Effective value of myocardial tissue oxygen pressure monitoring during cold ischaemia and reperfusion

Introduction

Recent studies have shown a relation between altered myocardial function and the cardiac cellular changes that are noted with hypothermic cardioplegic arrest, such as energy store depletion and intracellular acidosis. The aim of the study was to evaluate the link between myocardial energy metabolism (high-energy phosphorylated compounds and intracellular pH), as measured using ³¹phosphorus nuclear magnetic resonance spectroscopy (³¹P-MRS) and myocardial tissue oxygen pressure (ptiO₂) in isolated rabbit hearts subjected to 2 h of cold cardioplegic ischaemia and reperfusion.

Method

Ten New Zealand White rabbits (male, 2.5 ± 0.5 kg body weight) were anaesthetized with sodium pentobarbital (45 mg/kg intravenous) and heparinized (700 IU/kg intravenous). The heart was rapidly excised, immersed in physiological salt solution, cannulated and perfused in the Langendorff mode at 37°C. After placing a minimally invasive, flexible catheter partial oxygen tension microprobe (polarographic Clark-type cell O₂-sensor; Licox^® system, GMS, Kiel, Germany) into the left ventricular anterior wall, baseline data were obtained after an equilibration period of 40 min. Hearts were then subjected to 2 h at 10°C of cardioplegic ischaemia and reperfused. The status of phosphorylated cardiac energy metabolites (measured using a 4.7-T high-field ³¹P-MR spectrometer) was assessed, and myocardial tissue oximetry, including temperature compensation, was measured using a microsensor catheter probe (Licox^®). Linear correlation was performed between ³¹P-MRS data and ptiO₂ readings.

Results

Intracellular pH (r = 0.58; P < 0.05), phosphocreatine (r = 0.71; P < 0.01) and inorganic phosphates (r = 0.62; P < 0.05) measured after cardioplegic infusion and onset of ischaemia correlated significantly with the decline in ptiO₂. During reperfusion, only intracellular pH (r = 0.76; P < 0.005) and phosphocreatine (r = 0.84; P < 0.005) values correlated significantly with ptiO₂.

Conclusion

On the basis of these findings, we conclude that ptiO₂ monitoring during surgically induced cold cardioplegic ischaemia and reperfusion appears to provide a real-time minimally invasive estimate of cardiac oxidative metabolism and cellular energy consumption.