INTERSTITIAL TRANSUDATE PURINES IN NORMOXIC AND HYPOXIC IMMATURE AND MATURE RABBIT HEARTS

Interstitial transudate and coronary venous concentrations of adenosine, inosine, and hypoxanthine were determined in isolated isovolumic immature and mature rabbit hearts during normoxia and hypoxia. During normoxia, interstitial transudate adenosine was lower in immature hearts compared with mature hearts. Interstitial transudate concentrations of adenosine, inosine, and hypoxanthine were 130 ± 16 nM, 699 ± 88 nM, and 392 ± 80 nM, respectively, in immature rabbit hearts and 228 ± 35 nM, 1154 ± 126 nM, and 287 ± 30 nM, respectively, in mature rabbit hearts. Interstitial transudate adenosine was significantly lower in the immature hearts. Coronary venous purine concentrations were 6- and 8-fold lower than their respective interstitial transudate concentrations during normoxia in both age groups. Hypoxia significantly increased interstitial transudate purines in both age groups. Interstitial transudate adenosine, inosine, and hypoxanthine increased to 1180 ± 231 nM, 4049 ± 500 nM, and 1099 ± 98 nM, respectively, in immature hearts and to 1225 ± 300 nM, 5220 ± 1217 nM, and 876 ± 147 nM, respectively, in mature hearts. The age-related difference in transudate adenosine levels present during normoxia was not detected during hypoxia. Venous purine levels increased during hypoxia and the gradient from interstitial transudate fluid to venous effluent was abolished for adenosine in both groups. In immature hearts, hypoxia led to higher venous effluent adenosine levels than in the mature hearts. Coronary resistance correlated with interstitial transudate adenosine in both groups, although immature hearts displayed lower resistances at all adenosine levels. The results indicate that 1) interstitial transudate adenosine may regulate coronary resistance during hypoxia in isolated hearts from both age groups, 2) age-related differences exist in the normoxic release of interstitial transudate adenosine, and 3) age-related differences appear to be present in the release of purines into the coronary venous effluent during hypoxia. © 1990 International Pediatric Research Foundation, Inc.