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J Pisanty

Publications and source records attributed to J Pisanty.

7 recordsLinked to original sources

Glucose stabilization and coronary infarction with artificial pancreas in heart-lung preparation.

In the performance of heart-lung preparations, after 4-8 hours, it is an usual feature to have multiple microinfarctions, and, finally, heart failure and ventricular fibrillation. We have studied glucose, triglycerides and conjugated fructose consumption by the heart-lung preparation and found a very fast glucose depletion (30 to 90 minutes to glucose 0, starting with glucose 120 mg/dl). The depletion has been slower for triglycerides and even slower for conjugated fructose. Ventilation with pure oxygen has not modified itself the coronary deterioration, but if a Biostator has been used in order to maintain the glucose levels at 100-110 mg/dl., the isolated heart-lung does not deteriorate in 16-24 hours, nor show electrical signs of coronary impairment; after this time, the respirator is disconnected and the preparate discarded. The above mentioned experiments demonstrated the need of artificial control of glycemia in isolated organ experiments and suggest the convenience to use more widely the artificial pancreas (Biostator in our case) for better treatment no only in diabetic or pancreatic patients, but also in many circumstances in which the glucose utilization is impaired.

Animals↗

[Increase of conjugated bilirubin in diabetics].

Three hundred patients were studied: 150 had NIDDM and the other 150 were non diabetics. Serum glucose and total and fractionated bilirrubin were measured in samples taken after night fasting. The mean glucose in the NIDDM group was 180.4 +/- 17.9 mg/dL (+/- SD) and 82.7 +/- 4.4 mg/dL in the non diabetic (p < 0.001). The levels of total bilirrubin were similar in both groups (0.84 +/- 0.04 vs 0.81 +/- 0.02 mg/dL, p > 0.40) but there were group differences in direct bilirrubin (NIDDM 0.52 +/- 0.03 vs 0.20 +/- 0.01 mg/dL, p < 0.001) and in indirect bilirrubin (NIDDM 0.32 +/- 0.03 vs 0.61 +/- 0.02 mg/dL, p < 0.001). Thus, 62% of the circulating bilirrubin was conjugated in the diabetics and only 25% in the non diabetics. We believe that at least part of the UDP-glucose pathway is altered in NIDDM and leads to an increase in the levels of glucouronic acid and, in turn, may cause a rise in direct bilirrubin at the expense of indirect bilirrubin.

Adult↗