Profound Arterial Hypotension in Dogs

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Abstract
To determine whether non-invasive measuremnt of brain electrical activity can predict ischemic brain damage, the EEG and somatosensory- (SEP) and auditory-evoked (AEP) potentials were recorded before, during and after trimethaphum-induced profound arterial hypotension in dogs. The change in electrical activity were compared with the degree of brain damage, as determined by microscopic examination. Dogs were anesthetized with halothane (1.4 vol% inspired), maintained lorisontal (head at the level of the heart), and ventilated mechaniically (FIO2 0.5); deviations from normal acid-base status were corrected. Twenty animals received a 1.5-mg/kg i.v bolus of trimethaphan. Three animals were resistant to the drug. The remaining animals had profound hypotension [mean arterial blood pressure (MABP) at some steady level between 12 and 25 mm Hg] for 1 h. Of these animals, 8 died during or soon after the hypotensive period as a consequence of cardiac arrest (3), intestinal bleeding (3) or unknown causes (2). In all survivors, EEG intensity and the amplitude of the SEP decreased during hypotension; both variables recovered with restoration of MABP. All 9 animals surviving hypotension had no apparent neurologic or behavioral deficit nor any histologic evidence of ischemic brain cell injury. Neither a MABP threshold for brain injury or the degree of electrical change correlated with minimal brain injury could be determined. Apparently, there is a great margin of tolerance for profound hypotension by the brain in this species. Other organ system (the heart, gastrointestinal tract and liver) proved to be more susceptible to ischemic damage. Of the 9 surviving animals, 8 had elevations in serum alanine transaminase (SGPT), aspartate transaminase (SGOT) and alkaline phosphatase. Animals with the greatest increases in these enzymes showed centrilobular hepatocyte degeneration.