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Senor Attikan wrote <<<<<<CO2 production is thought to be independent of ppO2, but metabolic rate dependent - There is no direct relationship between ppO2 inhaled & CO2 that evolves (O18 tagged inhaled gas would appear in CO(18)2 with a delay). Hold your snide comments about CO2 production will be zero irrespective of the ppO2 if organism is dead - Let's keep this to alive humans.>>>>> Just so that people do not confuse things, the CO2 produced does not come from the O2. The CO2 comes from the carboxylic acid cycle oxalosuccinic ------> CO2 + alpha-ketoglutarate alpha-ketoglutarate -----> CO2 +SuccinylCoA The consumption of O2 occurs in oxidative phosphorylation, the O2 is used up and H2O produced (1/2 O2 produces 3 ATP and produces 1 H2O) So the formtion of CO2 18 from labelled O2 18 is not direct and probably due to some oxygenase or other on a fatty acid or amino acid break down. It would be far more interesting to do the same experiment under hyperbaric conditions and find out which metabolic products have been labelled the most in comparison to normobaric O2 or air. As too why we get an increase in CO2 retention in divers under hyperbaric air, heliox, trimix etc.., I liked the idea that it is not just a product of gas density but also of anaesthesia ( I forget who suggested this). The comparison with anaesthetised patients was good. I have not heard anybody mention this so I will add my two cents about O2 transport and CO2 by red blood cells. If you look at the binding coefficient of Hb and O2 with respect to pH you will see that the binding is reduced in conditions of low pH (more acidic). This adaptation probably came about in order for the body to release O2 from RBC at the site where it is metabolically most active. Since CO2 is converted to carbonic acid by the enzyme carbonic anhydrase, areas with high CO2 levels will be more acidic and be able to recieve more O2. If under hyperbaric oxygen or other gases we have a higher level of O2 being transported not by the RBC and Hb but by O2 dissolved in the blood as a gas. This will probably affect the ability of the RBC to convert CO2 to carbonic acid as the raised levels of O2 in the plasma will cause the RBC to keep O2 bound to the HB and not release it to the tissues. With the Hb still bound up with O2 it will not be able to buffer the hydrogen ions and may affect the Chloride shift. Since 70% of CO2 is carried by the blood as carbonic acid we would then end up with some CO2 retention. All this above is just my opinion of what could happen in cvonditions of high O2 partial pressures. The physiology is right (I think) it just wants tidying up. So gas density, aneasthesia (narcosis) and reduced capacity of RBC to produce carbonic acid may all play their parts. Any other physiologist or Medics out there want to comment on this, is it right or wrong, and have any studies been done on it. J. Gibbo John M. Gibbons 0171-793-1101 Home Univ. London School of Pharmacy 0171-582-6561 Fax Dept. of Pharmaceutical Chemistry 0171-753-5800 Wk ex 4882 jgibbo@cl*.ul*.ac*.uk* or jgibbo@ul*.ac*.uk*
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