Glassman wrote on May 3rd, 2011 at 10:37pm:I'm going to be lazy

and rely on a posting by Batch that goes a long way to explaining the dilation/constriction effect. Much better than my spending a long time basically re-typing what he so conveniently has already written.
It's under "Your Brain on Oxygen" reply #30 on March 17th 2011.
I had read Batch's explanation of how oxygen works and am in total agreement with it. However, the one area that seemed less understood is how the uptake of carbon dioxide is done. I read "cast off" but eventually remembered something else involved, like a missing link.
from Batch's explanation:
Quote:When the chemo sensors in the brain detect an elevation in CO2 levels and drop in arterial pH, an acid-base homeostatic mechanism kicks in and the brain signals the heart to beat faster, the lungs to breath faster and the arteries to dilate. It does all this to pump more blood to the lungs where the excess carbonic acid can be cast off or downloaded from blood hemoglobin as CO2 and oxygen in uploaded.
This increased respiration rate and heartbeat will continue until the excess CO2 is cast off...
I remembered something I read in 2008 by Michael Trachtenberg at Harvard, who did his early work on carbon dioxide removal for NASA, building carbon dioxide-capture systems for spacesuits and for the ship being developed for the first manned mission to Mars.
I looked back to where I read this and will recap. Batch, your comments are welcome and I hope this will maybe add to your description of how oxygen works. You seem to have the rest.

Here was the interesting thought Batch left us with:
Quote:Clearly, there are other mechanisms involved in the cluster headache abort process with oxygen therapy and that's what Ricardo wants to learn. That leads us to a possible question as to which is the predominant mechanism in play, acid-base homeostasis, or a cocktail of hormones, enzymes, and chemical messengers triggered by hyperoxia?
I don't know... The neurochemistry involved is well above my pay-grade.
The problem here being - it does not involve neurochemistry, but neurobiology instead. It is biological, a physiological processes evolved over million of years and used by virtually every organism on earth. Clinical research on the role of glial brain cells in epilepsy and head trauma were revealing for this.
Trachtenberg's explanation:
Glial cells bring in nutrients, including oxygen, and carry away pathogens and
carbon dioxide. Since 1967, Trachtenberg had been investigating a mystery: given the large distance in the brain between neurons and blood vessels, it seemed impossible that the glial cells could scavenge carbon dioxide fast enough to prevent a dangerous buildup. Increased carbon dioxide would increase acidity, which in turn would change the "excitability" of the neurons, causing them to fire at the wrong time.
Nature solved the problem, evolution had borrowed the same high-speed carbon dioxide shuttle used in nearly every plant, animal, and bacteria on earth: an enzyme called
carbonic anhydrase. Plants use carbonic anhydrase to help them absorb carbon dioxide from the atmosphere. Mammals use it to help them move carbon dioxide from tissues into capillaries and from there to the lungs to be expelled from the body.
One driver of this movement is a simple pressure differential: a gas will always flow from a region of higher concentration and pressure to one of lower pressure. But the second driver - the one that homes in on only carbon dioxide is the carbonic anhydrase contained in each of our cells. The enzyme catalyzes a reaction that turns carbon dioxide to bicarbonate, which can be carrried in large volumes in the blood plasma to the lungs, exhalations have a concentration of about 4% carbon dioxide.
The reason I bring this up is because Batch had everything involved in his explanation, except I saw no mention of the enzyme carbonic anhydrase, which is what homes in on carbon dioxide and accelerates its uptake.
The only reason I remembered reading this though, is this sentence here:
Quote:Increased carbon dioxide would increase acidity, which in turn would change the "excitability" of the neurons, causing them to fire at the wrong time.
I thought about cluster headaches when I read this and if this had a connection -- do we maybe have a problem with carbonic anhydrase?
I found this similar to the question Batch left us with in his post:
Quote:That leads us to a possible question as to which is the predominant mechanism in play, acid-base homeostasis, or a cocktail of hormones, enzymes, and chemical messengers triggered by hyperoxia?