Years ago, I believe the 3M company showed a TV ad with a mouse submerged in a liquid that it was supposedly breathing. Then a few years ago the movie "Abyss" had a human being breathing a liquid. I heard that the liquid actually exists but I have heard nothing more about it. It has a fairly long name which I can't remember plus I heard years ago that it was going to be the substitute for blood transfusions because of its oxygen content.

Did something go horribly wrong somewhere and was the product banned? Can anyone shed some light on the fate of this liquid?

http://en.wikipedia.org/wiki/Perfluorocarbons
http://en.wikipedia.org/wiki/Liquid_breathing

In Mission to Mars 2...the guy who leaves for the aliens breathes liquid with oxygen as well

http://chem.ch.huji.ac.il/history/clark_leland.htm

After bubbling oxygen through the fluorocarbon, the oxygenated fluid was pumped into the animals' lungs, and recirculated (about 6 cycles of inhalation and exhalation per minute). Most of the animals who were kept in the fluid for up to an hour survived for several weeks after their removal, before eventually succumbing to pulmonary damage. Autopsies uniformly revealed that the lungs appeared congested when collapsed but normal when inflated. Some of the early problems Clark encountered seemed to be due to the size of the animals' airway. The tiny size physically limited the amount of fluid that could get into the lungs. For that and other reasons, carbon dioxide tended to build up in the system: it simply couldn't be removed fast enough.
http://chem.ch.huji.ac.il/history/clark_leland_blood.jpg

To my knowledge, morbidity of test subjects has been approximately 100%, although some of that may be due to impurities in teh PFC's.

Finally, AFAIK, it has yet to be sucessfully tested on Humans (and some sources suggest it may not be feasible on the grounds of viscosity, and the required fluid exchange rates in the lungs to remove adequite CO_2.

"Some of the early problems Clark encountered seemed to be due to the size of the animals' airway. The tiny size physically limited the amount of fluid that could get into the lungs."

so Clark is suggesting to us to test it on humans? After all our airways are much bigger.

As previously stated, and as stated in at least one of the links I've provided, some indications are that it simply may not be practicle for human use - because of the physics of gas transfer.

um trippy, acording to the wikipedia link they already ARE using a form of it in med

um trippy, acording to the wikipedia link they already ARE using a form of it in med

Correct, but the methods that have been used are PLV, PFC Vapor, and PFC aerosol - technically liquid breathing, because the lungs inhale liquid and extract oxygen from the liquid, but, AFAIK, different from Total Liquid Ventilation which is what we see in The Abyss, and what I was assuming was being refered to.

I'm under the scientific opinion that human lungs simply can't pump liquid and keep it self oxygenated/decarbonated well enough without causing extensive damage to the lungs. An alternative approach might be to hook up an artificial lung to the cardiovascular system.
http://www.novalung.com/eng/Default.asp

um EF, the lungs DO breath liquid before your born. In fact the hardest breath ever taken is that first one where the lungs are collapsed because of they are full of emniotic fluid insted of air and surficant

Now your right if you say "but we dont get oxygen from that" but there is no theoritical reason why you couldnt. Actually it may be a good treatment for Acute Pulmonry Odema (APO) because the increased pressure of using a liquid for breathing would stop the fluid leaving the capilleries and flooding the lungs

um EF, the lungs DO breath liquid before your born. In fact the hardest breath ever taken is that first one where the lungs are collapsed because of they are full of emniotic fluid insted of air and surficant

Now your right if you say "but we dont get oxygen from that" but there is no theoritical reason why you couldnt. Actually it may be a good treatment for Acute Pulmonry Odema (APO) because the increased pressure of using a liquid for breathing would stop the fluid leaving the capilleries and flooding the lungs

I am tempted to try this wit V8, everything the body needs right? :shrug:

It just takes a little getting used to....

um EF, the lungs DO breath liquid before your born. In fact the hardest breath ever taken is that first one where the lungs are collapsed because of they are full of emniotic fluid insted of air and surficant

Now your right if you say "but we dont get oxygen from that" but there is no theoritical reason why you couldnt. Actually it may be a good treatment for Acute Pulmonry Odema (APO) because the increased pressure of using a liquid for breathing would stop the fluid leaving the capilleries and flooding the lungs

The only problem I have with this is that for it to be effective at decarbonating the blood, either it need to be partial infusion, or mechanically driven - it takes something like 5 litres per second of fluid flow to remove the carbon dioxide from resting metabolism alone.

um EF, the lungs DO breath liquid before your born. In fact the hardest breath ever taken is that first one where the lungs are collapsed because of they are full of emniotic fluid insted of air and surficant

You did not read what I said: fetuses do not breath for oxygen and carbonic acid homeostasis do they? No their breathing is merely reflexive, a pratice for the real thing perhaps, and does not strain them. Now imagine having to breath something with hundreds of times the density and viscosity of air at ~350 liters per hour! No wonder animals test subjects die of internal bleeding from the lungs after testing!

