Pulmonary lymphatic flow alterations during intracranial hypertension in sheep.

Abstract

The role of intracranial hypertension in the genesis of neurogenic pulmonary edema was studied in 25 sheep; cardiopulmonary hemodynamics (aortic, pulmonary arterial, and left atrial pressures and cardiac output) and fluid and protein movement across the pulmonary capillary bed (efferent pulmonary lymph flow and lymph/plasma protein ratio) were monitored. Only when intracranial pressure was raised to equal the baseline mean systemic pressure (75 to 120 Torr) did we observe the expected Cushing response of increased aortic pressure, or any alteration in pulmonary hemodynamics or fluid movement. When pulmonary changes did occur, they included an increase in pulmonary arterial pressure of between 5 and 15 Torr without any notable rise in left atrial pressure, and a sustained doubling of the pulmonary lymph flow with no dilution of the lymph/plasma protein ratio. In 3 additional animals cerebral ischemia alone produced an elevation in systemic pressure (74 Torr over baseline) without change in pulmonary arterial pressure, left atrial pressure, or pulmonary lymph flow. Thus, intracranial hypertension and ischemia both affect systemic pressure, but only the elevated intracranial pressure is followed by changes in the pulmonary circuit. We suggest that these changes in pulmonary vascular pressure, independent of changes in left atrial pressure, produce increased pulmonary transcapillary fluid flux that may result in neurogenic pulmonary edema.