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Hi Chuck

    I'll offer my take on this, for what it's worth.  Hb is affected physically
by CO2...It changes the conformation of the proteins and affects O2 binding in
this manner.  I think that the figure of 75% saturation refers to the amount of
Hb molecules that have O2 bound to them - not the amount of O2 bound to the Hb.
This is a slight difference, but I think it makes sense.  Before the
dissociation
curve shifts (although I think you might have got the numbers reversed (i.e.
lower saturation PP after CO2 shift, but I could be wrong), 50% of the Hb
molecules have O2 molecules (I think it's four each) attached to them (or an
average of two O2 molecules on every Hb molecule - either way) at 40 mmHg. Once
the shift occurs, 75% of the Hb molecules (or 75% of the binding sites) are
bound
at the same pressure.  This change is due to the physical change in the Hb
molecule.  There's no Partial Pressure associated with the O2 molecules once
they're bound.  If they're dissolved in plasma it's another story, but in terms
of hemoglobin, PP only affects the speed with which they bind...

    HTH...

Ben

CHKBOONE@ao*.co* wrote:

>     Supposedly the venous Hb is still 75% saturated and we only use about 25%
> of the arterial O-Hb.   However;
>
>    The unshifted dissociation curve shows Hb as about 50% saturated at a PPO2
> of 40 mm Hg.   Various agents shift the curve so that in the venous flow Hb
> is reportedly 75% saturated at this same O2 concentration (40mm Hg).    Is
> this 75% of what Hb is capable of carrying after the influence of CO2, H+,
> and 2-3 BPG shifts the curve?
>    If so, then it appears that we use more than 25% of the O-Hb stores at
> rest.  ? ? ?
>
> Anybody got a handle on this ?
>
> Chuck
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