Experimental neurogenic pulmonary edema

Abstract

Neurogenic pulmonary edema (NPE) was produced consistently in normal cats by increasing intracranial pressure with an intraventricular infusion of mock cerebrospinal fluid. The usual elevation of systemic arterial pressure (SAP) that follows severe intracranial hypertension (the "Cushing response") was controlled by blood withdrawal at variable rates to achieve and maintain constant cerebral perfusion pressure (CPP) in three groups of cats of 50, 20, and 0 mm Hg, respectively, for 30 minutes. In this model, NPE occurs in the absence of increased SAP and in the presence of decreasing CPP. These results indicate that systemic arterial hypertension is not an essential stimulus for the development of NPE, and suggest that the lungs are directly affected by the intense sympathetic discharge evoked by severe intracranial hypertension.