Mailing List Archive Mailing List Archive
Senor Attikan wrote
<<<<<<CO2 production is thought to be independent of ppO2, but
metabolic rate dependent - There is no direct relationship
between ppO2 inhaled & CO2 that evolves (O18 tagged inhaled gas
would appear in CO(18)2 with a delay). Hold your snide comments
about CO2 production will be zero irrespective of the ppO2 if
organism is dead - Let's keep this to alive humans.>>>>>
I am not sure who Senor Attikan is but
Esat Atikkan responds:
John Gibbon wrote:
>"Just so that people do not confuse things, the CO2 produced
>does not come
>from the O2. The CO2 comes from the carboxylic acid cycle
>
>oxalosuccinic ------> CO2 + alpha-ketoglutarate
>alpha-ketoglutarate -----> CO2 +SuccinylCoA"
Actually CO2 comes from
1. Pyruvate via the Rx:
Pyr-H + CoA + NAD ----> Ac-CoA + CO2 + NADH + H+
This is the anaerobic phase of the respiratory pathway & 1
equivalent of CO2 is produced w/o the direct involvement of
molecular O2
2. The Krebs cycle which yields the protons and electrons for
DPNH & TPNH [the nicontinamide adenine dinucleotides] for the
terminal respiratory chain yielding H2O and ATP
isocit + NADP ----> alpha-ketoglut + CO2 + NADPH + H+
alpha-ketoglut + ADP + Pi + NAD ----> succinate + CO2 + NADP
+ ATP + H+
This is the aerobic phase of the respiratory pathway, yet
again 2 equivalents of CO2 along with ATP are produced w/o the
direct involvements of molec O2. That occurs further down the
cascade.
3. The Pentose Shunt via 6-phosphogluconic acid, yielding
ribose, H+, CO2 and NADPH
4. The decarboxylation of amino acids to the corresponding
amine.
The alternate pathways of Amino-H oxidation or deamination
yield either Keto acid, NH3, H2O2 or Hydroxy acid, NH3
>The consumption of O2 occurs in oxidative phosphorylation, the
>O2 is used
>up and H2O produced (1/2 O2 produces 3 ATP and produces 1 H2O)
Agreed
>So the formtion of CO2 18 from labelled O2 18 is not direct and
>probably
>due to some oxygenase or other on a fatty acid or amino acid
>break down.
Agreed - the idea here is demo that CO2 production is not
directly linked to the that is inhaled - If we label the inhaled
O2, it will not appear immediately in the expired CO2. The
primary fate of that O2 is H2O via the terminal phase of aerobic
respiration (oxidative phosphorlation)
>It would be far more interesting to do the same experiment under
>hyperbaric
>conditions and find out which metabolic products have been
>labelled the
>most in comparison to normobaric O2 or air.
This assumes that hyperoxia and/or hyperoxia with different
diluents is going to impact the fate of the H2O generated by oxis
PO4'lation.
>As too why we get an increase in CO2 retention in divers under
>hyperbaric
>air, heliox, trimix etc.., I liked the idea that it is not just
>a product
>of gas density but also of anaesthesia ( I forget who suggested
>this). The
>comparison with anaesthetised patients was good.
I am not discounting the anesthesia effect - however the study
should be relatively easy, actually even available data should
show if the CO2 retention for gases with varying anesthetic
potency show a difference.
>I have not heard anybody mention this so I will add my two cents
>about
>O2 transport and CO2 by red blood cells.
>If you look at the binding coefficient of Hb and O2 with respect
>to pH you
>will see that the binding is reduced in conditions of low pH
>(more acidic).
>This adaptation probably came about in order for the body to
>release O2
>from RBC at the site where it is metabolically most active.
No question evolution had to come up with a molecule that would
tightly bind O2 when ppO2 is high, yet readily release it when
ppO2 was low without itself getting oxidized. It achieved the
trick by a pH sensitivity
>Since CO2 is
>converted to carbonic acid by the enzyme carbonic anhydrase,
>areas with
>high CO2 levels will be more acidic and be able to recieve more
>O2. If
>under hyperbaric oxygen or other gases we have a higher level of
>O2 being
>transported not by the RBC and Hb but by O2 dissolved in the
>blood as a
>gas. This will probably affect the ability of the RBC to convert
>CO2 to
>carbonic acid as the raised levels of O2 in the plasma will
>cause the RBC
>to keep O2 bound to the HB and not release it to the tissues.
Here again the compartmentalization of the carbonic anhydrase rx
inside the RBC is what permits the fine tuning.
Once CO2 diffuses into the RBC the rx
CO2 + H2O ----ca----> H3CO2 proceeds rapidly
It is slow in the absence of carbonic anhydrase (ca)
H2CO3 however, readily dissociates into
H2CO3 ----> H+ + HCO3-
When [HCO3-] rises it diffuses out. But H+ can not diffuse
out as readily (memb is not very permeable to cations). The
resulting ionic disequilibrium is eliminated by a Cl- shift
(Gibbs-Donnan equilibrium).
Hb & HbO2 have different pK's. Some liberated H+ bind Hb
because Hb is less acidic (better proton acceptor) than HbO2
Or
HbO2 + H+ ----> HHb + O2,
with a concomittant increase in CO2 carrying ability and
increased O2 yield.
The true statement of the Haldane effect is: deoxygenation of
blood increases ir CO2 carrying ability.
>With the Hb
>still bound up with O2 it will not be able to buffer the
>hydrogen ions and
>may affect the Chloride shift. Since 70% of CO2 is carried by
>the blood as
>carbonic acid we would then end up with some CO2 retention.
Actually this is independent of Cl- shift. It is the increased
H+ that is produced due to greater CO2 entry into RBC. The [Cl-]
appears to have no role in the final HHb/HbO2 ratio, which is
what determines O2 release & blood [HCO3-].
>All this above is just my opinion of what could happen in
>cvonditions of
>high O2 partial pressures. The physiology is right (I think) it
>just wants
>tidying up. So gas density, aneasthesia (narcosis) and reduced
>capacity of
>RBC to produce carbonic acid may all play their parts.
My view is that assuming CO2 ventilation at lungs at higher
ambient P will be decreased if overall gas viscosity is
decreased is not an easyassumption to make. One has to look at
actual CO2 retention at depths were CO2 viscosity is significant
while using gases w/ varying viscosities.
>Any other physiologist or Medics out there want to comment on
>this, is it
>right or wrong, and have any studies been done on it.
>John M. Gibbons 0171-793-1101 Home
>Univ. London School of Pharmacy 0171-582-6561 Fax
>Dept. of Pharmaceutical Chemistry 0171-753-5800 Wk ex 4882
>jgibbo@cl*.ul*.ac*.uk* or
>jgibbo@ul*.ac*.uk*
--
Esat Atikkan
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]