供应减少和冠状动脉流量降低不是影响缺血期间ANP释放的主要因素，并且心肌温度的改变可能在这一现象中起主要作用。
