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Biomedical subjects

C Holliger

Publications and source records attributed to C Holliger.

29 records · Page 2Linked to original sources

Methyl-coenzyme M reductase of Methanobacterium thermoautotrophicum delta H catalyzes the reductive dechlorination of 1,2-dichloroethane to ethylene and chloroethane.

Reductive dechlorination of 1,2-dichloroethane (1,2-DCA) to ethylene and chloroethane (CA) by crude cell extracts of Methanobacterium thermoautotrophicum delta H with H2 as the electron donor was stimulated by Mg-ATP. The heterodisulfide of coenzyme M (CoM) and 7-mercaptoheptanoylthreonine phosphate together with Mg-ATP partially inhibited ethylene production but stimulated CA production compared Mg-ATP alone. The pH optimum for the dechlorination was 6.8 (at 60 degrees C). Michaelis-Menten kinetics for initial product formation rates with different 1,2-DCA concentrations indicated the enzymatic character of the dechlorination. Apparent Kms for 1,2-DCA of 89 and 119 microM and Vmaxs of 34 and 20 pmol/min/mg of protein were estimated for ethylene and CA production, respectively. 3-Bromopropanesulfonate, a specific inhibitor for methyl-CoM reductase, completely inhibited dechlorination of 1,2-DCA. Purified methyl-CoM reductase, together with flavin adenine dinucleotide and a crude component A fraction which reduced the nickel of factor F430 in methyl-CoM reductase, converted 1,2-DCA to ethylene and CA with H2 as the electron donor. In this system, methyl-CoM reductase was also able to transform its own inhibitor 2-bromoethanesulfonate to ethylene.

Ethyl Chloride↗

Reductive dechlorination of 1,2-dichloroethane and chloroethane by cell suspensions of methanogenic bacteria.

Concentrated cell suspensions of methanogenic bacteria reductively dechlorinated 1,2-dichloroethane via two reaction-mechanisms: a dihalo-elimination yielding ethylene and two hydrogenolysis reactions yielding chloroethane and ethane, consecutively. The transformation of chloroethane to ethane was inhibited by 1,2-dichloroethane. Stimulation of methanogenesis caused an increase in the amount of dechlorination products formed, whereas the opposite was found when methane formation was inhibited. Cells of Methanosarcina barkeri grown on H2/CO2 converted 1,2-dichloroethane and chloroethane at higher rates than acetate or methanol grown cells.

Biodegradation, Environmental↗

Prostaglandin synthesis inhibitors and vasa recta erythrocyte velocities in the rat.

Vasa recta erythrocyte velocities (VRBC) in the exposed renal papilla of anesthetized water-loaded rats were determined before and 60 min after intravenous administration of a prostaglandin synthesis inhibitor (indomethacin, meclofenamate) or the inhibitor vehicle alone. The change in VRBC of ascending and descending vasa recta for the inhibitor group [-17 +/- 5% (SE)] was different from that for controls (+12 +/- 4%, P less than 0.002). Erythrocyte velocities were also determined in vasa recta of antidiuretic rats before and 30 min after administration of indomethacin or vehicle alone. Prostaglandin synthesis inhibition was again associated with a significant decrease in VRBC compared with control (-24 +/- 4% vs. +28 +/- 20%, respectively, P less than 0.025). These findings suggest that prostaglandins play a similar role in regulating blood flow in the renal medulla in water diuresis and antidiuresis.

Animals↗

Direct determination of vasa recta blood flow in the rat renal papilla.

