Time course of ischemic alterations during normothermic and hypothermic arrest and its reflection by on-line monitoring of tissue pH.
Currently there are no techniques available for the intraoperative on-line assessment of the adequacy of myocardial preservation during cardiac operation. The efficacy of a new intramyocardial pH electrode in quantitating myocardial ischemic damage and monitoring myocardial preservation was investigated by correlating changes in intramyocardial pH with the time course of metabolic, histologic, and ultrastructural alterations during global ischemia. Seventeen open-chest dogs were placed on cardiopulmonary bypass and the aorta was cross-clamped for 2 hours. In Group I (n = 8), aortic cross-clamping was performed under normothermia. Group II (n = 9) received 4 degrees C potassium cardioplegia immediately after cross-clamping and consecutively every 30 minutes thereafter. Intramyocardial carbon dioxide tension (Pco2) and intramyocardial pH were measured continuously. Serial transmural biopsies were obtained before and at 5, 15, 30, 60, 90, and 120 minutes after cross-clamping for biochemical and structural analysis. During the period of cross-clamping, mean myocardial temperature was 33 degrees C in Group I and 19 degrees C in Group II. Intramyocardial pH at the end of 2 hours of anoxic arrest reached 5.39 +/- 0.08 in Group I and 6.49 +/- 0.13 in Group II (both values p less than 0.01 compared to prebypass values). Intramyocardial Pco2 rose from 41 +/- 4 to 234 +/- 13 mm Hg in Group I (p less than 0.001) and did not change in Group II. Tissue content of adenosine triphosphate (ATP) decreased by 51% in Group I and by 14% in Group II (p less than 0.01 compared to prebypass value). Tissue creatine phosphate was depleted in Group I and decreased by 48% in Group II. The degree of ischemic damage assessed by a mean ischemic score was 2.15 +/- 0.06 in Group I and 0.75 +/- 0.19 in Group II (p less than 0.001). Irreversible structural damage assessed by electron microscopy occurred in Group I 60 to 90 minutes after cross-clamping and was associated with an intramyocardial pH below 6.2. No such damage was observed in Group II. Therefore, intramyocardial pH is shown to be a reliable indicator of the severity of ischemic damage during anoxic arrest under normothermic conditions and of the adequacy of preservation under hypothermic conditions. Measurement of intramyocardial pH may provide a potentially useful tool for the intraoperative on-line monitoring of the adequacy of myocardial preservation in patients undergoing cardiac operation.
D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D002245:Carbon Dioxide / Q000032:analysis; D004285:Dogs; D005260:Female; D006324:Heart Arrest, Induced; D006863:Hydrogen-Ion Concentration; D007035:Hypothermia; D007511:Ischemia / Q000503:physiopathology*; D008297:Male; D008991:Monitoring, Physiologic; D009206:Myocardium / Q000032:analysis / Q000378:metabolism* / Q000648:ultrastructure; D010725:Phosphocreatine / Q000032:analysis; D013997:Time Factors
D010725:Phosphocreatine; D002245:Carbon Dioxide; D000255:Adenosine Triphosphate