Cardiopulmonary bypass impairs vascular endothelial relaxation: Effects of gaseous microemboli in dogs

Gaseous microemboli during hypothermic cardiopulmonary bypass (CPB) may injure the vascular endothelium and interfere with intrinsic vasomotion. We tested whether gaseous microemboli reduced the vasodilator response to acetylcholine (ACh, 10^-9-10^-6 M) and potentiated the vasoconstrictor response to norepinephrine (NE, 3 x 10^-8-10^-4 M). Arteries from 18 dogs were excised before and after 120 min 28°C CPB using membrane (n = 9) and bubble (n = 9) oxygenators to produce microemboli, which were quantitated by Doppler. Five nonbypassed dogs were controls. In isolated vessel rings, the 50% effective dose (ED₅₀) values for ACh (10^-8 M) and NE (10^-7 M) responses were calculated. Mean microemboli count per minute was 0 ± 0 in the control group, 1.0 ± 0.4 in the membrane group (P < 0.05 vs. controls), and 46.9 ± 8.4 in the bubble group (P < 0.05 vs. control and membrane groups). ACh ED₅₀ values did not change in controls but increased in the membrane group from 4.01 ± 1.52 to 5.66 ± 1.39 (P < 0.05) and in the bubble group from 2.32 ± 0.56 to 7.21 ± 1.90 (P < 0.05). The change in ED₅₀ was greater for bubble than for membrane animals (P < 0.05) but did not correlate with microemboli number (bubble: r = 0.392, P = 0.297; membrane: r = 0.058, P = 0.802). NE responses were similar in all groups. Hypothermic CPB reduces ACh-induced dilation of the canine femoral artery independent of the incidence of gaseous microemboli. The vasoconstrictor response to NE is preserved after CPB regardless of whether membrane or bubble oxygenators are used.