Cerebral tissue lactate in experimental oligemic shock.

Abstract

✓ Eleven anesthetized dogs underwent bilateral craniectomies. Four control dogs had serial resections of cerebral tissue in the normotensive state. After one control sample was removed from the remaining seven dogs, they were bled to a mean arterial pressure of 30 to 35 mm Hg and had cerebral tissue samples resected at 0, 30, and 60 min after the onset of hypotension. The tissue samples from the four normotensive dogs averaged 4.83 mM lactate/kg tissue with a range of 4.67 to 7.22 mM/kg. At 0 time post-shock the samples averaged 7.18 mM/kg, at 30 min post-shock 14.31 mM/kg, and at 60 min 18.76 mM/kg. It can be concluded that hemorrhagic shock causes a progressive elevation in cerebral tissue lactate, which correlates with the duration of shock. At low mean arterial pressures the brain is susceptible to the effects of poor tissue perfusion, which results in both inadequate oxygenation and lactate washout in spite of well-established mechanisms for preferential shunting of blood to the brain.