• M Inoue and A Kohyama.
• Department of Anesthesiology, Tokushima Prefectural Central Hospital.
• Masui. 1994 Feb 1; 43 (2): 182-9.

AbstractEffects of NaHCO3 on metabolic acidosis during hypoxia and after reoxygenation were studied in 18 anesthetized dogs. Metabolic acidosis was produced by inhalation of low fraction of oxygen (9%) for 2 hours. NaHCO3 1M was infused intravenously during hypoxia (n = 12) and 30 minutes after reoxygenation (n = 6) at the rate of 100 ml.min-1 (total 0.2 x body weight x base excess mEq). After reoxygenation, NaHCO3 significantly increased blood and intramyocardial pH and decreased blood lactate (LA) level. Maximal rate of rise of left ventricular pressure (LV dP/dt max) and cardiac index (CI) increased significantly, and left ventricular end-diastolic pressure (LVEDP) and LVEDP/left ventricular pressure (LVP) were unchanged. During hypoxia, NaHCO3 also significantly increased blood and intramyocardial pH but those changes were less than the values after reoxygenation, while blood LA level increased significantly. LVP and LV dP/dt max tended to decrease, while LVEDP and LVEDP/LVP increased significantly. In 8 of 12 dogs, myocardial glucose uptake increased but was not correlated with myocardial LA uptake and LV dP/dt max. Blood LA level correlated significantly with LV dP/dt max (r = 0.534, P < 0.01). It appears that during hypoxia, differing from reoxygenation, NaHCO3 may depress cardiac function due to intramyocardial acidosis.

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