INCREASED PULMONARY VASCULAR-PERMEABILITY FOLLOWS INTRACRANIAL HYPERTENSION IN SHEEP

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Abstract
Neurogenic pulmonary edema is probably due to rupture of lung vessels by marked but transitory pulmonary hypertension. The effects of increased intracranial pressure in a sheep model in which the flow rate and protein content of lung lymph could be measured to detect changes in pulmonary vascular permeability was studied. Increasing intracranial pressure to amounts near systemic arterial pressure produced a 3-fold increase in the flow of protein-rich lymph, which indicates increased lung vascular permeability. The high permeability developed and persisted, without extraordinary increases in pulmonary vascular pressures. Apparently increased lung vascular permeability may follow intracranial hypertension and extreme pulmonary hypertension is not a prerequisite. Barotrauma to exchange vessels may cause capillary damage, but perhaps local permeability release mediators may be involved.

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