I have heard of the use of partial liquid breathing procedures for premature babies, where their little lungs are filled partially with PFC and it assists in their undeveloped respiratory system by preventing lung collapse.

You did not read what I said: fetuses do not breath for oxygen and carbonic acid homeostasis do they? No their breathing is merely reflexive, a pratice for the real thing perhaps, and does not strain them. Now imagine having to breath something with hundreds of times the density and viscosity of air at ~350 liters per hour! No wonder animals test subjects die of internal bleeding from the lungs after testing!

I should point out that it has been suggested by several sources (including the one's I've linked to) that the damage to the lungs was caused by impurities in the PFC's, and they treat the build up of Carbon Dioxide as a seperate issue.

Rats can breath oxygenated water for some time. (I forget how long -more than 15 minutes, I think.) The main problem is that drawing it in and expelling it requires a lot of effort and energy, which makes the CO2 in the blood increase as transport of it into the water is not rapid enough. This CO2 make them breath faster.*

Few know that we will not notice the lack of oxygen in the "air" we breath. I.e. we have no urge to breath because we are not getting enough O2. We breath because the urge to breath is related to the CO2 accumulating in your blood. (It just make sense - the exhalled air is nearly as rich in O2 as the inhalled air - so hard to sense a change in O2 concentration, but the exhaled CO2 concentartion is much higher than the inhaled concentration. (I am just guessing as have forgotten the facts, but at least an order of magnitude higher concentration I think.- An easy change for the body to sense.)

At APL two men working on a satellite inside a bell jar for later thermal test in vacuum died because of this fact. The huge steel bell jar they were working in was cranked up by hand. They had cranked it up only enough to squeeze between its lower lip and the base plate. Unforutantely, they had not turned off the dry N2 feed so slowly the O2/N2 ratio became very low. They could have left at any time, but did not notice anything wrong as they were getting rid of the CO2 building up in their blood normally. They were found by their car pool driver when they did not show for the ride home.

*The smaller blood vessels in the brain are unique. They expand as the CO2 concentration increases. Nature has developed this clever adaptation to reduce the resistance to blood flow in those part of the brain which are working the most. The brain is only about 2% of body weight but can take 20% of the O2 from the blood. It needs to get to the more active parts of the brain - CO2 expanding those capilaries is how that is done.

billy your answer is only PARTUALLY correct

Chemo receptiors on the arch of the aorta are responcable for the CO2 drive to breath (they also respond to Ph levels and what i have read is contradictor as to wether this is the way they find out how much CO2 is in the blood or if they are seprate)

However the brain itself (specifically the medulla) CAN detect O2 levels directly, the problem is that this requires a MASSIVE drop in O2 before it kicks in and the CO2 receptors are alot faster. This is why CO2 retrainers will stop breathing if you put them on 100% O2 (you can actually suffercate them with O2) but it will eventually kick in that the brain is being staved of O2

billy your answer is only PARTUALLY correct...I don't think I said anything wrong. - I just did not tell (as did not know- thanks) where the CO2 that causes normal urge to breath was detected. I did know that CO2 disolved in water tends to make it more acidic and suspected strongly that what was really detected was this change in pH and not the CO2 directly.

I.e. My answer was "fully correct" but not as complete as it might have been (few answers ever "exhaust the subject"). Mine tend to be too long as it is.

God help Sicforums with storage space if I were to try to give exhaustive answers. :D

Can I get my breathable liquid with THC added to it?...that would be sweet. :)

I can testify from personal experience that you do have an "urge to breath more" when the partial pressure of O2 gets too low, even if the overall atmospheric pressure is still acceptable high. You start to feel out of breath, as if you were running hard (even though you're not).

