We investigated microcirculatory changes in sodium taurocholate (ST)-induced pancreatitis. Groups of rats received as tracer either fluorescein isothiocyanate-dextran or acridine orange intravenously. The microcirculation of the exposed pancreas was observed by use of a video camera attached to an epi-illumination microscope. Vessel diameters and plaques of adherent leukocytes were measured with a digital image-analyzing system. In contrast to 0.4 ml of saline, intraductal infusion of ST (4%, 0.4 ml) induced a constriction of interlobular pancreatic arteries of 79 +/- 2% (P < 0.01) within 2 min. This constriction could not be antagonized by the leukotriene antagonist CGP-35949B. The radical scavengers superoxide dismutase (SOD) and N-(2-mercaptopropionyl)glycine (MPG) prevented the arterial constriction. Constriction of pancreatic arteries was accompanied by a decrease of erythrocyte velocity in the pancreatic capillaries. Flux in the head of the pancreas measured by laser-Doppler velocimetry decreased from 300 +/- 69 to 74 +/- 23 perfusion units (P < 0.01) after 446 +/- 159 s. Subsequently an increase of perfusion values was observed indicating reperfusion phenomena. ST induced leukocyte adherence to the walls of interlobular veins forming plaques constituting 39% of the observed venular cross section within 6 min. The leukotriene antagonist, SOD, or MPG prevented leukocyte adherence. Arterial constriction followed by ischemia-reperfusion and leukocyte adherence to venular endothelium during the reperfusion period represented the sequence of microcirculatory changes in ST-induced pancreatitis. The radical scavengers SOD and MPG prevented arterial constriction and leukocyte adherence to venular endothelium, indicating the involvement of free radicals in the pathogenesis of ST-induced pancreatitis in the rat.
Using an in vivo microscopy technique, we studied the microcirculatory changes in sodium taurocholate-induced pancreatitis in rats. With a computerized image analyzer system, blood flow, vascular permeability changes, and capillary densities were measured. Intraductal infusion of 0.4 ml saline had only minor effects on the microcirculation. Various concentrations and volumes of sodium taurocholate solutions were infused into the pancreatic duct. Sodium taurocholate (0.4 ml, 4%) led to increased vascular permeability preceding stasis within 232 +/- 47 s, followed by hemorrhagic necrosis in the head of the pancreas. In the corpus close to the tail of the pancreas capillary blood flow was maintained. In conclusion, this study shows that the microcirculation of the pancreas can be excellently investigated with in vivo microscopy. With this method, tremendous distribution disturbances of the microcirculation in the pancreas can be seen in the course of acute pancreatitis. Vascular permeability changes and stasis of the microcirculation represent the primary microcirculatory events in acute pancreatitis induced by sodium taurocholate in the areas where hemorrhagic necrosis occurs.
Background: In patients with diabetic gastroparesis, delayed food delivery to the intestine may become a major obstacle to post‐prandial glycaemic control. Aim: To investigate whether cisapride accelerates gastric emptying in the long term or improves diabetes control in patients with diabetic gastroparesis. Methods: Eighty‐five patients with long‐standing insulin‐dependent diabetes mellitus (glycosylated haemoglobin (HbA1c) > 7.0%), dyspepsia and diabetic neuropathy were tested for impaired gastric emptying of solids by the 13C‐octanoate breath test. Nineteen of these patients with severe diabetic gastroparesis (i.e. t1/2 > 170 min) were randomly treated with 10 mg cisapride t.d.s. (n=9) or placebo (n=10) for 12 months. Thereafter, the breath test, dyspeptic symptoms and HbA1c values were reassessed. Results: Half emptying times in nine patients with diabetic gastroparesis were significantly shortened by cisapride (175 ± 46 min vs. 227 ± 40 min; P < 0.03). Half emptying times in the 10 patients taking placebo did not change (205 ± 37 min vs. 211 ± 36 min, P=0.54). Cisapride significantly reduced dyspepsia (score: 4.1 ± 1.6 vs. 2.0 ± 0.5, P=0.002). HbA1c values after 12 months of treatment were not different (cisapride: 7.7 ± 0.4% vs. 7.6 ± 0.9%, P=0.76; placebo: 7.5 ± 0.6% vs. 7.6 ± 1.5%, P=0.89). Conclusions: Prokinetic treatment with cisapride accelerates gastric emptying of solids and improves dyspeptic symptoms in diabetic gastroparesis. Glycaemic control, however, is not affected by cisapride.
Ischemia-reperfusion injury is a pathogenic factor in the course of many clinical disorders, such as myocardial infarction, stroke, organ transplantation, burns, and circulatory shock. The extent of ischemia-reperfusion injury is dependent on the number of infiltrating leukocytes. With in vivo microscopy, we evaluated the effect of the recombinant form of soluble murine intercellular adhesion molecule-1 (ICAM-1) on ischemia-reperfusion injury in an animal model. A mesenteric vein was occluded with a clamp for 45 min. During a reperfusion period of 30 min, the number of leukocytes rolling along the endothelium and the number of adherent leukocytes were measured with and without pretreatment with recombinant ICAM-1. The number of leukocytes rolling along the endothelial surface increased more than twofold during postischemic perfusion ( P < 0.05). Recombinant ICAM-1 had no effect on leukocyte rolling. In the control group, firm adherence of leukocytes was increased 10-fold. Recombinant ICAM-1 dose dependently reduced firm adhesion to the endothelium in response to prior ischemia. After 30 min, reperfusion pretreatment with recombinant ICAM-1 inhibited leukocyte adherence from 512 ± 123 to 166 ± 34 leukocytes/mm2( P < 0.01). We demonstrate here for the first time that soluble recombinant ICAM-1 is able to reduce leukocyte adherence to mesenteric venules in postischemic reperfusion injury dose dependently. Because soluble ICAM-1 is naturally circulating in human serum, the therapeutic use of soluble recombinant forms of ICAM-1 may represent a physiological way to protect against ischemiareperfusion injury.
In this crossover study, two days of oatmeal intervention allowed a highly significant reduction of required daily insulin doses while maintaining adequate metabolic control as compared to a diabetes adapted diet only. The beneficial effects of the intervention might last for several weeks as shown by the lower HbA1c four weeks after the intervention.
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