Summary.
The effects of adrenaline. noradrenaline. lactic acid and sodium lactate. in intravenous infusion. upon the cardiac output. blood pressure. oxygen consumption. heart and respiration rates, and lactic, acid content of the blood were investigated in unanesthetized rabbits. Control experiments were performed with infusion of saline alone.
Both adrenaline and lactic acid infusions were followed by a rise in the cardiac output but no change in blood pressure, which finding indicated a reduction of the total peripheral resistance. The increase in cardiac output was greater than the rise in oxygen consumption.
After sodium lactate the cardiac output rose only to the same degree as the oxygen consumption.
Noradrenaline elevated the cardiac output. oxygen consumption and lactic. acid production very slightly. concurrently with a pressor effect.
The stimulating action of adrenaline in a low‐ concentration on the cardiac output is thought to be largely of reflex origin. resulting from a primary vasodilator effect. caused by adrenaline's stimulation of the lactic acid production in skeletal muscle. Lactic acid induces vasodilatation in the following ways: (1) Through the rise in the lactic acid content of skeletal muscle, CO, is liberated from the tissue bicarbonate and vasodilatation is produced via the increased CO2 tension. (2) When the lactic acid content rises in the blood, the latter's CO2 transporting capacity is impaired, and this also tends to raise the CO2 tension in the tissues. (3) With oxidation of the lactate the blood flow increases, chiefly in the liver.
The discrepancies in the hemodynamic effects of adrenaline and noradrenaline are attributed to the fact that the former hormone, even in low concentrations, has a powerful stimulatory action on the lactic acid production, but the latter almost none.
The lactic acid producing effect of adrenaline in muscle is assumed to be a phase of the mechanism by which it elicits an emergency reaction in the organism.
