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本研究选用健康杂种犬35只,随机分为正常组（n=5）,缺血对照组（n=15）、及给药组（n=15）。在左冠状动脉前降支第2～3分支间结扎冠脉,造成心肌缺血模型,观察药物对心肌二氧化碳代谢和冠脉血PH的影响。结果表明:心肌缺血后,对照组PV—_aCO_2。增加,PHV降低,与缺血前及正常组比较均有显著性差异（P<0.05 P<0.01）,提示缺血导致了心肌代谢产物的堆积,血液变酸;给药组在药后60min时与对照组相比PV—_aCO_2显著为低,PHV显著为高（均P<0.05）。表明药物在抑制缺血导致的二氧化碳产生增多,防止血液酸化方面有一定的作用。
In this study, 35 healthy mongrel dogs were randomly divided into normal group (n=5), ischemic control group (n=15), and drug administration group (n=15). The coronary artery was ligated between the branches 2 to 3 of the left anterior descending coronary artery, resulting in a model of myocardial ischemia. The effects of drugs on myocardial carbon dioxide metabolism and coronary blood PH were observed. The results showed that after myocardial ischemia, the control group PV-_aCO_2. Increased PHV decreased compared with pre-ischemic and normal groups (P<0.05 P<0.01), suggesting that ischemia caused the accumulation of myocardial metabolites and blood acidification; the administration group was 60 min after drug administration. Compared with the control group, PV-_aCO 2 was significantly lower and PHV was significantly higher (all P<0.05). It shows that the drug has a certain role in inhibiting the increase of carbon dioxide production caused by ischemia and preventing blood acidification.