Effects of sepsis-induced acute lung injury on glycogen content in different tissues.

The metabolic profile is very affected in sepsis, which is the most important cause of extrapulmonary acute lung injury (ALI-EX). The aim of the present study was to investigate whether sepsis-induced ALI-EX in mice affects the glycogen content in different tissues. This measurement could indicate performance limitations of tissues and constitute a novel biochemical aspect of ALI. ALI was induced by cecal ligation and puncture (CLP), which is a model that reproduces clinical and pathological alterations stemming from sepsis. Control group mice were sham-operated. Glycogen content (mg/g tissue) from different tissues was measured using the anthrone reagent. Glycogen content in the diaphragm (0.3 +/- 0.1) and gastrocnemius muscle (0.4 +/- 0.1) was lower in the sepsis group than the control group (0.9 +/- 0.1 and 1.1 +/- 0.2, respectively). However, there were no significant differences in glycogen content in the heart and kidney. Sepsis caused a greater thickening of the alveolar walls, more areas of atelectasis, and a greater abundance of inflammatory cells in comparison to the control group. These results demonstrate that glycogen content in sepsis-induced ALI-EX is altered in different tissues.

Effects of vasoactive intestinal polypeptide microinjected into the nucleus tractus solitarius on jejunal electrolytes absorption in rats.

It has been shown that vasoactive intestinal polypeptide (VIP) injected into the nucleus tractus solitarius inhibits alanine absorption across the jejunum. The aim of the present study was to investigate the effects of VIP injection into the nucleus tractus solitarius on jejunal absorption of electrolytes in the rat. Fifty-three Wistar rats were submitted to midline laparotomy to expose and isolate 20 cm of jejunal loop and to perform a subdiaphragmatic troncular vagotomy. Saline or VIP (10 pg 100 nl(-1)) was injected into the rostral nucleus tractus solitarius using a stereotaxic instrument. Tyrode solution, pH 8, containing twice glucose, sodium and potassium concentration was infused (0.5 ml min(-1)) into the jejunal loop. Samples were taken at 10-min intervals during the 40-min-experiment. Injection of VIP into the nucleus tractus solitarius increased jejunal potassium absorption. Moreover, VIP associated with vagotomy resulted in inhibition of jejunal potassium absorption by VIP alone at 40 min after perfusion (5.99 +/- 0.74 vs. 9.83 +/- 0.57 microM). There was no change in jejunal sodium absorption in any of the experimental groups. VIP had a modulatory action on jejunal potassium absorption when injected into the nucleus tractus solitarius.

Effects of vasoactive intestinal polypeptide microinjected into the nucleus tractus solitarius on jejunal glucose absorption in rats.

It has been shown that vasoactive intestinal polypeptide (VIP) injected into the nucleus tractus solitarius and into the dorsal motor nucleus of the vagus inhibits alanine absorption across the jejunum. The aim of the present study was to investigate the effects of VIP injection into the nucleus tractus solitarius on jejunal absorption of glucose in the rat. Forty Wistar rats were submitted to midline laparotomy to expose and isolate 20 cm of jejunal loop and to perform a subdiaphragmatic troncular vagotomy. Saline or VIP (10 pg 100 nl(-1)) was injected into the rostral nucleus tractus solitarius using a stereotaxic instrument. Tyrode solution, pH 8, containing twice glucose, sodium, and potassium concentrations was infused (0.5 ml min(-1)) into the jejunal loop. Samples were taken at 10-min intervals during the 40-min experiment. Injection of VIP into the nucleus tractus solitarius associated with vagotomy resulted in inhibition of jejunal glucose absorption by VIP alone at 10 and 40 min after perfusion (2.75+/-0.19 vs. 3.53+/-0.29 mg). The vagal outflow tract maintained jejunal glucose absorption even when VIP was microinjected into the nucleus tractus solitarius.

Peripheral glucose metabolism is altered by epileptic seizures.

The aim of the present study was to investigate the status of jejunal absorption and peripheral metabolism of glucose in Wistar Audiogenic Rats (WAR), a genetic model of epilepsy, after seizures induced by intensive sound exposure. The jejunal loop of rats was isolated and infused (0.5 mL min(-1)) with Tyrode solution containing twice the normal concentrations of glucose, sodium, and potassium. Samples were taken at 5 or 10-min intervals over a 40-min period. At the end of the experiment, samples of liver and gastrocnemius muscle were taken to measure the levels of glycogen, glucose-6-phosphate, fructose-6-phosphate and glucose transporter-4 (GLUT4). Hepatic glucose-6-phosphate increased in WAR submitted to audiogenic seizure (21.90 +/- 3.08) as compared to non-susceptible Wistar rats (8.12 +/- 0.87) and to WAR not submitted to audiogenic stimulation (5.17 +/- 0.97). In addition, an increase in hepatic fructose-6-phosphate, an intermediate metabolite of the glycolytic pathway, was observed in WAR submitted to audiogenic seizure (5.98 +/- 0.99) compared to non-susceptible Wistar rats (2.38 +/- 0.53). According to the present results, jejunal absorption of glucose was not changed by seizures. However, generalized tonic-clonic seizures produced by sound stimulation resulted in a decrease in muscle glycogen content. In addition, our results demonstrated that the concentration of GLUT4 in the gastrocnemius muscle of WAR was 1.6-fold higher than that observed in resistant rats and that the audiogenic stimulus led to decreased concentration of this receptor in the muscle of WAR animals.

Route of jejunal mucosa absorption of trypsin demonstrated by immunofluorescence.

Previous studies have demonstrated the absorption of porcine trypsin in isolated jejunal loops from male Wistar rats by open-loop perfusion. The possible routes of absorption were examined in the study reported here. Trypsin (0.5 mg/ml) was dissolved in tyrode solution and perfused at a rate of 0.5 ml/min, at 37 degrees C, for 40 min. Using immunoperoxidase and immunofluorescence techniques, strong reactivity towards anti-TLCK-trypsin antibody was demonstrated through out the enterocyte cytosol. The present data indicate that trypsin was absorbed by enterocytes, probably through a transcellular route.