Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027960 (mole)
 21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The effect of acid-base changes on hepatic lactate utilization was investigated in anaesthetized, mechanically ventilated dogs.2. Portal vein flow and hepatic artery flow were measured with electromagnetic flowmeters, lactate concentration of portal vein, arterial and mixed hepatic venous blood was determined by an enzymatic technique, and hepatic lactate uptake was calculated using the Fick principle.3. Respiratory alkalosis (Delta pH 0.25 +/- 0.02) in four dogs resulted in a significant fall in total hepatic blood flow (-22 +/- 4%) and a significant rise in both arterial lactate concentration (2.18 +/- 0.32 m-mole/l.) and hepatic lactate utilization (3.9 +/- 1.2 mumole/min.kg).4. 0.6 M-Tris buffer infusion (Delta pH 0.21 +/- 0.02) in four dogs produced no significant changes in liver blood flow, arterial lactate concentration or hepatic lactate uptake.5. Respiratory acidosis (Delta pH -0.20 +/- 0.03) in six dogs and metabolic acidosis (Delta pH -0.20 +/- 0.02) in four dogs produced no significant changes in liver blood flow, decreases in arterial lactate concentration of 0.38 +/- 0.09 m-mole/l. (P < 0.05) and 0.13 +/- 0.13 m-mole/l., respectively, and no significant changes in hepatic lactate uptake.6. A significant correlation (r = 0.63; P < 0.01) was found between hepatic lactate utilization and arterial lactate concentration during the hyperlactataemia associated with respiratory alkalosis.7. Hyperlactataemia induced in four dogs by infusion of buffered sodium lactate (Delta pH 0.05 +/- 0.01;% Delta liver blood flow 29 +/- 7%) was also significantly correlated with hepatic lactate utilization (r = 0.70; P < 0.01) and the slope of the regression was similar to that during respiratory alkalosis.8. These data suggest that the hyperlactataemia of alkalosis is not due to impaired hepatic utilization of lactate and that the principal determinant of hepatic lactate uptake during alkalosis or lactate infusion is blood lactate concentration, rather than liver blood flow or acid-base status.
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PMID:Effect of acid-base alterations on hepatic lactate utilization. 503 74

Serotonin transporters (SERTs) are targets for drugs such as Prozac that increase serotonin (5HT) levels by blocking 5HT reuptake. Although SERTs saturate in the micromolar range, synaptic 5HT may exceed 1 mM. To examine SERT's response to high 5HT concentrations, we expressed Drosophila SERT (dSERT) in Xenopus oocytes and found that transport continued to increase with concentration up to 0.3 mM 5HT. As 5HT is a monovalent cation, its entry through an ion channel in SERT might explain uptake at high concentrations. We therefore investigated dSERT using traditional ion channel methods, including mole-fraction experiments under voltage clamp. We propose that SERTs may function as 5HT-permeable channels, and that this mechanism may be important for clearance of the neurotransmitter at high concentrations.
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PMID:Ionic interactions in the Drosophila serotonin transporter identify it as a serotonin channel. 1040 79