The synthesis of [Ru(NO(2))L(bpy)(2)](+) (bpy = 2,2'-bipyridine and L = pyridine (py) and pyrazine (pz)) can be accomplished by addition of [Ru(NO)L(bpy)(2)](PF(6))(3) to aqueous solutions of physiological pH. The electrochemical processes of [Ru(NO(2))L(bpy)(2)](+) in aqueous solution were studied by cyclic voltammetry and differential pulse voltammetry. The anodic scan shows a peak around 1.00 V vs. Ag/AgCl attributed to the oxidation process centered on the metal ion. However, in the cathodic scan a second peak around -0.60 V vs. Ag/AgCl was observed and attributed to the reduction process centered on the nitrite ligand. The controlled reduction potential electrolysis at -0.80 V vs. Ag/AgCl shows NO release characteristics as judged by NO measurement with a NO-sensor. This assumption was confirmed by ESI/MS(+) and spectroelectrochemical experiment where cis-[Ru(bpy)(2)L(H(2)O)](2+) was obtained as a product of the reduction of cis-[Ru(II)(NO(2))L(bpy)(2)](+). The vasorelaxation observed in denuded aortic rings pre-contracted with 0.1 mumol L(-1) phenylephrine responded with relaxation in the presence of cis-[Ru(II)(NO(2))L(bpy)(2)](+). The potential of rat aorta cells to metabolize cis-[Ru(II)(NO(2))L(bpy)(2)](+) was also followed by confocal analysis. The obtained results suggest that NO release happens by reduction of cis-[Ru(II)(NO(2))L(bpy)(2)](+) inside the cell. The maximum vasorelaxation was achieved with 1 x 10(-5) mol L(-1) of cis-[Ru(II)(NO(2))L(bpy)(2)](+) complex.
SUMMARY The effect of pentagastrin in step-wise increasing doses of 0.02, 0.2, 2.0, and 20 nmol/kg/h (0.01, 0 1, 1.0, and 100 ,ug/kg/h) on pepsin and acid secretion was studied in seven healthy subjects. The study was repeated on another day during infusion of glucagon in a dose of 103 pmollkg/h (0.36 ug/kg/h) which results in plasma-glucagon concentrations comparable with those seen after a protein-rich meal. Pepsin output was maximal after 0.2 nmol/kg/h (0. 1 ,ug/kg/h) of pentagastrin and 20 nmolkg/h (10 ,ug/kg/h) resulted in a marked decrease. The dose of pentagastrin required for half-maximal pepsin output was less than 0. 1 nmollkg/h (0.05 ,ug/kg/h). When the study was repeated during infusion of glucagon, the dose-response curve was shifted to the right. The highest pepsin output was obtained with 20 nmol/kg/h (10 ,uglkg/h) of pentagastrin and D50 increased to well over 1 ug/kg/h. The dose of pentagastrin required for half-maximal acid secretion was about 0 3 nmollkg/h (0. 15 ug/kg/h) indicating that the sensitivity of the chief cells to pentagastrin is more than three times that of the parietal cells.There is evidence that pancreatic glucagon participates in the physiological inhibition of gastric acid secretion.1 2 Whether glucagon is involved in the physiological control of pepsin secretion also is unknown, as previous studies on glucagon and pepsin secretion have been performed with supraphysiological doses of glucagon.35The present study investigates the dose-response relationship of pentagastrin and pepsin secretion and the effect on the dose-response curve of glucagon administered exogenously in a dose resulting in plasma concentrationsa comparable with those seen after a protein-rich meal. Each subject was studied twice on separate days. On the first day a step dose-response study of the effect of pentagastrin on gastric acid and pepsin secretion was performed. After an overnight fast, a Levin tube was positioned under fluoroscopic control and the stomach was emptied. Through a thin polyvinyl tube welded to the Levin tube 51Cr-EDTA dissolved in 0.9% saline was infused with a flow of 30 ml/h in order to determine recovery. Basal secretion was collected for one hour. Pentagastrin was administered by continuous intravenous infusion in doses of 0.02, 0-2, 2.0, and 20 nmol/kg/h (0.01, 01, 1.0, and 100 ,ug/kg/h), each dose being administered for one hour. (These doses of pentagastrin were the same as those used in a previous study of pentagastrin glucagon interaction on acid secretion.1) On the second day the step dose-response study with pentagastrin was repeated but now on a background infusion of glucagon in a dose of 103 pmol/kglh (0.36 Methods
Amylase activity was measured in normal sera and serum of patients with acute pancreatitis and mumps. A significant decrease of enzyme activity in patients with acute pancreatitis was observed after incubation with specific antibody against hog pancreas amylase. A minimal effect of the antibody on normal serum and on that from mumps patients was noted. A comparable effect was observed in the presence of glyceraldehyde used as an amylase differentiating factor.
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