RECOVERY OF EVOKED-POTENTIAL AMPLITUDE AFTER CEREBRAL ARTERIAL AIR-EMBOLISM IN THE RABBIT - A COMPARISON OF THE EFFECT OF CARDIOPULMONARY BYPASS WITH NORMAL CIRCULATION
Bj. Hindman et al., RECOVERY OF EVOKED-POTENTIAL AMPLITUDE AFTER CEREBRAL ARTERIAL AIR-EMBOLISM IN THE RABBIT - A COMPARISON OF THE EFFECT OF CARDIOPULMONARY BYPASS WITH NORMAL CIRCULATION, Anesthesiology, 88(3), 1998, pp. 696-707
Background: Cerebral arterial air embolism (CAAE) may cause neurologic
injury during cardiac surgery. It is not known whether cardiopulmonar
y 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 mu l/kg air into the internal carotid artery of methoh
exital-anesthetized New Zealand white rabbits. Somatosensory-evoked po
tential (SSEP) amplitude was measured serially as a marker of neurolog
ic recovery. In experiment A, saline rather than air was injected to c
ontrol for surgical manipulation and time in CPB (n = 4) and nonhepari
nized non-CPB (n = 4) animals. In experiment B, 50 mu l/kg air was inj
ected 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 bem een CPB and non-CPB conditions. In
experiment B, there was no SSEP recovery 5 min after CAAE in either CP
B or non-CPB animals. Thereafter, SSEP recovery was less in CPB animal
s than in non-CPB animals at 30 min (9 +/- 12% as. 29 +/- 20%; P = 0.0
09) and 60 min <18 +/- 15% vs. 39 +/- 22%; P = 0.030) after CAAE. Nine
ty-minute SSEP recovery did not differ bem een 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 CA
AE was 67 +/- 48%, 72 +/- 47%, 80 +/- 35%, and 77 +/- 35%, respectivel
y. Conclusions: Somatosensory-evoked potential recovery after CAAE is
no better (and is probably worse) during CPB than during normal circul
ation. The adverse effect of CPB occurs despite heparinization, which,
under non-CPB conditions, appears to be protective. Therapies in addi
tion to heparin are needed during CPB to reduce neurologic injury from
CAAE.