Relationship between hypoxemia and urinary catecholamine excretion in stroke (II)

In our previous report, it was suggested that sympathetic hypertonic state is probably the cause for hypoxemia in the patients with acute stage of cerebrovascular disease. In the present study, 43 cases with cerebrovascular accident were studied with PaO2, PaCO2, AaDO2 (alveolar-arterial PO2 difference), physiologic dead space, and urinary catecholamine excretion. Increase in AaDO2 is positively correlated to increase in urinary catecholamine excretion. In the cases with cerebral infarction, increases in AaDO2 and in urinary catecholamine excretion are higher in cases with occlusion of the internal carotid artery than in cases with infarction of the perforaters. In 3 cases with internal carotid occlusion or middle cerebral arterial occlusion, increase in AaDO2 is observed during period of marked cerebral edema. In the cases with supratentorial hemorrhage, maximal diameter of the lesion in CAT scan, urinary adrenalin excretion and AaDO2are all positively correlated. In 5 cases with increased AaDO2, reductions of AaDO2 and of Qs/Qt were ovserved with administration of phenotolamine and/or trimetaphan. It is considered that the present authors further accumulated evidences of symphathetic overflow that plays an important role, if any, in hypoxemia of acute stage of cerbrovascular accidents and that is probably due to elevated intracranial pressure or hypothalamic dysfunction.