I can testify from personal experience that you do have an "urge to breath more" when the partial pressure of O2 gets too low, even if the overall atmospheric pressure is still acceptable high. You start to feel out of breath, as if you were running hard (even though you're not).How did you know the pratial O2 pressure was low yet total pressure was normal? And if you did know, how do you rule out the effects of conscious recognition that you need to breath more often or deeper and if not doing that you would / should feel out of breath?

I do not doubt that you are telling the truth, only that results measured when you were not aware that the partial presure of O2 was sub normal would have shown that you breath more deeply or more rapidly. At best, I think, you might notice you were getting tired or getting sleepy, before passing out and dying. - That seems to be the case of the two men who died as the O2/N2 ratio slowly decreased. - See post 15.

How did you know the pratial pressure was low? And if you did, how do you rule out the cosciious recognition that you need to breath more often or deeper and if not doing that you would /should feel out of breath?

I do not doubt that you are telling the truth, only that the results measured when you were not aware that the partial presure of O2 was sub normal would have shown that you breath more deeply or more rapidly. At best, I think, you might notice you were tired or getting sleepy, before passing out and dying - that seems to be the case of the two men who died was the 02/N2 ratio slowly decreased.
I should clarify that my only experience with low O2 pressures comes from being on mountains above 15k feet. At that altitude the atmospheric pressure is about .6 ATM or less. That's still more than enough pressure for lungs to function without drying out etc, but the partial pressure of O2 is only around 0.14 ATM. If you go high enough, eventually simply walking around will make you pant and feel "out of breath" as if you were exercising hard.

My father mentioned using a breathable liquid while he was in the military. He along with his colleagues tested it for use underwater, but they couldn't breathe it for very long, so I guess it was back to the drawing board. But seeing as my father was in the military over 30 years ago and still alive, I guess whatever they used wasn't fatal.

I should clarify that my only experience with low O2 pressures comes from being on mountains above 15k feet. ... I have been to top of Pike's Peak. 14,110 FT. Girl I was with got altitude sick, as unlike me she did not consciously breath deeply.

Fact that you feel adverse effects from low pressure atmosphere is not proof that you are sensing O2 to stimulate breathing at normal atmospheric pressure. To refute what I posted (that under normal condition your urge to breath is due only to CO2 accumulation in blood) you need to show in experiment that people not aware the the O2/N2 ratio is dropping breath deeper or more rapidly. Only evidence I have is that two guys died unaware there was any problem as the O2/N2 ratio dropped plus some reading long ago that stated what I have stated (Excessive CO2 in blood will make you breath.)

Also note there is still lots of un used O2 in your lungs when you hold your breath as long as you can.

billy what i ment was that your answer missed that there actually IS a bodly responce to falling O2 levels in the blood. Its there, its just not as quick as the responce to CO2 and the body shouldnt be relying on it in normal conditions as the driving resp responce

billy what i ment was that your answer missed that there actually IS a bodly responce to falling O2 levels in the blood. Its there, its just not as quick as the responce to CO2 and the body shouldnt be relying on it in normal conditions as the driving resp responceNot only "shouldn’t be relying on it in normal conditions as the driving respiratory response" – Low blood oxygen does not produce the normal urge to breath.

BTW there are at least two other "bodly responce to falling O2 levels in the blood." The ones you forgot to mention are loss of consciousness and death. So I guess you are only "partially correct" :D

Re read my post. - I did not try to discuss abnormal reactions or responses. I was clearly speaking of the normal urge to breath. Most people erroneously think it is to get Oxygen. I was just correcting that. (I.e. it is to get rid of CO2 that makes you breath, under normal circumstances). There are several abnormal circumstances related to breathing, including the “iron lungs" of an early era when polio was more common and brain stem electrical stimulation. Neither of us mentioned them. Almost every post at scifourms is only "partially correct" if mine was.

death is not a bodly responce:p Necrosis MAY be concidered a bodly responce but "death" is the ABSANCE of a bodly responce:p

And the medulla reaction is not "abnormal" its just that it takes a very low Sp02 reading to get it to kick in. Your right that CO2 is the normal driving responce for respiration though i do admit and your right that alot of people (including myself until last year) think that the drive to breath is low O2 not high CO2.

Oh incidently did you hear about the study on frebile convolsions and extreemly low levels of SpCO2?

