Cerebral hypotension and shock lung syndrome

Abstract

Pressure studies of systemic hemorrhagic hypotension at 40 mm. Hg for 2 hours showed the initial change to be small pulmonary vein (SPV) constriction. 1 Subsequently, during shock and particularly after reinfusion, gradients developed across the alveolar capillary bed. Hypoxia of the central nervous system is considered to be one of the prime factors in the pathogenesis of the shock lung syndrome. Cerebral hypotension can be produced by slight hemorrhage and ligation of both the right brachiocephalic and the left subclavian arteries. By this procedure, we maintained the cerebral blood pressure at 40 mm. Hg while keeping the systemic blood pressure at control levels. Nevertheless, the pulmonary pressure studies conducted in animals with cerebral hypotension did not show any significant pressure or gradient changes even though cerebral neurologic disorders were caused by the procedure. Cinemicroscopically, damage was minimal, and the microcirculatory pattern was that of the normal animal.