Blood flow in vasa recta capillaries of the exposed renal papilla of young antidiuretic rats (n = 18) was determined by an adaptation of the video-photometric technique of Intaglietta. The erythrocyte velocity and capillary diameter in vasa recta (n = 97) were measured at the same location by means of fluorescence video microscopy, with fluorescein-labeled bovine gamma-globulin as a plasma marker. A factor relating erythrocyte velocity to mean cross-sectional blood velocity was determined in vitro to permit the calculation of single vasa recta blood flows from the measured indices, erythrocyte velocity and capillary diameter. Mean blood flow in descending vasa recta was 8.83 +/- 0.96 (SE) nl/min, significantly greater than that in ascending vasa recta, 4.82 +/- 0.34 nl/min. The total numbers of ascending and descending vasa recta at the base of the exposed papilla were also determined. Over 1500 vasa recta were identified as ascending vasa recta or descending vasa recta in electron micrographs of three papillas. At this level in the papilla (2 mm from the tip), there were four ascending vasa recta for each descending vas rectum. From the total numbers of ascending vasa recta and descending vas rectum, single vessel blood flows were converted to total blood flow. Total blood outflow in all ascending vasa recta, 11.3 microliter/min, substantially exceeded total blood inflow in all descending vasa recta, 5.2 microliter/min. The difference between outflow and inflow (6.1 microliter/min) represents an estimate of water by the papillary microcirculation, and is more than adequate to accommodate the known rate of water reabsorption from the collecting ducts of the exposed papilla.

Animals↗

Effects of glucagon, vasoactive intestinal peptide, and vasopressin on villous microcirculation and superior mesenteric artery blood flow of the rat.

The effects of the peptide hormones glucagon, vasoactive intestinal peptide, and vasopressin on the microcirculation of single jejunal villi were studied in anesthetized rats. By means of a recently developed in vivo video-microscopy technique, the red blood cell velocity (pretreatment value: 2.1 +/- 0.1 mm X s-1) and the diameter of the red blood cell column (5.5 +/- 0.2 micron) were measured in the villous arcade vessels. From these parameters, an index of blood flow was calculated in order to determine changes in response to intravenous infusions of the peptides. During the infusions of glucagon and vasopressin, simultaneous measurements were made of superior mesenteric artery blood flow and villous arcade flow. Glucagon (1 microgram X kg-1 X min-1) increased villous arcade flow markedly to 150.1 +/- 13.7% of control, while superior mesenteric artery flow remained unchanged. Vasoactive intestinal peptide (1 microgram X kg-1 X min-1) produced a dilation of the arcade vessel with a commensurate reduction of red cell velocity, leaving the flow index unaltered. Vasopressin (14.3 mU X kg-1 X min-1) was found to be a potent vasoconstrictor at the mucosal level, and since red cell velocity also decreased, villous flow was reduced substantially, paralleling a reduction of superior mesenteric artery flow. After the vasopressin infusion, a reactive hyperemia occurred in the villous arcades. No such increase in blood flow was observed in the superior mesenteric artery. From these findings, we conclude that the villous microvasculature is influenced by various hormones and, therefore, must occupy a prominent position in control of the circulation of the small intestine.

Animals↗

[Microcirculation studies on rat small intestine villi in vivo].

A method of observing and studying the microcirculation in the jejunal villus of the living rat is described. It permits measurement of the velocity of plasma gaps and of the diameters of the various vessels, and is based on transillumination of the exposed mucosa. The motility of the gut is overcome by allowing the intestine to adhere to the water-immersion lens. The problems of mucous secretion are resolved by administration of N-acetyl-L-cystein. A direct arteriovenous connection between arterioles and the venous system of the villus is postulated. Plasma gap velocity is 1.78 +/- 0.62 mm/sec in the arterioles and 0.42 +/- 0.08 mm/sec in the capillaries. The measured diameter of the of the erythrocyte column in the vessels is: central artery: 9.14 +/- 1.89 micron; "arcade" arteriole part I, II and III respectively: 5.88 +/- 1.05 micron, 6.69 +/- 1.04 micron, 8.86 +/- 1.63 micron; venule: 13.58 +/- 2.67 micron; capillaries: 4.56 +/- 0.57 micron. The method also allows puncture of the villus vessels.

Acetylcysteine↗