Recovery of Evoked Potential Amplitude after Cerebral Arterial Air Embolism in the Rabbit

Background Cerebral arterial air embolism (CAAE) may cause neurologic injury during cardiac surgery. It is not known whether cardiopulmonary bypass (CPB) increases or decreases brain injury from CAAE compared with the normal circulation. Methods A model of CAAE was produced by injection of 50 microl/kg air into the internal carotid artery of methohexital-anesthetized New Zealand white rabbits. Somatosensory-evoked potential (SSEP) amplitude was measured serially as a marker of neurologic recovery. In experiment A, saline rather than air was injected to control for surgical manipulation and time in CPB (n = 4) and nonheparinized non-CPB (n = 4) animals. In experiment B, 50 microl/kg air was injected in CPB (n = 11) and nonheparinized non-CPB (n = 11) animals. In experiment C, non-CPB animals (n = 6) were given heparin according to the same protocol as for CPB. Results In experiment A, SSEP latencies and amplitudes did not differ between CPB and non-CPB conditions. In experiment B, there was no SSEP recovery 5 min after CAAE in either CPB or non-CPB animals. Thereafter, SSEP recovery was less in CPB animals than in non-CPB animals at 30 min (9 +/- 12% vs. 29 +/- 20%; P = 0.009) and 60 min (18 +/- 15% vs. 39 +/- 22%; P = 0.030) after CAAE. Ninety-minute SSEP recovery did not differ between CPB and non-CPB groups (at 24 +/- 19% vs. 39 +/- 24%, respectively; P = 0.146). In experiment C (heparinized non-CPB), SSEP recovery 5, 30, 60, and 90 min after CAAE was 67 +/- 48%, 72 +/- 47%, 80 +/- 35%, and 77 +/- 35%, respectively. Conclusions Somatosensory-evoked potential recovery after CAAE is no better (and is probably worse) during CPB than during normal circulation. The adverse effect of CPB occurs despite heparinization, which, under non-CPB conditions, appears to be protective. Therapies in addition to heparin are needed during CPB to reduce neurologic injury from CAAE.