Oxygen dissociation curve!!!

[peacefulheart]

In EK book, it says "Carbon monoxide has more than 200 times greater affinity for hemoglobin than does oxygen but shifts the curve to the left."

If carbon monoxide has greater affinity for hemoglobin than oxygen, then when exposed to carbon monoxide, oxygen should have less affinity for hemoglobin and then the dissociation curve should shift to the right .


thanks a lot!

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[TieuBachHo]

In EK book, it says "Carbon monoxide has more than 200 times greater affinity for hemoglobin than does oxygen but shifts the curve to the left."

If carbon monoxide has greater affinity for hemoglobin than oxygen, then when exposed to carbon monoxide, oxygen should have less affinity for hemoglobin and then the dissociation curve should shift to the right .


thanks a lot!

It's due to the allosteric and cooperative effects of hemoglobins upon CO bindings. The same way that can be explained with O2 bindings. The first (one or two) bindings doesn't have so much of allosteric and cooperative effects, but the subsequent bindings (three and four) enhances O2 binding affinity. CO can only bind to one or two subunits. Therefore, the curve shifts to the left. Why is it a bad thing? Well, an increase in O2 affinity is one thing but the releasing of O2 is another. O2 high affinity will cause hemoglobins being less able to release Oxygens to the tissues.

 

[image187]

It's due to the allosteric and cooperative effects of hemoglobins upon CO bindings. The same way that can be explained with O2 bindings. The first (one or two) bindings doesn't have so much of allosteric and cooperative effects, but the subsequent bindings (three and four) enhances O2 binding affinity. CO can only bind to one or two subunits. Therefore, the curve shifts to the left. Why is it a bad thing? Well, an increase in O2 affinity is one thing but the releasing of O2 is another. O2 high affinity will cause hemoglobins being less able to release Oxygens to the tissues.

in addition, if you look at the dissociation curve in the context of CO toxicity, the total O2 saturation of Hb is severely limited. So not only is much less oxygen allowed to bind to hemoglobin, but out in the tissues that need it, O2 is more tightly bound in the blood

 

[Captain Sisko]

in addition, if you look at the dissociation curve in the context of CO toxicity, the total O2 saturation of Hb is severely limited. So not only is much less oxygen allowed to bind to hemoglobin, but out in the tissues that need it, O2 is more tightly bound in the blood

Does this mean that venous return will be oxygenated?

 

[peacefulheart]

It's due to the allosteric and cooperative effects of hemoglobins upon CO bindings. The same way that can be explained with O2 bindings. The first (one or two) bindings doesn't have so much of allosteric and cooperative effects, but the subsequent bindings (three and four) enhances O2 binding affinity. CO can only bind to one or two subunits. Therefore, the curve shifts to the left. Why is it a bad thing? Well, an increase in O2 affinity is one thing but the releasing of O2 is another. O2 high affinity will cause hemoglobins being less able to release Oxygens to the tissues.

I am still confused. Do you mean because of CO bindings and cooperative effects, the O2 's affinity for hemoglobin increased?


thanks a lot.

 

[Captain Sisko]

I am still confused. Do you mean because of CO bindings and cooperative effects, the O2 's affinity for hemoglobin increased?


thanks a lot.

Yeah, as I understand it, carbon monoxide will bond to the iron which is bound to the proximal histidine of the F helix, thus forcing the hemoglobin into the R conformation. When in the R state, bpg won't bind in the central cavity and O2 affinity will remain high.

 

[image187]

Does this mean that venous return will be oxygenated?

This is sort of tricky. The "oxygenation" of the blood takes into account a few different things, but essentially it is equal to 1) the oxygen carried by hemoglobin and 2) the diffused oxygen in the blood. If youre measuring the oxygenation of venous return (a venous gas is rarely really done, but theoretically I guess...) you're getting the "PvO2", which will be normal, and this will be true for PaO2 (ABG) of the arterial blood as well. This is because the CO bound to hemoglobin doesn't affect solubility of O2 at all. The total blood oxygen saturation, however will be decreased throughout because CO does all those things stated from the other posters. In the lungs it diffuses way faster than O2 into the blood and then binds to Hb with about 200x greater affinity and stubbornly hangs on there, causing O2 to actually bind tighter than normal through allosteric effects. If you look at the carboxyhemoglobin graph, there is a certain PO2 range where there is more O2 bound than normal (shift to the left), and then at a certain PO2 the binding becomes less than normal due to the crowding out by CO (google this graph, it's probably way easier to understand). So, while through most of this phsiological range Hb is not adequately filled with oxygen during CO poisoning, yes, the oxygenation of hemoglobin will technically be greater than normal in venous blood.

 

[peacefulheart]

Yeah, as I understand it, carbon monoxide will bond to the iron which is bound to the proximal histidine of the F helix, thus forcing the hemoglobin into the R conformation. When in the R state, bpg won't bind in the central cavity and O2 affinity will remain high.

1. Thanks for the explanation.

2. I thought CO and O2 compete each other for binding to hemoglobin.

3. By the way , what does bpg stands for ?

thanks

 

[dan123]

bpg is bisphosphoglyceric acid. an increase of this of this in an o2-hb curve will create loose binding (sigmoidal curve will shift to right)