Dogs were anesthetized with pentobarbital 30 mg/kg. Cannulas were placed for measurement of arterial and central venous blood pressures. The left femoral artery was cannulated and attachment was made to a reservoir set to maintain arterial blood pressure at 40 mm Hg. Blood pH, pCO2, and pO2 were obtained concomitantly with measurements of blood epinephrine levels utilizing the rat uterus assay method. Rapid hemorrhage to 40 mm Hg blood pressure elicited increments in blood epinephrine levels that closely followed the development of uncompensated acidosis. Correction of the acidosis by intravenous administration of tromethamine or sodium bicarbonate at a blood pressure of 40 mm Hg reduced the blood epinephrine levels by at least 50%, markedly improved cardiac function, increased hemorrhage volume, reduced respiratory rate, and, paradoxically, increased arterial pO2. In vitro studies showed that acidosis did not inhibit destruction of epinephrine added to blood. It was concluded that the adrenal gland is stimulated by acidosis to secrete epinephrine. This stimulation is an important source of blood epinephrine during periods of hypotension associated with shock.
