Canine myocardial adenosine and lactate production, oxygen consumption, and coronary blood flow during stellate ganglia stimulation.

Publisher Website
Google Scholar
Abstract
The vasodilator adenosine is produced continuously by the normal dog myocardium. The relation of adenosine production to increased cardiac metabolism is unclear. The hypothesis that increased myocardial O2 demand promotes increased adenosine production to match coronary blood flow (CBF) to metabolic requirements was studied. Increased adenosine production should correlate with increased CBF and myocaridal O2 consumption (M.ovrhdot.VO2). Graded changes in CBF were induced through bilateral stellate ganglia stimulation (SGS) in open-chest dogs. Left CBF, M.ovrhdot.VO2, and the adenosine and lactate contents of pericardial infusate (Krebs-Henseleit solution) were measured. Pericardial infusate was placed in contact with the epicardium through a cannula introduced through the otherwise intact pericardium. Left ventricular tissue samples frozen in situ also were obtained after the infusate was withdrawn and analyzed for adenosine and lactate. The correlation of infusate adenosine concentration with CBF was significant, as was the correlation of adenosine concentration with M.ovrhdot.VO2. Tissue adenosine levels increased significantly with SGS and were reflected in significant increases in pericardial infusate adenosine content. Adenosine concentration of the infusate was measured after contact for different times with the epicardium (0.5-18 min) and increased continually throughout the times studied, but it did not reach equilibrium with tissue adenosine levels. Loss of adenosine from the infusate was rapid, indicating a high turnover of pericardial fluid adenosine. Results support adenosine as a coupler of myocardial metabolism to CBF and the use of pericardial infusate adenosine content as an index of tissue adenosine production.