Introduction:. Previous studne haw demonstrated (he rapid lots of myocaroW creaane phosphate (CP) with the onset of ventneUar fibriation (VF), but a more gradual toss of adenoone triphoaphata (ATP) .It Is undear the tow (tow generated by eartyreeuacrtaoonfU CPR) is sufficient to regenerate nryocanial high-energy phoaphate (HEP) stores andtor protect against further losses. Methods: To characterize the changes In myocardal HEP'S during low-flow reperfusion of VF, six swine (21±3 kg) received 10 min of non-perfused VF, Mowed by cardnpuknonary bypass reperfusion of 30-40 rnVkgMw) for up to 120 max MyocaroU creatine phosphate (CP) and adenine tiphoaphato (ATP) ware determined at baseline and parioofcafty during VF w#i "P NMR spectrasoopy n mo using a large bore 4.7 Testa magnat Öfter cotected data indudect coronary perfusion pressure (CPP mean aortic pressure - mean right atrial pressure) and lactate flux (LFLUX=artarial - canfac vein lactato) Results: Hernodynamic and HEP data are summarized below (meantSO): Baseline 15mnVF 3T>60rrinVF 60-90 min VF 90-120 rrin VF :PP(rnmHgK 84.3±20.5 48.2±9.6 39.2±13.4 324±12.2 26.fetft2 JLUX 0.24±0.29 -0.66±1.14 -0.89±2.13 -0.07±1.48 0.15±1.46 (mmoM.) CP 100±0 71.9A38.2 S47t32.7 59.a±31.5 41±24.1 CTPT 53.6113.0 35.1A10.0 262±16.3 19.1±3 13.6±5.2 a pO.05 for basefina vs. 30-60, 60-90. 90-120 min VF by ANOVA wäh Tukey Poethoctast b pO.05 for beseane vs. al others by ANOVA with Tukay PosHwc teat ATP levels correlated with CPP (R=0.56. p=0.04). At the conclusion. WB animals ware defcrilated, but ncne ovekped ixrtractle hixtioa Conclusions: Low flow reperfusion of VF resutts in continued loss of ATP stores over fme and is correlated wrth CPP. Maximizing early reperfusion of VF is needed to prevent ongoing myocanJal HEP depletion teadng to an irrewrsUe rovfunctfcnal stata.
|Original language||English (US)|
|Journal||Critical care medicine|
|Issue number||1 SUPPL.|
|State||Published - Dec 1 1998|
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine