Mechanisms of neurogenic pulmonary edema during intracranial hypertension / 中国病理生理杂志

ABSTRACT

The neurogenic pulmonary edema (NPE) was produced consistently in rabbits by raising intracranial pressure (ICP) with an infusion of anticoagulat rabbit blood into subarachnoid space of the bilateral parietal regions. When ICP increased from 60mmHg to 140 mmHg, There was a rapid decrease in blood flow volume of the bilateral internal carotid arteries (ICABFV). At the same time, the frequency of cervical sympathetic discharge and the concentrations of plasma noradrenaline and adrenaline increased acutly accompanied by a rapid elevation of systemic arterial pressure (SAP). There was a decline in SAP and a further decrease in ICABFV and the animal died as ICP was sustained at 140mmHg for 5-20min. Autopsy revealed severe hemorrhagic pulmonary edema and the left ventricular and atrial enlargement. In the period of ICP rising, the NPE was prevented if SAP was kept at the baseline levels by withdrawing blood from femoral artery, The results suggest that decreased cerebral blood supply due to ICP rising is responsible for the massive sympathetic discharge and catecholamine release which contribute to SAP elevtion and left ventricular overload, the NPE is mediated by hemodynamic mechanism.