I agree with the tenet that cardiovascular parameters may not have any relevance to O2 transport or cellular physiology. However, I disagree with the interpretations of this study. There is no question that measurements of blood pressure, pulse rate, CVP, PAWP, and cardiac output must be related to the clinical situation and to measures of metabolic requirements. Theye, Perry and Brzica demonstrated the false security of maintaining blood pressure when they showed that cyclopropane supported blood pressure at the expense of tissue perfusion, an unacceptable trade.1 Other studies have examined O2 consumption and delivery under anesthesia in man and animals. These studies established that O2 delivery and consumption decline during anesthesia. The question “Why” is only partially answered. Two common factors are a decrease in body temperature and a decrease in organ function. Merin has shown that, although the myocardium may be profoundly affected by anesthetics, myocardial metabolism appears to remain normal.2 Thus, it is difficult to know exactly when the cardiovascular system reflects cellular deterioration. If a patient is mildly cold, and deeply anesthetized, should we expect a normal hemodynamic profile? Where does abnormal begin? I believe some measure of cellular integrity is needed to correctly interpret the hemodynamics. Shibutani believes that his group has found a measure. They interpret the decline in O2 delivery (ḊO2) as the cause for decreased O2 consumption (O2). Such a relationship is purported to be adverse. Since the experimenters did not control all other variables and did not systematically change only ḊO2, they need evidence that ḊO2 below 330 ml. per min. per M2 indicates inadequate tissue oxygenation. Their only piece of evidence is an increase in lactate. What the authors do not reveal is that, despite the increase in lactate, the values were still in the normal range (9 to 16 mg/dl).3 Well, is not any increase in lactate an indication that tissue metabolism is abnormal? It turns out that lactate is produced in most tissue beds; under normal circumstances, 70 mg. of lactate are produced hourly. About 50 per cent is metabolized by the liver, 30 per cent is excreted by the kidney, and the rest is used by the heart and perhaps the muscles.4 Lactate levels rise when production exceeds excretion. Therefore, in order to prove abnormal cellular metabolism, excretion has to be shown to be constant. In Shibutani's study, there are reasons to believe that lactate removal decreased from factors other than tissue hypoxia. First, those patients with the lowest O2 delivery had extraordinary elevations of peripheral vascular resistance—3,900. (Even the patients with DO2) 330 had resistances averaging 2,686.) This high resistance implies high cate- cholamine levels, and catechols increase lactate levels without the accompaniment of tissue hypoxia.5 Additionally, lactate clearance may have been decreased in the patients with low DO2 because patients had low outputs (cardiac index = 1.7); renal and hepatic blood flows may have been markedly diminished. A lowered clearance rate would allow a gradual accumulation of lactate. This lactate accumulation was never severe, and acidosis never occurred. Thus, I suggest that there is little evidence to warrant Shibutani's conclusions.