Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003129 (Anoxia)
 551 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A defect in isolated perfused rat-liver (IPRL) preparations has been proposed to explain discrepancies between in vivo and in vitro findings regarding hepatic glucose metabolism. The aim of the present study was to investigate whether a preparation of IPRL using a synthetic hemoglobin-free perfusate was capable of net glucose uptake and glycogen deposition at physiological portal substrate concentrations. Livers from fed anaesthetized rats were perfused in a recirculating system using a fluorocarbon emulsion as artificial oxygen carrier. Depending on the prevailing glucose concentration, livers exhibited net glucose uptake or release with a threshold value of 5.5-6.0 mM glucose. Net glucose uptake was associated with net glycogen deposition (+0.23 to +0.59 mumol C6 min-1 g-1). From 5.8 mM (n = 3) and 10.0 mM (n = 8), initial concentration glucose levels fell to 5.3 +/- 0.2 mM after 210 min (n = 3) and 6.3 +/- 0.9 mM after 120 min (n = 8), respectively. This was equivalent to a net glucose uptake of -0.16 and -0.45 mumol min-1 g-1. Anoxia reversibly switched hepatic glucose balance from net uptake (-0.42 mumol min-1 g-1) to release (+0.69 mumol min-1 g-1) followed by net uptake (-0.50 mumol min-1 g-1) after reinstitution of aerobic conditions. We conclude that the composition of perfusion media might play a pivotal role for studies of glucose metabolism in the isolated perfused rat liver. In our experimental model, using a hemoglobin-free synthetic medium, net glucose uptake was readily demonstrated at physiological portal substrate concentrations similar to the in vivo situation.
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PMID:Use of an artificial oxygen carrier in isolated rat liver perfusion: first demonstration of net glucose uptake at physiological portal glucose concentrations using a hemoglobin-free perfusate. 175 45

Net Cl- absorption by Amphiuma small intestine is electrogenic but associated with the secretion of HCO3-. To define the mechanisms of Cl- entry into the enterocytes the initial rate of uptake of 36Cl into isolated segments of small intestine was measured. Luminal extracellular space was measured using [3H]inulin. Cl- influx was saturable with a Km of 5.3 mM. When the mucosal medium Cl- concentration was 20 mM influx was linear for 5 min. Cl- influx in 5 min (JiCl) was not reduced by 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid added to the serosal medium, although the Cl- current was abolished. Hence the luminal membrane was the barrier to Cl- uptake. Monovalent anions blocked Cl- influx in the order I- = SCN- = NO3- greater than Br- greater than F-. Anoxia and dinitrophenol reduced JiCl 33 and 71%, respectively. Substitution of medium Na+ with choline or N-methyl glucamine reduced JiCl 60-70%. Removal of medium K+ reduced influx 51%. After medium Na+ and K+ were both replaced influx was stimulated upon reexposure to (Na+ + K+); Na+ alone did not stimulate. JiCl was reduced 34% by furosemide. Neither amiloride nor SITS in the mucosal medium altered influx. JiCl was reduced by replacement of the HCO3- -CO2 buffer with either phosphate or N-2-hydroxyethyl-piperazine-N'-2-ethanesulfonic acid and by exposure to acetazolamide. Theophylline reduced influx 60%, whereas the Ca ionophore A23187 reduced net Cl- absorption and lowered JiCl by 17%. Norepinephrine (10(-5) M) in the serosal bathing medium stimulated Cl- influx 51%. These results indicate that Cl- influx into the intestinal mucosa occurs by a Na+- and, possibly, K+-dependent pathway. Cl- entry is under adrenergic influence.
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PMID:Characteristics of chloride ion influx in Amphiuma small intestine. 253 36

The relations among alkaline secretion, short-circuit current (Isc), and fluxes of Na+ and Cl- are examined. The Isc (1.15 +/- 0.03 microeq.cm-2.h-1) was significantly greater than the rate of alkaline secretion (1.02 +/- 0.02 microeq.cm-2.h-1). Regression analysis (n = 300) showed a highly significant correlation between alkaline secretion and Isc and indicated a residual Isc of 0.26 microeq.cm-2.h-1. In the absence of HCO3-, there was a residual Isc of 0.25 +/- 0.04 microeq.cm-2.h-1. This residual Isc is accounted for by an observed net Na+ absorption of 0.28 +/- 0.04 microeq.cm-2.h-1. Fluxes of Na+ fail to fit the flux-ratio equation and were not significantly affected by 2 X 10(-6) M ouabain, 5 X 10(-5) M amiloride, or anoxia but were significantly reduced by 2,4,6-triaminopyrimidine. The net Cl- flux was not significantly different from zero. Cl- fluxes conform to the flux-ratio equation and were reduced by anoxia or 2,4,6-triaminopyrimidine but were not affected by 4-acetamido-4'-isothiocynostilbene-2,2'-disulfonic acid (SITS). Anoxia or ouabain significantly inhibited alkaline secretion and Isc without affecting net fluxes of Na+ or Cl-, whereas amiloride or SITS had no effect on any of these parameters. There is no NaCl-coupled transport nor anion exchange, but solute-coupled Na+ absorption is demonstrated. We conclude that alkaline secretion by the duodenum involves a transcellular, energy-requiring, Na+-dependent, ouabain-sensitive, electrogenic mechanism that accounts for at least 80% of the Isc. Net Na+ absorption accounts for the residual Isc. Movements of Cl- are passive, do not contribute to Isc, and are not involved in the mechanism of alkaline secretion. Two hypothetical models of transcellular alkaline secretion are proposed.
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PMID:Alkaline secretion by amphibian duodenum. II. Short-circuit current and Na+ and Cl- fluxes. 697 2