Adenosine is a potent
vasodilator whose concentration has been shown to increase in cardiac tissue in response to
hypoxia. However, the time-dependent relationship between the levels of myocardial interstitial
adenosine and tissue oxygenation has not yet been completely established. Therefore, the purpose of this study was to investigate the complex relationship between tissue myocardial
oxygen tension (
PtiO(2)) and interstitial myocardial
adenosine and
lactate concentrations by developing a new technique which combines a cardiac microdialysis probe and a Clark-type P O(2)
electrode. The combined and the single microdialysis probes were implanted in the left ventricular myocardium of anesthetized pigs. The consequences of the combined use of microdialysis and P O(2)probes on myocardial
PtiO(2)and microdialysis performances against
glucose were evaluated. A moderate but significant reduction in the relative recovery against
glucose of the combined probe was observed when compared to that of the single microdialysis probe (42+/-2 v 32+/-1%, mean+/-S.E. M.n=5 P<0.05), at 2microl/min microdialysis probe perfusion flow. Similarly, myocardial
oxygen enrichment, measured by the P O(2)
electrode, was negligible when microdialysis probe perfusion flow was 2microl/min. Systemic
hypoxia (FiO(2)=0.08) resulted in a significant decrease in
PtiO(2)from 30+/-4 to 11+/-2 mmHg, limited increase in coronary blood flow (CBF), and a significant increase in myocardial
adenosine and
lactate concentrations from 0.34+/-0.05 to 0.98+/-0.06micromol/l and from 0.45+/-0.05 to 0.97+/-0.06 mmol/l respectively (P<0.05). Increasing the FiO(2)to 0.3 restored the
PtiO(2)and hemodynamic parameters to baseline values with no changes in interstitial
adenosine and
lactate concentrations. Nevertheless, myocardial interstitial
adenosine remained significantly higher than baseline values. In conclusion, this study demonstrates the ability of a combined probe to measure simultaneously regional myocardial
PtiO(2)and metabolite concentration during
hypoxia. The
hypoxia-induced increase in myocardial
adenosine persists after correction of
hypoxia. The physiological significance of this observation requires further studies.