Hemodynamic mechanisms of neurogenic pulmonary edema.

Acute lung injury has been reported in man and animals with intracranial disorders, head trauma or cerebral compression. Early studies in our laboratory demonstrated that pulmonary hemorrhagic edema (PHE) of acute and fulminating type occurred accompanying severe hypertension and bradycardia (Cushing responses) in animals following cerebral compression (CC) or intracranial hypertension (ICH). The lung pathology was prevented by spinal transection and sympathoadrenergic blocking agents, but was not affected by decerebration, adrenalectomy, vagotomy and atropine. The effects of central sympathetic activation due to ICH on the systemic and pulmonary resistance and capacitance vessels were studied in dogs with a total heart bypass preparation. ICH caused an increase in vascular resistance with a reduction in the vascular capacity of the systemic and pulmonary circulation. The relative importance of hemodynamic changes was further analyzed with the measurement of aortic and pulmonary flows and the use of right and left heart bypass. The overall pattern of imbalance in the right and left cardiac output was characterized by an immediate fall in aortic flow accompanying a slower decline in pulmonary arterial flow. In rats with a right heart bypass, ICH produced severe pulmonary venous hypertension and PHE. In the left heart-bypassed rats, ICH induced systemic hypertension, whereas no significant changes occurred in the lungs. Our studies reveal that: (1) ICH elicits vasoconstriction of the systemic and pulmonary resistance and capacitance vessels and (2) the major cause of volume and pressure loading in the pulmonary circulation is acute left ventricular failure resulting in a dramatic decrease in aortic flow.