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> > > The discussion of cold vs hot narcosis has been interesting to >watch. One comment on the following; > >> >> The "Cold Narc" effects do seem to be related to higher than normal CO2. >> This could be related to the inability of the blood to xfer O2 and CO2 to/from >> the lungs and tissues properly due to raised levels of gases in all three. >> When the pressure in the lungs increases it is xfered to the blood and from >> the blood to the tissues. Reversing this action with CO2 on the return trip. >> As the level in the tissues increases eventually the level in the blood >> reaches the point at which it can no longer effectively absorb/bond with >> more gases. Therefore on the return trip it fails to bond with enough CO2. >> >> (Please be kind, this is not based on anything other than the first thing >> that came to my wandering mind) >> >> Have Fun, >> >> Scooter > > CO2 is a 'special' gas in my book because its transport in the >body is unusual and not what was stated above. Haemoglobin does not >bind CO2, only O2 and CO. If it binds CO, it does not readily release >it, which is why one dies from CO inhalation. Wrong, a significant portion of CO2 in the blood is carried by haemoglobin, off the top of my head I think it is 5% in venous blood, and this binding of CO2 causes a left shift in the Hb-O2 dissociation curve. > O2 as we all know is primarily transported by hemoglobin in >the red blood cells (at one atmospere! At pressure, I don't know what >the loading levels are, but this is known.). In the tissues, CO2 is >produced by the metabolism of O2. Unlike N2 or Ar, or most other >gases, CO2 is NOT transported in the blood as a neutrally dissolved >gas. some must be in solution by definition of an equilibrium, and CO2 is highly soluble in blood. >CO2 is dissolved in the blood liquid as H2CO3 (Carbonic acid), >which changes the pH and helps release the O2 from the haemaglobin, >along with Di-Phospho-Glycrerol(DPG) in the tissues. During the >transport of the blood from the tissue to the lungs and back, only a >small percentage of the total CO2 present in the blood (at 1 atm!) is >released in the lungs. When the H2CO3 passes through your lungs, the >carbonic acid is converted to CO2 by an enzyme (carbonic anhydrase) at >rapid speeds in your lungs, thus causing the CO2 to outgas in a 'safe' >area. I know that model calculations have been done to model the >effect of higher CO2 levels on the action of the enzyme, but since the >enzyme is limited by the rate of diffusion of CO2 INTO the enzyme, it >should (that's an opinion folks) work at at least the same RATE as on >the surface. However, because the partial pressures in the lungs are >higher at depth, plasma loading of carbonic acid will increase. The >(probable) shift in pH and the presence of more CO2 may well cause the >effects mentioned by Rich Pyle and others. > David Doolette ddoolett@me*.ad*.ed*.au*
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