Jaimie Polson <jaimiep at cortex.physiol.su.oz.au> wrote in article
<jaimiep.855667949 at cortex.physiol.su.oz.au>...
> In <01bc17cd$42cb8560$b049bacd at dnawten.ix.netcom.com> "Nate"
<dnawten at ix.netcom.com> writes:
> So presumably, this means that with a higher PCO2 in the blood, less O2
> would bind for a given PO2 - but I don't know how significant this would
> be at any imaginable increase in CO2 levels.
> (And also, this does not account for the body's homeostatic responses to
> reduce the high CO2 - that were kindly explained to me earlier.)
>But this is due to the acidity of the blood, not necessarily the pCO2. The
more CO2 dissolved in the blood, the more acidic it becomes (due to the
action of carbonic anhydrase). When this occurs, the excess protons will
interact with the globin portion of the hemoglobin molecule, decreasing its
O2 affinity. Therefore, in the arterial circulation, the CO2 content is
low relative to the venous circulation, and therefore, the pH is slightly
higher. On the venous side, the pH is lower due to protons released by an
increasing concentration of CO2 (from metabolizing tissues). This
decreased pH changes the configuration of the O2-hemoglobin complex which
causes the hemoglobin protein to lose its affinity for O2, releasing it to
be consumed by the tissues. This is called the Bohr effect, and is well
documented in any physiology text.
What you may be referring to, as far as feeling drowsy in a crowded lecture
hall is popularly known as the BORE effect. Although very similar in name,
they are in fact quite different.