Brain injury after cerebral arterial air embolism in the rabbit as determined by triphenyltetrazolium staining

Background: Microscopic cerebral arterial air embolism (CAAE) occurs common ly during cardiac surgery and causes acute and chronic nonfocal neurologic dysfunction. Nevertheless, most neuroimaging studies do not detect brain in jury after cardiac surgery. Using a rabbit model, the authors hypothesized they could detect and quantitate severe brain injury and infarction 24 h af ter microscopic CAAE using the vital stain triphenyltetrazolium chloride. Methods: Experiments were conducted in methohexital anesthetized New Zealan d white rabbits. Surgical shams (n = 5) underwent surgery but had no neurol ogic insult. Positive controls (n = 3) received 200 mu l/kg of intracarotid air. Other animals were randomized to receive either 50 mu l/kg intracarot id air, which produces microscopic CAAE (n = 18), or 300 mu l intracarotid saline (control n = 18). Outcomes included somatosensory evoked potential a mplitude at 90 min, neurologic impairment score at 4 and 24 h (0 [normal] t o 99 [coma]), and percentage of nonstaining brain at 24 h using color-discr imination image analysis. Severely injured or infarcted brain does not stai n with triphenyltetrazolium chloride. Results: Surgical shams had little neurologic impairment and a small amount of nonstaining brain at 24 h (5.2 +/- 2.4%; mean +/- SD). Positive control s had profound neurologic impairment and large amounts of nonstaining brain (40-97%). Ninety-minute somatosensory evoked potential amplitude was less in animals receiving 50 mu l/kg air versus saline: 38 +/- 28% versus 102 +/ - 32%, respectively, P < 1 x 10(-7). Neurologic impairment scores were grea ter in animals receiving 50 mu l/kg air versus saline: at 4 h, 43 +/- 16 ve rsus 23 +/- 9, P < 1 x 10(-7); at 24 h, 24 +/- 12 versus 15 +/- 8, P = 0.01 3. Nevertheless, there was no difference between 50 mu l/kg air and saline in nonstaining brain: 5.5 +/- 2.9% versus 6.8 +/- 5.4%, P = 0.83. Conclusions: Neurologic injury after (CAAE is dose-dependent. Although micr oscopic CAAE causes somatosensory evoked potential abnormalities and neurol ogic dysfunction, severe cerebral injury or infarction Is not present at 24 h The author's findings are consistent with clinical imaging studies that suggest microscopic CAAE causes neurologic dysfunction even though overt in farction is absent.