Direct measurement of myocardial oxygen tension and high energy phosphate content under varying ventilatory conditions in rabbits.

Effective myocardial oxygen supply should not be compromised during cardiac surgery as it is essential to avoid circulatory and cardiac dysfunction. Local measurement of myocardial oxygen partial pressure (pO2) was therefore introduced into the operative monitoring of myocardial ischemia. The aim of the present study was to assess whether myocardial oxygen partial pressure correlates with the content of high energy phosphates (HEPs). Seven male rabbits were examined in parallel with measurement of myocardial pO2 by an implanted Clark electrode and 31phosphorus-NMR spectroscopy. The ventilatory management established hyperoxygenation followed by systemic hypoxia with hypercapnia for 20 min. Additionally, analysis of end-expiratory gas composition in combination with blood gas analysis was performed simultaneously, and hemodynamic parameter was recorded. Under hypoxic conditions the cardiovascular system was severely compromised, whereas the myocardial pO2 was only moderately impaired (pO2M 45.0+/-16.0 mm Hg). Immediately before cardiac arrest, low values of arterial and venous pO2 were found (17.6+/-6.0 and 12.9+/-6.1 mm Hg). In contrast to near normal myocardial pO2, HEP content in the myocardium was considerably reduced and inorganic phosphorus was increased. Artificial ventilation leading to systemic hypoxia and eventually circulatory arrest resulted in almost normal myocardial pO2 but severely compromised HEP content. This somewhat unexpected finding requires further clarification, but is in accordance with findings reported previously where regulatory mechanisms have been shown to play a role in the pathophysiology of severe hypoxic conditions such as those for cellular oxygen delivery and demand, P/O coupling and finally control of HEP production facilitating the interaction between respiratory chain and myoglobin oxygen transport.