The contribution of adenosine to myocardial protection mechanisms has proven to be highly complex. Experimental works on the isolated heart and cell systems have shown that adenosine is distributed in different regions coupled to a variety of metabolic processes. Thus, even simple flow experiments with input-output measurements of adenosine concentrations are hard to interpret. To overcome analytical limitations in 1992 Kroll, Deussen, and Sweet established a mass conserving mathematical model including vascular, endothelial, interstitial, and parenchymal regions as well as production and degradation processes of adenosine. Classical blocking experiments of adenosine receptors helped to set the parameters of the model. Now the availability of knock-out mice provides new ways to study the system. Experiments of our group have show that global adenosine production rates of mice hearts are similar to guinea pig hearts. However, recent literature data indicates that transport and metabolic processes are differentially regulated. Thus, the application of a comprehensive mathematical model permits the in-silico evaluation of biological effects. The application of Bayesian data analysis allows a logically consistent inclusion of prior knowledge about the setup, facilitates model comparisons, and delivers a reliable estimation of parameter values and errors.