Postoperative hyperglycemia and previously undiagnosed diabetes are associated with development of SSIs among cardiothoracic surgery patients. Screening for diabetes and hyperglycemia among patients having cardiothoracic surgery may be warranted to prevent postoperative and chronic complications of this metabolic abnormality.

SUMMARY1. 31P nuclear magnetic resonance was used to measure the relative concentrations of phosphorus-containing metabolites in Langendorff-perfused ferret hearts. Intracellular concentrations of inorganic phosphate ([Pi]i), phosphocreatine ([PCr]i), ATP ([ATP]i) and H+ (pHi) were monitored under control conditions and while oxidative phosphorylation and/or glycolysis were prevented. Mechanical performance was assessed by recording the pressure developed in a balloon placed in the left ventricle.2. Oxidative phosphorylation was prevented either by replacement of 02 with N2 or by addition of cyanide. When the rate of oxidative phosphorylation was reduced by either method, developed pressure fell to a stable level of about 35 % of control after 5 min. The pHi (control value 6 98) first increased to a peak of 7 07 after 2 min but then decreased to give a stable acidosis (pH 6 85).[PCr]i decreased rapidly to about 15 % of the control value after 5 min whereas [ATP]i declined very slowly, reaching about 90 % of the control value after 10 min.3. Reduction in the rate of glycolysis was achieved either (i) by removal of external glucose and depletion of glycogen stores by a long (1-2 h) period of stimulation or (ii) by removal of glucose and application of 2-deoxyglucose (1 mM) for 30-60 min.These procedures had only a small effect on pressure development, [ATP]i, [PCr]i and pHi. Measurements of lactate production showed that these procedures reduced the rate of glycolysis by a factor of about 10.4. When oxidative phosphorylation was prevented during periods when the rate ofglycolysis was reduced, developed pressure fell to less than 5 % of control after 5 min and there was a subsequent increase in resting pressure hypoxicc contracture). pHi (control value 7 03) first increased to a peak of 7-12 and then declined to about pH 7 00, but there was no subsequent acidosis. [PCr]i fell rapidly to about 10 % of control after about 5 min while [ATP]i declined to about half of its control value over 10 min.5. It is concluded that (i) when oxidative phosphorylation alone is prevented, the

3. In conditions of Ca overload, the systolic light signal was either similar in amplitude or larger than the systolic light observed under conditions which did not lead to Ca overload. Oscillations of diastolic light were invariably present under conditions of Ca overload. These oscillations were accompanied by after-contractions which were small in relation to the magnitude of the aequorin light oscillations.4. During Ca overload, the variance of the amplitude of the systolic light signal was greater than could be accounted for by the random nature of the arrival of photons. Small systolic light signals occurred when there had been an oscillation of light in the diastolic period immediately preceding the systolic light signal. Large systolic light signals occurred when the preceding period (-1 s) was free of oscillations of light.5. These observations suggest that if the sarcoplasmic reticulum (s.r.) has spontaneously released its contents of Ca as shown by a diastolic [Ca2+], oscillation, then a stimulated systolic Ca signal occurring within about the next second is smaller, possibly because it takes longer than this period for the s.r. to reload with Ca. If this process occurs randomly in the various cells of the preparation, developed tension will be reduced because those cells which have a small Ca release will act as a compliance in series with cells which have a large Ca release.

The reasons for the marked variability in expansion of myocardial infarcts are unknown. To examine this question, the hearts in 204 patients with a single myocardial infarct, autopsied at The Johns Hopkins Hospital and studied after coronary arteriography and fixation in distension, were reviewed. There were 58 (28%) hearts with marked infarct expansion, 34 (17%) with moderate expansion and 112 (55%) with no or minimal expansion. The degree of expansion was greater in larger, more transmural infarcts (p less than 0.001). Infarcts with greater expansion had significantly more endocardial thrombus (p less than 0.001) and endocardial fibroelastosis (p less than 0.01). Larger heart weight and degree of left ventricular hypertrophy had a significant negative correlation with infarct expansion (p less than 0.05). A markedly greater degree of expansion was noted in the 101 infarcts (50%) caused by lesions in the distribution of the left anterior descending coronary artery as compared with the 57 infarcts (28%) secondary to right coronary lesions and the 46 infarcts (23%) in the distribution of the left circumflex coronary artery (p less than 0.001). The results show that expansion is associated with large infarcts but is less marked in hearts with ventricular hypertrophy. Expansion occurs predominantly in infarcts in the left anterior descending coronary artery distribution, that is, regions of the left ventricular myocardium with the greatest curvature. These results suggest that the degree to which an infarct expands may be influenced by the preinfarction thickness of the ventricular wall.

Studies of myocardial function during ischaemic or anoxia would be assisted if it were possible to inhibit glycolysis completely and reversibly. Three methods of preventing glycolysis in isolated perfused ferret hearts were studied: (a) the removal of glucose from the perfusate followed by manoeuvres designed to deplete glycogen stores, (b) the use of 2-deoxyglucose, and (c) the use of iodoacetate. The rate of glycolysis before and after applying the three methods was assessed by measuring lactate production during short periods of anoxia. Metabolic changes associated with each method were investigated with phosphorus nuclear magnetic resonance, and other side effects associated with each method were assessed by measuring developed pressure. The results show that removal of glucose followed by glycogen depletion reduced the rate of glycolysis to any chosen extent and that the method was reversible. 2-Deoxyglucose treatment did not lead to complete inhibition of glycolysis, was not reversible, and reduced the concentrations of phosphocreatinine and adenosine triphosphate in the heart. Iodoacetate treatment completely blocked glycolysis, but it was not reversible and subsequent periods of anoxia lead to a rapid fall in adenosine triphosphate owing to the accumulation of phosphorylated glycolytic intermediates.