I wish i could find the study because i only herd about it second hand and it was a fair while ago but its hypothisis was that frebile convolsions were caused by an increase in the Ph of the babies blood caused by hyperventaliation due to increased external temp. I belive what they wanted to try was to put the baby in a high CO2 enviroment (i honestly dont know how, possably by using a non rebreather mask and under inflating the bag so that the baby would be forced to breath a higher than atmospheric concentration of its own CO2) and seeing if that stopped the convolsions

… And the medulla reaction is not "abnormal" its just that it takes a very low Sp02 reading to get it to kick in. ...Earlier you had mentioned that the aortic arch was site of body noting low SpO2. I almost commented on that then as I think that is more likely to be the fourth backup to keep heart beating. I think, but it was a long time ago when I knew, primary beat rate control is mid brain function with a rate boost by cortical recognition of danger. Then the brainstem or medulla (for those who know the term) is secondary driver. The third is the SAN (sinal atrial node) which operators like a relaxation oscillator to send signals electrical pulses down the bundle of Hess nerve fibers, which spread out to most of heart muscle. The SAN usually is triggered before it will independently fire by signals from the brain.

I once caught a large pike or Muskie in Canada and it heart was still beating when I cleaned it hours later, but otherwise it was without life. I made salt solution (by taste as I remember sea water taste) and put heart in that solution. It kept slowly beating many hours more. Still was when I went to bed, but had stopped by time I got up the next day. When I went to bed the rate was slower than when first placed in the salt solution. I think at bed time, it was on the fourth backup mode, which I believe is the low oxygen sensed trigger. I had left a good part of the arteries attached so if that low SpO2 is sensed there it could have been detected. Fish are cold blooded so this probably helped keep the O2 demand low. I do not actually remember, but bet I had shaken the solution well, both to make sure all the salt was disolved and to add O2 to the water.

Are you sure that the low SpO2 sensing (in aortic arch) you mentioned earlier will stimulate breathing? I would think that might even be counterproductive O2 demand increase. For example, when very cold circulation shuts down except for vital organs (I am not sure but think kidneys, etc. get greatly reduced blood flow as they are not immediately needed to preserve life.) Essentially the same thing happens when you are drowning, especially in the young. - some timed called the "diving reflex" as many sea creatures that dive deep do this also.

If I have errors here, please correct where you can - this is all from very old memory - even if I remembered correctly, the "facts" may have changed by now.

PS I hope I always said "not normal" or "not normally" as I agree these backup modes are not "abnormal."

Fact that you feel adverse effects from low pressure atmosphere is not proof that you are sensing O2 to stimulate breathing at normal atmospheric pressure.
About a million references say you are correct. I wonder now if the excess urge to breath more that I experienced was caused by respiratory alkalosis.

About a million references say you are correct. I wonder now if the excess urge to breathe more that I experienced was caused by respiratory alkalosis.Do any of them support my guess that one is actually responding to a slightly acidic change in the Ph, instead of the excess of CO2 in the blood?

On respiratory alkalosis: My first reaction is NO, - you are dropping your blood CO2, but I guess that is possible if you were doing what I did on top of Pike's Peak. (Body is so complex I hesitate to ever say anything is "impossible")* - Namely I was consciously compensating by breathing deeply, especially if also fully exhaling and breathing more rapidly - neither of which did I do. If ever there again, take a paper bag to breath into (recirculate the CO2) and you can probably breathe more rapidly and exhale more fully with no respiratory alkalosis, or if you have it, cure it with the paper bag recirculating your exhaled CO2..

Blood sucking mosquitoes are exquisitely sensitive detectors of CO2. That is how the find you from far away on a nearly windless eve. (They fly up your CO2 enriched air stream tail.) And why open fires make it harder for them too (Saturates their CO2 detectors).
------------
* I try to stay far away for doctors or at least resist their "help" whenever I reasonably can. One of my favorite (and original) sayings is: "My body is smarter than all the world's doctors combined." Only when it gives no sign of curing me, do I seek their help. My father was a rural MD, before specializing in Psychiatry (Fortunately for me only after I left for college and told him I did not want to be a MD doctor.) He would occasionally say (not to patients of course): that "He was in partnership with Mother Nature. - She cured them and he sent out the bills."

billy i will need to recheck my post but if i did say that i wrote it wrong (if so im sorry about that). What i MENT to say is that the receptors in the aortic arch detect rising PH and\or (no one that i know of is sure) SpCO2. Its the medulla which directly detects O2. So no its the first line in dectecting hypoxia because thats where the blood goes first (well second or third if you count the pulmonry vain and the left side of the heart but *shrug*) and it should be almost compleatly free of CO2.

