NEUROHORMONAL REGULATION OF SYSTEMATIC HEMOSTATIC FUNCTION

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Unexplained acidosis occurs in up to 15% of patients following cardiac surgery, Since this disorder resolves spontaneously and cardiac output is similar in patients with and without lactic acidosis, it is likely this represents a type 2 lactic acidosis. Little is presently known regarding the mechanism responsible for this apparent Type 2 lactic acidosis. This study, which stems from a previous investigation on the neurohormonal regulation of systemic hemostatic function, is designed to evaluate the impact of stress hormones on acid-base balance and lactate concentrations. Volunteers in the original study on hemostatic function were noted to develop an apparent Type 2 lactic acidosis when randomized to the stress hormone infusion that contained epinephrine, cortisol, glucagon, angiotensin Ii, and vasopressin. Subsequently we have studied healthy volunteers receiving stress hormone infusion of all f hormones, four hormones (without angiotensin II), three hormones (without angiotensin or vasopressin) and during all of these infusions the volunteers have developed an apparent Type 2 lactic acidosis of the same magnitude. Presently we are studying healthy volunteers receiving epinephrine alone. The initial volunteer also has developed a type 2 lactic acidosis and given the cost of routinely evaluating postoperative lactic acidosis we are eager to evaluate subsequent volunteers.