Abstract

The influence of acidosis and hypoxia upon the isolated pressor and depressor elements of the epinephrine response was studied by pharmacologically dissociating the two components by the use of DCI and phentolamine, respectively. Ventricular contractile force, arterial pressure and femoral blood flow were measured to determine the extent of cardiac and vasomotor participation in the isolated pressor and depressor responses to epinephrine during acidosis.

It was demonstrated that hypoxia and acidosis can strikingly reduce the amplitudes of the pressor and depressor responses to epinephrine. Consistently, the depressor component was more readily obliterated by respiratory acidosis than was the pressor component. This differential sensitivity can, in large measure, be attributed to the fact that the epinephrine-responsive vasodilator mechanism is more susceptible to suppression by acidosis than is the vasoconstrictor mechanism. Failure to eliminate the pressor response cannot be attributed to the persistence of a positive inotropic action of epinephrine during severe acidosis. The roles of acidosis and hypoxia in the development of epinephrine refractoriness are briefly discussed.