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Acidosis


Findings from University of Arizona, Medical Department broaden understanding of physiology



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This article was published in Drug Law Weekly, which you can subscribe to online.

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2009 JUL 21 - (NewsRx.com) -- According to recent research from the United States, "Pilarski JQ, Solomon IC, Kilgore DL Jr, Hempleman SC. Effects of aerobic and anaerobic metabolic inhibitors on avian intrapulmonary chemoreceptors."

"Am J Physiol Regul Integr Comp Physiol 296: R1576-R1584, 2009. First published March 18, 2009; doi:10.1152/ajpregu.90608.2008.-Birds have rapidly responding respiratory chemoreceptors [intrapulmonary chemoreceptors (IPC)] that provide vagal sensory feedback about breathing pattern. IPC are exquisitely sensitive to CO2 but are unaffected by hypoxia. IPC continue to respond to CO2 during hypoxic and even anoxic conditions, suggesting that they may generate ATP needed for signal transduction anaerobically. To assess IPC energy metabolism, single-cell action potential discharge and acid-base status were recorded from 26 pentobarbital-anesthetized Anas platyrhynchos before and after intravenous infusion of the glycolytic blocker iodoacetate (10-70 mg/kg), mitochondrial blocker rotenone (2 mg/kg), and/or mitochondrial uncoupler 2,4-dinitrophenol (5-15 mg/kg). After 5 min exposure at the highest dosages, iodoacetate inhibited IPC discharge 65% (15.9 +/- 0.3 s(-1) to 5.5 +/- 0.3 s(-)1, P< 0.05), rotenone inhibited discharge 80% (12.9 +/- 0.5 s(-1) to 2.6 +/- 0.6 s(-1), P< 0.05), and 2,4-dinitrophenol inhibited discharge 19% (14.0 +/- 0.3 s(-1) to 11.3 +/- 0.3 s(-1), P< 0.05). These results suggest that IPC utilize glucose, require an intact glycolytic pathway, and metabolize the products of glycolysis to CO2 and H2O by mitochondrial respiration. The small but significant effect of 2,4-dinitrophenol suggests that ATP production by glycolysis may be sufficient to meet IPC energy demands if NADH can be oxidized to NAD experimentally by uncoupling mitochondria, or physiologically by transient lactate production," wrote J.Q. Pilarski and colleagues, University of Arizona, Medical Department.

The researchers concluded: "A model for IPC spike frequency adaptation is proposed, whereby the rapid onset of phasic IPC discharge requires ATP from anaerobic glycolysis, using lactate as the electron acceptor, and the roll-off in IPC discharge reflects transient acidosis due to intracellular lactic acid accumulation."

Pilarski and colleagues published their study in American Journal of Physiology - Regulatory Integrative and Comparative Physiology (Effects of aerobic and anaerobic metabolic inhibitors on avian intrapulmonary chemoreceptors. American Journal of Physiology - Regulatory Integrative and Comparative Physiology, 2009;296(5):R1576-R1584).

For additional information, contact J.Q. Pilarski, University of Arizona, College Medical, Dept. of Physiol, POB 210093, Tucson, AZ 85721, USA.

Publisher contact information for the American Journal of Physiology - Regulatory Integrative and Comparative Physiology is: American Physiological Society, 9650 Rockville Pike, Bethesda, MD 20814, USA.

Keywords: United States, Tucson, Comparative Physiology, Drugs, Metabolism, Pentobarbital, Pharmaceuticals, Therapy, Treatment, University of Arizona, Medical Department.

This article was prepared by Drug Law Weekly editors from staff and other reports. Copyright 2009, Drug Law Weekly via NewsRx.com.

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