Stimulus for vasopressin release during elective intra-abdominal operations.

In 12 patients undergoing an upper abdominal operation, blood pressure and peripheral venous blood samples were taken at intervals throughout the procedure. There was no significant increase in plasma vasopressin concentration after induction of anaesthesia or skin incision; within 3 min of opening the peritoneum and commencing intraperitoneal manipulation there was a highly significant rise (P less than 0.01), maintained with fluctuations until closure of the abdomen. There was no correlation between the changes of blood pressure and those in plasma vasopressin level. In 16 patients undergoing elective cholecystectomy similar observations were made to coincide with events believed, on the basis of the first study, to be related to changes in the concentration of vasopressin. There was a significant rise in vasopressin concentration (P less than 0.01) after incision of the peritoneum, 1 min after the start of intraperitoneal manipulation (P less than 0.01) and after deliberate traction on the stomach (P less than 0.01). During operative cholangiography, when there was no intraperitoneal manipulation, there was a significant fall in the vasopressin level. There was no correlation between changes in vasopressin concentration and blood pressure. These findings indicate that during an abdominal operation nervous stimuli, arising from within the peritoneal cavity and probably mediated via the autonomic system, are an important factor responsible for the increased secretion of vasopressin, and, at least in the absence of major changes in blood pressure and osmolality, the determinant factor.

The stimulus for vasopressin release during laparoscopy.

The results of our study have demonstrated raised AVP secretion during laparoscopy, which was stimulated by the maximal increase in IAP. We propose that this relationship is mediated by way of known hemodynamic pathways occurring during laparoscopy involving a reduction in intrathoracic blood volume.

Non-enzymatic glycosylation of keratin from the stratum corneum of the diabetic foot.

Non-enzymatic glycosylation of keratin from the stratum corneum of the sole of the foot was measured by the thiobarbituric acid technique in thirty diabetic and thirty control subjects. A significant increase in the level of glycosylation was demonstrated in the diabetic subjects (P less than 0.001). HbA1 levels were measured in a further eighteen subjects at the same time as keratin was removed, and in this group a significant association between non-enzymatic glycosylation of that protein and diabetic control was demonstrated (P less than 0.01). In vitro incubation of keratin in the presence of free glucose produced increased non-enzymatic glycosylation (P less than 0.01) and this effect was blocked by incubation in the presence of increasing concentrations of aspirin (P less than 0.01). Measurement of non-enzymatic glycosylation of keratin in a further group of twenty diabetics with neuropathic ulceration showed a significant increase in levels when compared with a group of diabetics without ulcers (P less than 0.05). As keratin is the principle structural protein of the stratum corneum of the sole of the foot, it is possible that changes in this protein associated with non-enzymatic glycosylation may contribute to abnormalities seen in the skin of the feet of diabetics.