Bishop S P, White F C, Bloor C M
Am J Pathol. 1977 Dec;89(3):541-53.
Chronic hypoxemia was produced in 16 dogs by surgical transposition of the caudal vena cava to the left atrium to determine if chronic hypoxemia would alter the response of the myocardium to acute ischemia. An electromagnetic aortic flow probe, left atrial tube, and occlusive cuff on the left circumflex coronary artery were permanently implanted in 11 hypoxemic and 26 normal control dogs. The animals were studied in the conscious state after recovery from the surgery. Dogs with hypoxemia had a blood hematocrit value of 54.3 +/- 1.0% (SE), arterial PO(2) of 43.2 +/- 1.4 mm Hg, and 80.2 +/- 1.6% oxygen saturation. There was no difference from control animals in the ratio of left ventricular weight to body weight, but the right ventricular weight was significantly decreased in the hypoxemic dogs. Cardiac output from the left ventricle was twice that of the right ventricle. Aortic blood flow was 3.68 +/- 0.22 liters/min in hypoxemic animals and 2.64 +/- 0.19 liters/min in normal dogs. Myocardial blood flow measured with 15-mu diameter tracer microspheres was increased from 79 +/- 10 and 59 +/- 8 ml/100 g/min in left ventricular endocardial and epicardial halves, respectively, in normal dogs to 212 +/- 48 and 172 +/- 39 in dogs with chronic hypoxemia. There were no deaths in 10 hypoxemic dogs within 24 hours after complete circumflex coronary artery occlusion; 7 of 26 (27%) normal dogs died after circumflex coronary artery occlusion during the conscious state. Gross infarct size was extremely variable in both groups. Median infarct size was smaller in dogs with hypoxemia and was directly correlated with arterial PO(2) in hypoxemic dogs. There was a mild, but statistically not significant, increase in the anastomotic index of hypoxemic dogs compared with that of normal animals, suggesting that a metabolic adaptive change rather than increased collateral circulation may have been responsible for the decreased mortality and smaller infarct size in hypoxemic dogs.
通过将尾腔静脉手术转位至左心房，在16只犬中制造慢性低氧血症，以确定慢性低氧血症是否会改变心肌对急性缺血的反应。在11只低氧血症犬和26只正常对照犬中永久植入电磁主动脉血流探头、左心房导管和左旋支冠状动脉上的闭塞袖带。动物在手术后恢复至清醒状态时进行研究。低氧血症犬的血细胞比容值为54.3±1.0%（标准误），动脉血氧分压为43.2±1.4毫米汞柱，氧饱和度为80.2±1.6%。低氧血症犬的左心室重量与体重之比与对照动物无差异，但右心室重量显著降低。左心室的心输出量是右心室的两倍。低氧血症动物的主动脉血流量为3.68±0.22升/分钟，正常犬为2.64±0.19升/分钟。用直径15微米的示踪微球测量的心肌血流量，在正常犬的左心室心内膜和心外膜半部，分别从79±10和59±8毫升/100克/分钟增加到慢性低氧血症犬的212±48和172±39。10只低氧血症犬在左旋支冠状动脉完全闭塞后24小时内无死亡；26只正常犬中有7只（27%）在清醒状态下左旋支冠状动脉闭塞后死亡。两组的大体梗死面积差异极大。低氧血症犬的梗死面积中位数较小，且与低氧血症犬的动脉血氧分压直接相关。与正常动物相比，低氧血症犬的吻合指数有轻度但无统计学意义的增加，这表明代谢适应性变化而非侧支循环增加可能是低氧血症犬死亡率降低和梗死面积较小的原因。
