In pentobarbital-pancuronium anesthetized open chest dogs, left ventricular pressure (LVP), first derivative of LVP (dp/dt) and left ventricular end-diastolic pressure (LVEDP) were measured by a micromanometer tipped catheter, stroke volume and cardiac output (CO) by an electromagnetic flow meter and coronary sinus blood flow (CSBF), by a thermal dilution catheter, respectively. Mean arterial pressure (mAP), mean pulmonary arterial pressure (mPAP), lead II of ECG and esophageal temperature were monitored. Blood gas, catecholamines and lactate of arterial blood and coronary sinus blood were measured and myocardial lactate extraction ratio (MCL) was calculated. As an index of contraction, maximum positive dp/dt (+dp/dt max), and as an index of relaxation, the time constant (T) of isovolumic left ventricular pressure fall were employed, respectively. Acute hypoxia was induced by the inhalation of a 5% O2-95% N2 gas mixture and arterial blood oxygen pressure was maintained between 15 and 20 mmHg. Along with the advancement of hypoxia, +dp/dt max, CO and mAP gradually increased and peaked in 5 minutes. Thereafter, these parameters began to decrease and CO fell to zero in 20 minutes. mPAP and HR slowly increased and peaked in 9 and in 12 minutes, respectively. T was progressively prolonged throughout the hypoxia. CSBF/CO ratio was increased and stayed at a high level even after CO began to decrease. MCL decreased and changed from positive values to negative ones in 5 minutes. Epinephrine and norephinephrine concentrations slowly increased and peaked in 16 minutes. A gradual decrease in the R wave, shortening of the R-R interval and lengthening of the QTc interval were observed in ECG. This study indicated that the left ventricular relaxing function was impaired earlier than contracting function by acute hypoxia and that conversion of the augmented left ventricular contractile state to the depressed one coincided with conversion of myocardial lactate extraction to its production.