Back to the reinnervation of the pancreas after transplantation? (Experimental study on dogs, cats, and rats).

BACKGROUND: Significant functional decrease and sclerosis of the pancreas graft in late delays cannot only be related to chronic rejection. Any transplantation leads to graft denervation, which may be an important cause of dysfunction. Studies concerning graft reinnervation were controversial. PURPOSE OF THE STUDY: The purpose of this study was to investigate the feasibility and pertinence of a surgically directed reinnervation (SDR) of denervated/neuro-reflex isolated (NRI) or autotransplanted (aTx) pancreas. BASIC PROCEDURES: Anatomy of the nerves penetrating into the pancreas was studied in humans, dogs, cats, and rats. Surgery and physiological investigations were performed in dogs, cats, and rats. Nervous conductivity between NRI, NRI+SDR pancreas, and brain was tested. Load tests with glucose, insulin, and adrenalin were performed; amylase and lipase were determined in fasted and not fasted animals to evaluate the influence of NRI and SDR on pancreatic function. Histology was provided. Observation delays were 6 months. MAIN FINDINGS: Anatomic feasibility of SDR in humans and animals was proved. Models of pancreatic tail NRI and surgical reconstitution of the interrupted nervous pathways (SDR) were elaborated in animals. The restoration of the pancreas-brain reflex axis after SDR was electro physiologically proved. As blood glucose curves after load test, exocrine amylase and lipase determination have shown that pancreas NRI or aTx leads to an exaggerated reaction to usual stimulations that may cause the observed graft functional exhaustion in late delays. SDR shortened the period of the graft neuro-reflex isolation, contributed to a quick normalization of its function, and prevented its late degradation. CONCLUSION: SDR was shown to be a simple surgical technique, easily performed after the graft surgical revascularization. Its functional and morphological efficiency was tested and proved. Thus, SDR may be recommended in human pancreas transplantation as pertinent.

Use of a temperature gradient measuring device in monitoring of diabetic and critically ill patients.

A device realizing the simultaneous measure of the central body temperature (Tc), the superficial one (Ts) and their difference (Dt), was proposed for permanent energetic balance evaluation in humans. A program was elaborated to command the intravenous delivery of insulin by a pump depending on the value and trends of Dt. The use of this device for monitoring of decompensated diabetic patients allowed their easier stabilization. In critically ill patients (post transplantation, myocardium infarction) it had a diagnostic and prognostic value, and was helpful for optimization of conventional and insulin therapy.

[Effect of pentagastrin on the survival of allogenic grafts from fetal rat intestine]. / Influence de la pentagastrine sur la survie des greffons allogéniques d'intestin foetal chez le rat.

OBJECTIVES: Pentagastrin is not known as an immunomodulatoring drug. The aims of the present study were to create an optimal schedule for pentagastrin administration and to evaluate its influence on the allogenic foetal intestinal graft survival and the recipient condition in rats. METHODS: An allogenic foetal intestinal graft was performed in rats treated by pentagastrin 1 mg/kg/day and in controls. Biomorphometry and histology of the graft was regularly studied and biochemical, hematological, immunological and morphological parameters were determined in a maximal observation time of 19.5 months. RESULTS: Pentagastrin treatment, 1 mg/kg/day, significantly increased the graft survival in rats and. In 50% of the cases, tolerance was reached without any damage for the recipients. This may be due to additional effects of mild immunodepressive and trophic influences of pentagastrin, which have to be confirmed and which could be useful in adult intestine transplantation.

Preservation of the anomeric specificity of glucose-induced insulin release in partially pancreatectomized rats.

Attenuation, suppression or even inversion of the normal preference of glucose-stimulated insulin release for the alpha-anomer of the hexose was recently proposed to represent a feature of Beta-cell glucotoxicity in Type 2 (non-insulin-dependent) diabetes mellitus. Since recent reports emphasize the possible significance of Beta-cell secretory hyperactivity as a determinant of such a glucotoxicity, the anomeric specificity of glucose-induced insulin release was examined in normoglycaemic partially pancreatectomized rats. About 80-85% of the pancreas was removed, the animals then being given sucrose via their drinking water up to the time of killing. In these animals, alpha-D-glucose was more efficient than beta-D-glucose in stimulating insulin release from the perfused pancreas, the alpha/beta ratio in insulin output not being significantly different from that found in control rats. It is concluded, therefore, that the anomeric malaise, taken as a manifestation of Beta-cell glucotoxicity, it attributable to hyperglycaemia rather than to Beta-cell secretory hyperactivity.

[Reaction of intercellular contacts of the intestinal epithelium to a non-specific stress]. / La réaction des contacts intercellulaires de l'épithélium intestinal à une agression non spécifique.

The influence of a short-term ischemia on the small intestinal epithelial cell contacts was studied in the rat. The cell contact condition was evaluated by the parameters of the paracellular ionic permeability and the cell adhesion. A severe diminution of the adhesion is noted immediately after the ischemia and during the next 4-8 h, after what it is replaced by an increase above the control values while the mitotic index is reduced. On the 4th day an increase of the mitotic index is accompanied by a new reduction of the cell adhesion. The fluctuation of the cell adhesion is always accompanied by a fall of the transepithelial resistance and a modification of the relative ionic permeability PNa/PCl. These and other data may be a sign of deep and long alterations in the enterocyte plasmic membranes as an answer to the ischemic trauma, as well as a proof of the influence of the cell contact state on the cellular turn-over.