... it should be almost compleatly free of CO2.True the blood that has just come from the lungs will have the lowest SpCO2 of any in the body, but "almost completel free of CO2" I think is a stretch, unless there is some active transport of CO2 from blood to the air soon to be exhaled. Do you know if there is?

I assume that it is just a diffsuion across membrain gradient. I.e. the concentration of CO2 in the blood always being greater than in the air, even greater than lung's air soon to expelled, which is much richer in CO2 than the freshly inhaled air. I.e. I think the blood returning to the heart from the lungs is with higher CO2 concentration than the air leaving the lungs (if there is no active transport of CO2 into the lung air).

i did say almost, no there is no active trasport and some is retained as a weak acid to buffer the blood anyway. will try to post the various partial pressures later

ok arterial blood gasses (by coincidence todays lecture) PaCO2: 35-45 mmHg normal

ok arterial blood gasses (by coincidence todays lecture) PaCO2: 35-45 mmHg normalWhat fraction is this (of the more CO2 saturated blood) entering the lungs? The answer will tell if "almost completely free of CO2" was a "stretch" or not.

huh?

sorry i dont understand the question
are you asking the SvO2 or the difference in CO2 between atmospheric air and expired air?

Here's a bit of food for thought:

What if there was some way to reduce the ratio of exchange on O2 to CO2 in the airway by making it a one way transport?
Example being that snorkels are only made to a certain specific length, at some point if a snorkel gets too long the oxygen entering does not have enough pressure to reach the bottom of the tube into our mouths, nor does it have the density to push out CO2 from any residual CO2 that did not go into the ocean as bubbles. This would be able to be fixed by increasing the radius/diameter of the snorkel tube itself but alas, that is not practical. The exchange of gases and partial pressure due to the pressure of the water in the ocean would also prevent the oxygen from moving that far down that fast.

Theoretically speaking, the lungs would not have to actually move, as if you could passively train yourself to allow the transfer of gases in the PFC fluid, then you would not have to muscularly move the diaphragm and lungs to push the fluid out and in. Besides, regardless of how viscous or lubricated the fluid is, it would still create micro-friction in your alveoli and bronchioles, and would probably not feel good nevertheless, since we are accustomed to breathing air.

One way would be to increase the gaseous exchange rate within the fluids chemical characteristics, the way that copper has a higher heat exchange coefficient in relation to aluminum or steel, that way the removal of oxygen from the fluid inside the lungs and the accumulation of CO2 would cause a gradient that makes oxygen more likely to flow into the body, but only from a limited space we have in our trachea.
We'd also have to learn to train our swallowing the way we did when we learn not to breathe when we eat, except its all backwards. Expect a lot of swallowing of that fluid.

An alternative would be to just saturate the fluid with oxygen and insert some form of IV transfusion attached to a reservoir that had a high affinity for CO2, thus it would have to be emptied or replaced now and then as a kind of waste basket/waste removal system. That way oxygen uptake would be increased in the lungs, with the added decrease of CO2 leaving the lungs. It would only be a concentration gradient in the lungs at this point, more O2 would in when necessary and CO2 would leave through the lungs and hopefully mostly through the CO2 reservoir.
The reservoir itself would need to be insulated against the affinity binding surfaces otherwise the accumulation of CO2 in the reservoir would slow down over time.

Speaking of which... what would be the advantages of having fluid breathing, aside from saving space from building thicker walls to maintain the higher kinetic pressure/energy of gaseous containment.

huh? sorry i dont understand the question
are you asking the SvO2 or the difference in CO2 between atmospheric air and expired air?Sorry, it is not well worded. I added a pair of () to help but still poorly expressed question. Recorded local time of post shows it was 17 minutes past midnight here when I asked it - too late for me to still be up.)

Here is fraction I was asking about:

(SpCO2 leaving lungs & going to heart) / (SpCO2 entering the lungs from the heart) = ?

For me, that fraction would need to be 0.05 or less for numerator to be described as "almost completely CO2 free") I was guessing that it is more than that, when questioning your "almost completely CO2 free."