Venoarterial extracorporeal membrane oxygenation impairs basal nitric oxide production in cerebral arteries of newborn lambs.

Based on previous studies in our laboratory showing that exposure of newborn lambs to venoarterial extracorporeal membrane oxygenation (ECMO) alters cerebral blood flow autoregulation, we postulated that this altered vascular reactivity is mediated through changes in endothelial function caused by the pumping systems used in venoarterial ECMO. We tested that hypothesis in this study.Prospective, controlled, laboratory trial.Animal research laboratory.Two groups of newborn lambs.One group of animals was exposed to venoarterial ECMO (n = 6) and another group of control animals (n = 5) was maintained under similar conditions for 2 hrs on the ventilator without ECMO.Third-order branches of the middle cerebral arteries (140-300 microm diameter) were isolated from animals at the end of the experiment, mounted on glass cannulae in an arteriograph, and superfused with Krebs-Ringer buffer. Decrease in the diameter of the arteries induced by exposure of the vessels to nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (200 micromol/L) for 30 mins was significantly less (p <.05) in arteries from lambs exposed to ECMO compared with control animals. There were no significant differences between the two groups in myogenic response or in the contractile activity of the arteries to increasing concentrations of serotonin.These results demonstrate that 2 hrs of exposure of newborn lambs to venoarterial ECMO leads to a decrease in basal production of nitric oxide in cerebral arteries, and suggest that venoarterial ECMO selectively impairs cerebral arterial endothelial function.