von Oppell U O, King L M, Du Toit E F, Owen P, Reichart B, Opie L H
Ischaemic Heart Disease Laboratory, University of Cape Town Medical School, Republic of South Africa.
J Thorac Cardiovasc Surg. 1991 Sep;102(3):396-404.
The hypothesis tested is that shifts in pH, induced when a cardioplegic solution is oxygenated, can be detrimental. We added either 100% nitrogen, 95% nitrogen and 5% carbon dioxide, 100% oxygen, or 95% oxygen and 5% carbon dioxide to the cardioplegic solution (St. Thomas' Hospital No. 2 plus glucose 11 mmol/L), and determined postischemic recovery of isolated rat hearts after 3 hours of 10 degrees C cardioplegic protected ischemia. Hearts were arrested and reinfused every 30 minutes throughout the ischemic period with cardioplegic solution. When 5% carbon dioxide was added to nitrogen, the pH of the cardioplegic solution decreased from 9.1 (100% nitrogen) to 7.0 (95% nitrogen: 5% carbon dioxide), a change associated with improved postischemic functional recovery. Aortic output improved from 52.3% +/- 2.7% to 63.9% +/- 2.8%, p less than 0.05, and cardiac output from 60.8% +/- 3.6% to 75.4% +/- 3.3%, p less than 0.01. This improvement was associated with diminished efflux of lactate during ischemia but increased postischemic release of lactate dehydrogenase. When nitrogen was replaced with oxygen, the addition of 5% carbon dioxide resulted in a similar decrease of pH, which again was associated with improved postischemic functional recovery. Aortic output improved from 66.3% +/- 2.8% (100% oxygen) to 88.9% +/- 3.7% (95% oxygen: 5% carbon dioxide), p less than 0.005, and cardiac output from 75.3% +/- 4.1% to 88.9% +/- 2.4%, p less than 0.01. The efflux of lactate during ischemia and the postischemic release of lactate dehydrogenase were similar in both groups. Furthermore, provision of additional oxygen with perfluorocarbons in an electrolyte solution identical to the St. Thomas' Hospital plus glucose solution and oxygenated with 95% oxygen: 5% carbon dioxide conferred no extra protection. In conclusion, the St. Thomas' Hospital No. 2 plus glucose cardioplegic solution should be oxygenated but with 95% oxygen: 5% carbon dioxide and not 100% oxygen because of the additive effect of a relatively "acidotic" pH.
所检验的假设是,心脏停搏液充氧时所诱发的pH值变化可能是有害的。我们向心脏停搏液(圣托马斯医院2号配方加11 mmol/L葡萄糖)中分别添加100%氮气、95%氮气和5%二氧化碳、100%氧气或95%氧气和5%二氧化碳,并在10℃心脏停搏保护下缺血3小时后,测定离体大鼠心脏的缺血后恢复情况。在整个缺血期,每隔30分钟用心脏停搏液使心脏停搏并重新灌注。当向氮气中添加5%二氧化碳时,心脏停搏液的pH值从9.1(100%氮气)降至7.0(95%氮气:5%二氧化碳),这种变化与缺血后功能恢复的改善相关。主动脉输出量从52.3%±2.7%提高到63.9%±2.8%,p<0.05,心输出量从60.8%±3.6%提高到75.4%±3.3%,p<0.01。这种改善与缺血期间乳酸外流减少但缺血后乳酸脱氢酶释放增加有关。当用氧气替代氮气时,添加5%二氧化碳导致pH值出现类似下降,这同样与缺血后功能恢复的改善相关。主动脉输出量从66.3%±2.8%(100%氧气)提高到88.9%±3.7%(95%氧气:5%二氧化碳),p<0.005,心输出量从75.3%±4.1%提高到88.9%±2.4%,p<0.01。两组缺血期间的乳酸外流和缺血后乳酸脱氢酶的释放相似。此外,在与圣托马斯医院加葡萄糖溶液相同的电解质溶液中用全氟碳化合物提供额外氧气,并充入95%氧气:5%二氧化碳,并未提供额外的保护。总之,圣托马斯医院2号加葡萄糖心脏停搏液应充氧,但应充入95%氧气:5%二氧化碳而非100%氧气,因为相对“酸中毒”的pH值具有累加效应。