• T Tateyama, M Asada, H Suzuki, K Hashimoto, H Nose, K Okazaki, and Y Okutsu.
• Department of Anesthesiology, Yokohama City University School of Medicine.
• Masui. 1995 Jul 1; 44 (7): 932-6.

AbstractWe investigated the effects of increased arterial carbon dioxide (PaCO2 not equal to 60 mmHg) on myocardial tissue oxygen tension and metabolism in anesthetized dogs. Ten adult mongrel dogs weighing 15.3 +/- 4.1 kg were anesthetized with 0.5% isoflurane in 50% oxygen and ventilated mechanically to maintain normocapnia. After thoracotomy, regional myocardial tissue PO2 was measured using a monopolar polarographic needle electrode inserted in the myocardium. Electromagnetic blood flow probes were applied on the left anterior descending artery and the circumflex artery. A 23-gauge catheter was inserted into a coronary vein to obtain coronary venous blood for measuring oxygen content, lactate and pyruvate. After control normocapnic ventilation, hypercapnia (PaCO2 62.7 +/- 3.2 mmHg) was induced by adding 10% carbon dioxide to the inspired gas for 20 minutes. As a result, the coronary blood flow and myocardial oxygen tension increased during hypercapnia. The myocardial lactate extraction and coronary venous lactate were unchanged and excess lactate was kept below zero, although coronary venous L/P ratio increased during hypercapnia. These results indicate that hypercapnia (PaCO2 not equal to 60 mmHg) increases coronary blood flow and myocardial oxygen tension, while myocardial aerobic metabolism is not impaired under hypercapnia.

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