Comparison of myoglobin and creatine kinase MB levels in the evaluation of myocardial injury after cardiac operations.

Myoglobin was studied in 40 patients before, during, and after cardiac operations and was compared to the MB isoenzyme of creatine kinase to identify its possible role as a marker of perioperative myocardial damage. Myoglobin reached peak values during cardiac arrest in all patients and was significantly higher immediately after administration of the anesthetics, during cardiac arrest, and until the sixth postoperative hour in eight patients with a perioperative myocardial infarction. By contrast, the MB isoenzyme of creatine kinase reached peak values at the fourth postoperative hour and was significantly higher in patients with perioperative myocardial infarction from the fourth to the tenth postoperative hours. We conclude that myoglobin is a valuable marker of perioperative myocardial damage and is an earlier and more specific marker of perioperative myocardial infarction than creatine kinase MB.

[Myoglobin: an early indicator of myocardial infarction during heart surgery]. / La myoglobine: un marqueur précoce de l'infarctus myocardique au cours de la chirurgie cardiaque.

Plasma myoglobin was measured in 40 patients before, during and after cardiac surgery under cardiopulmonary bypass, in order to study its value as an indicator of intra-operative myocardial damage. Myoglobin levels rose at cannulation, further increased during the operation and reached a peak 2 hours later; they began to decrease 6 hours after surgery and were back to normal 24 hours later. Myoglobin levels from induction of the anesthetics to the 6th post-operative hour were significantly higher in the 8 patients who developed intra-operative myocardial infarction than in the other patients. Thus, myoglobin is an early indicator of intra-operative myocardial ischaemia. An abnormal rise of myoglobin at induction of the anesthetics characterizes a group of patients at high risk of myocardial infarction during surgery.

Effects of somatostatin added to insulin in a glucose-controlled insulin infusion system.

Five insulin treated diabetics were studied on three consecutive days. Overnight variable intravenous insulin infusions were used before each study to maintain normoglycaemia and to calculate the optimal basal insulin infusion rate (1.1 +/- 0.1 U/h) which ws then kept constant throughout the study day. A standard 400 kCal breakfast with 25 g xylose was given at 0800 h. When the blood glucose rose above 4.1 mmol/l, an external artificial pancreas was used to infuse either extra insulin (day INS) or somatostatin for either 3h (day som) or the entire 8h experimental period (day SOM). Peak post-prandial blood glucose values were similar on all three days. The blood glucose rebounded after the cessation of the somatostatin infusion on day som. Post-prandial blood xylose peaks were lowered by somatostatin on both days but rebounded after the cessation of the somatostatin infusion on day som. The area under the plasma and urinary xylose curves was lowered by somatostatin only on day SOM. Growth hormone and glucagon levels were not statistically different on all 3 days. Thus somatostatin, when added to an optimal insulin infusion, minimised the insulin requirements by slowing intestinal absorption, but led to rebound hyperglycaemia if not feed-back controlled.

Intestinal and renal handling of calcium in human diabetes mellitus: influence of acute oral glucose loading and diabetic control.

The intestinal absorption and the urinary excretion of calcium were compared in two groups of diabetic patients during periods of satisfactory and poor control. In a first group of ten patients, periods of isolated high glycosuria were obtained by giving an oral glucose load. The second group consisted of ten patients with a severe endogenous insulin deficiency. The subjects of this latter group were investigated before and after a few days of insulin therapy. In group I, the oral glucose load induced a significant increase in the intestinal calcium absorption and had a tendency to lower the urinary calcium excretion. Furthermore, an inverse relationship was found between the changes in the intestinal calcium absorption and the variations of the urinary calcium excretion. In group II, both intestinal absorption and urinary excretion of calcium fell significantly after recovery of satisfactory metabolic control by insulin therapy. From the results as obtained in group I one can conclude that glucose enhances the calcium transfer from the luminal to the serosal pole of both intestinal and renal tubular cells. During severe ketosis as observed in group II, calcium metabolism is considerably accelerated and the increase in the intestinal calcium absorption rate may be interpreted as compensatory mechanism for the high urinary loss of calcium.