Peripheral versus central cannulation for extracorporeal membrane oxygenation: a comparison of limb ischemia and transfusion requirements.

BACKGROUND: Extracorporeal membrane oxygenation (ECMO) can be instituted centrally, through the right atrium and ascending aorta, or peripherally, most commonly using the femoral artery and vein. We sought to investigate the impact of the mode of cannulation on the incidence of limb ischemia, perfusion and overall morbidity. METHODS: A retrospective analysis of 50 consecutive patients over 5 years who underwent ECMO by central or peripheral cannulation was performed. RESULTS: There was no difference in the incidence of limb ischemia and end-organ perfusion when peripheral and central cannulation cohorts were compared. Central cannulation was associated with a higher incidence of bleeding from the cannulation site (64% vs. 18%, P = 0.002), blood product utilization and reoperation (66% vs. 14%, P < 0.0001). 30-day mortality was similar in both cohorts (46% peripheral, 50% central, P = 0.8). CONCLUSION: Our results suggest that there is comparable tissue perfusion and limb ischemia with both cannulation techniques. Central cannulation is associated with a higher incidence of bleeding, higher transfusion rates, a greater need for reoperation and greater resource utilization. Therefore, peripheral cannulation is safe and may be advantageous in certain clinical scenarios.

Distinct myoprotective roles of cardiac sarcolemmal and mitochondrial KATP channels during metabolic inhibition and recovery.

The protective roles of sarcolemmal (sarc) and mitochondrial (mito) KATP channels are unclear despite their apparent importance to ischemic preconditioning. We examined these roles by monitoring intracellular calcium ([Ca]int), using fura-2 and fluo-3, in enzymatically isolated rat right ventricular myocytes. Myocyte mortality, estimated using a trypan blue assay, changed approximately in parallel with changes in [Ca]int. Chemically induced hypoxia (CIH), induced by application of cyanide and 2-deoxy-glucose, caused a steady rise in [Ca]int. Calcium increased more rapidly on 'reoxygenation' by return to control solutions. The protein kinase C (PKC) activator PMA abolished both phases of calcium increase. The mitoKATP channel-selective blocker 5-hydroxydecanoate partially prevented the PMA-induced protection during CIH, but not during reoxygenation. In contrast, HMR 1098, a sarcKATP channel-selective blocker, abolished protection only during the reoxygenation. Adenosine (A1) receptor activation prevented or reduced increases in [Ca]int and improved cell viability via a PKC and mito/sarcKATP channel-dependent mechanism. PKC-dependent protection against cytoplasmic calcium increases was also observed in a human cell line (tsA201) transiently expressing sarcKATP channels. Protection was abolished only during the reoxygenation phase by the amino acid substitution (T180A) in the pore-forming Kir6.2 subunit, a mutation previously shown to prevent PKC-dependent modulation. Our data suggest that sarc and mitoKATP channel populations play distinct protective roles, triggered by PKC and/or adenosine, during chemically induced hypoxia/reoxygenation.