Electrophysiological and biochemical changes in rabbit hearts stored at 4 degrees C for 6 or 24 h

This study examines the electrophysiological and metabolic changes that occ ur in rabbit hearts during hypothermic storage in vitro. Hearts were microp erfused at 4 degreesC for 6 or 24 h with either normal Krebs-Henseleit buff er (KHB) or KHB containing 2,3-butanedione monoxime (BDM). After hypothermi c storage, hearts were rewarmed to 37 degreesC with KHB. Cardiac function w as then assessed in Langendorff perfusion mode. Electrophysiological change s were also assessed from the ventricular paced-evoked responses. After sto rage, mitochondria were isolated from the hearts and their respiratory cont rol ratio, rate of ATP synthesis and outer membrane intactness were assesse d. Compared with values from fresh non-stored hearts, hearts stored hypothe rmically for 24 h showed significant decreases in both left ventricular dev eloped pressure and coronary flow when reperfused in Langendorff mode. On t he other hand, the decrease in left ventricular developed pressure in heart s that were stored for only 6 h (with or without BDM) was not significant. Compared with values obtained from fresh non-stored hearts, hypothermic sto rage significantly decreased the R-wave amplitude, and both the R-E and ST- E intervals of paced-evoked responses. This was true for hearts microperfus ed for 6 h (with or without BDM) and for hearts microperfused with buffer c ontaining BDM for 24 h. The ST-R intervals in hearts microperfused hypother mically for 6 h were prolonged, but this change was not statistically signi ficant compared with those obtained from unstored hearts. In hearts micrope rfused with KHB containing BDM for 24 h, the ST-R interval was significantl y prolonged. Hypothermic microperfusion for 24 h significantly decreased bo th the mitochondrial coupling ratio and the rate of ATP synthesis. In heart s microperfused with BDM for 6 h, mitochondrial coupling ratios and the rat e of ATP synthesis were not significantly different from those in fresh hea rts. In conclusion, the present study has shown that long-term hypothermic storage significantly impaired both paced-evoked responses and mitochondria l function. Inclusion of BDM in the perfusion buffer during storage signifi cantly ameliorated some of these changes.