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IN the majority of the reported cases of operated pheochromocytomas, prolonged postoperative shock has been a major problem,1 particularly in patients with sustained rather than intermittent hypertension.2 Shock after removal of a pheochromocytoma has been regarded as being due to a vasopressor deficiency. It seems logical to treat shock that follows the removal of an endogenous source of vasopressors by providing exogenous vasopressors, and this has been the routine procedure.However, little attention has been paid to the actual mechanism of this shock or the pathologic physiology of this dependence on vasopressors. It has even been postulated3 that the hypotensive . . .
Brunjes et al. (Thu,) studied this question.