Mailing List Archive Mailing List Archive
Rich Lesperance writes;
>>
>> Chuck,
>>
>> >> Obviously O2 gets into a pressurized tissue somehow but I can not
>> picture it migrating passively by random walk diffusion against the
>> onslaught of a pressure gradient even though that gradient is surely
>> quite small.<<
>>
>> I fear this physiology may be getting a little out of my league, but
>> here is my best guess for how it works. Any DMO/HMOs out there want to
>> take a stab at it and wade in??
>>
>> Diffusion works against pressure gradiants all the time. Your blood is,
>> at the capillary level, something like 40mm Hg higher than the
>> surrounding tissue pressure. It does decrease somewhat as it travels
>> through the capillary, but it has to remain higher than the surrounding
>> tissue pressure, or the capillary would collapse, and blood would not
>> circulate through it. Yet carbon dioxide and other waste products
>> diffuse from the cells into the blood stream just the same.
>>
=============================
Rich, I think you are talking about hydrostatic pressure here - a totally
different animal from the pressure exerted by the gasses in so-called
"solution". Hydrostatic pressure (that exerted on and by the liquid due
either to weight, mechanical pressure, or motion) does not effect the pressure
of gasses in solution because the liquid acts as an incompressible container
for the gas within it. The shape of the space within this container is
tortured and constantly changing and the fact that the gas molecules must
navigate a twisted path through this maze of liquid molecules is part of what
makes it diffuse about 10,000 times more slowly through a liquid than through
space (other gasses). (the mean free path of the gas molecules is reduced
and collisions are more frequent)
What causes the difference in solubilities of gasses is the very weak
electrical interactions between the liquid and gas molecules that distorts the
electron clouds of both to cause a temporary attraction between them as they
approach each other (London Dispersion Forces). This slows down the gas
molecules so that they can not exert quite as much pressure on the walls of
the liquid container or on more gas molecules trying to get into the liquid as
they could if they were in free space.
This is why helium, a relatively small tight entity (single atoms instead
of molecules), continues to exert more pressure on other molecules of both gas
and liquid when in solution and therefore is less soluble than O2 or N2. It
continues to push back harder than these larger molecules with electrons
farther away from their nuclei (electron clouds more easily distorted) and
maybe because it carries less charged particles to start with as well.
Because a liquid is incompressible (for our purposes) you can not squeeze
it's molecules closer together to reduce the internal volume and thus raise
the pressure of gasses contained within. These gasses are not in solution
as are salt and sugar in that they are not closely associated with the liquid
molecules as in the case of hydration. They are actually in a modified free
phase at all times (a better term would probably be freely diffusing) - if
they were not you would not be able to force them out of "solution" by
reducing the ambient pressure.
>> >> However, another factor that figures into this is that the release of
>> O2 from Hb raises the total plasma gas tension. <<
>>
>> I took a gander through one of my physiology textbooks, at the oxygen
>> dissociation curve for hemoglobin. It seems that as oxygen tension
>> increases, more of it is bound to the hemoglobin, so at higher tensions,
>> the oxygen would not be released at all - the only oxygen being
>> metabolized is that which is dissolved in the plasma.
>>
>> RIch L
>>
==========================
You and your textbook are correct - local PPO2 effects the Hb's affinity
for O2. But if you keep going you will find that a number of "known" factors
shift the oxygen dissociation curve to the right so that O2 is forced off the
Hb in environments of higher local PPO2 (a higher PPO2 is required to achieve
the same percentage of saturation). CO2, H+ ions, and a chemical called ' 2,
3 DPG ' act to shift the curve to the right. H+ concentration is controlled
or moderated by the reactions with CO2 during it's conversion into bicarbonate
in the RBC. If CO2 did not force some O2 off the Hb the CO2 concentration in
the tissues would rise when we breathed 100% O2 because of the reduced
capacity of the blood to carry CO2. (they used to think this was behind the
cause of O2 CNS toxicity - that it was actually CO2 poisoning)
I think it is likely that the presence of a high PPO2 in the capillaries
does indeed reduce the amount of O2 ultimately dissociated from Hb but keep in
mind that the Hb carries 70 times the amount of O2 that the plasma can at 1
ata of air. So, even a little is a lot.
We normally only use about 25% of the Hb bound O2 and the other 75% rides
back to the heart and lungs in the venous flow. CO2 binds to a different
site on the Hb molecule than O2.
The hemoglobin molecule is one of the most beautiful of evolutionary
devices, well worth an evening with your nose in a book just to give you an
appreciation for the incredible improbability of your odds of having ever come
to exist not to mention contemplate that existence.
In addition to the few gas transport events of which most of us are aware
is the action of P450, a protein that delivers O2 across membranes by active
transport and exists in high concentrations in pregnant women who must deliver
lots of O2 to babies - less in men and regular women (new to me and I know
little about it but O2 transport is not it's primary function, I don't think).
Another is called "filtration" whereby some blood plasma flows out of the
capillaries and through the interstitial spaces between somatic cells and back
into the capillary due to your 40 mmHg of hydrostatic pressure.
Another is colloid osmotic pressure or oncotic pressure which acts to pull
fluid from the tissue interstice into the plasma. This and the filtration
above result in a slow but definite movement of fluids between the plasma and
tissues and gasses in "solution" will move with them. All this is further
complicated by the Lymphatic system that very slowly drains fluid (full of
gas) from the tissues, possibly away from an effective influence of the
capillary beds or to other compartments.
One begins to wonder how anyone can presume to predict rates of
decompression with such variables at hand. It should inspire a new
appreciation for the value of the few things we have that we know work and
less of a tendency to experiment carelessly or push the tables.
I know this is a lot more than you bargained for but I thought some of you
might find some of these points interesting. For anyone else interested in
finding out more about all this physiology stuff there is a relatively simple,
well organized and illustrated, but surprisingly detailed book available at
most bookstores called the Physiology Coloring Book. It is easy to
understand and picture what they are talking about without a broad scientific
vocabulary and it will help the layman flesh out his perspective on some of
this stuff. Keep in mind that the specifics of normobaric gas transport are
not always directly applicable to the divers situation so if you start getting
deep you will have to be careful of exactly what is being said. The gas in
"solution" is a good example and the medical community measures blood gasses
as a combination of all gasses in any state whether they are bound to Hb, part
of other compounds such as bicarbonate or whatever - these do not exert a
partial pressure.
Thanks for the response Rich,
Chuck Boone
--
Send mail for the `techdiver' mailing list to `techdiver@aquanaut.com'.
Send subscribe/unsubscribe requests to `techdiver-request@aquanaut.com'.
Navigate by Author:
[Previous]
[Next]
[Author Search Index]
Navigate by Subject:
[Previous]
[Next]
[Subject Search Index]
[Send Reply] [Send Message with New Topic]
[Search Selection] [Mailing List Home] [Home]