Talk:Liquid breathing

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Contents 1 Move to Liquid breathing ? 2 Questions 3 RD article 4 Comments and Suggestions For Revision 5 Space application not possible 6 Removed from article 7 Space section is all wrong 8 Fiction 9 Filling all air-filled cavities

[edit] Move to Liquid breathing ?

This should really be cleaned up and moved to Liquid breathing. Although this article uses the terms "liquid breathing" and "fluid breathing" to mean the same thing, it in fact is referring to the breathing of a liquid. Since all breathing is breathing of a fluid, the improper use of that term should be removed. If nobody else does this first, I'll get around to it eventually. Merenta 20:34, 10 Nov 2004 (UTC)

so what happened?, the Liquid breathing just redirects to this page. I agree that "fluid breathing" is a misnomer, as air is fluid--JinFX HuangDi 1968 06:12, 2005 Feb 18 (UTC)

Argh! Air... is... a... fluid... 04:53, 24 June 2005 User:24.218.139.205

• Support, for the reasons suggested above. Alai 23:47, 27 August 2005 (UTC)
• Support. You're absolutely right, of course, Merenta. — Knowledge Seeker দ 00:34, September 1, 2005 (UTC)

This article has been renamed after the result of a move request. Dragons flight 22:47, September 2, 2005 (UTC)

[edit] Questions

After reading this fascinating article, I'm left with some questions. I don't know if the answers exist anywhere.

1. Does the subject breathe, using the muscles around the lungs? There is a mention of a pump in some studies. But could the lungs actually work to inhale/exhale liquid?

2. Has any subject been adult and conscious during any part of the process? Have their been any personal descriptions of the experience? I imagine that filling the lungs would be like drowning and very distressing, but what about the stable experience of breathing the liquid?

3. "The animal was tilted for 15 seconds and the liquid drained from the lungs". Is it really that simple? I am thinking of the efforts involved (it would seem) after a person has water in their lungs from a near-drowning. Much pumping of the chest, coughing etc. Or is all that just Hollywood? Notinasnaid 17:31, 8 November 2005 (UTC)

1. A fetus actually builds its muscles by breathing amniotic fluid, and so the subject's lungs could work pretty well at this. The pump is to bring the liquid through the rebreathing apparatus that scavanges CO2 and replenishes O2.
2. As mentioned in a few places, people have been awake for the "mist" style of this therapy, but this is a gradual process of alveoli filling up, rather than bronchi etc.
3. Water has a fairly low vapor pressure, and doesn't allow oxygen to pass through very well. As in the more moderate types of therapy, the alveoli can stay filled as the perfluorocarbon evaporates. However, in clinical trials, I'm sure that the animals cough and sputter, and the tilting is just to help with that process. Researchers tend to overlook the work that animals themselves do...--Joel 18:05, 8 November 2005 (UTC)

[edit] RD article

I'd read in a fairly recent article that one Dr. Shaffer of Temple University Hospital wanted to use PFC in premature babies since the procedure had worked fine in his experience. He claimed that his research was frustrated because he couldn't get the funding needed to apply for FDA approval. He said that the biggest reason critics object to its use is that it distracts from what causes much of premature births in the first place--drug and alcohol abuse by the mother. If this is a true claim by critics, its absurdity can be seen by all.Jlujan69 22:25, 10 August 2006 (UTC)

Last I looked into this, the problem was that the FDA forced Alliance in the clinical trials to compare partial liquid ventilation PLV (used with regular ventilators), to gas-only ventilation using top of the line high frequency oscillating ventilators (HFOV). When the PLV didn't show any better results, instead of saying "Gee, that's remarkable, just putting in some PFC with a regular vent does as well as using a state of the art new HFOV ventiation system!", they closed the tests down and didn't approve Perflubron for any more trials. Alliance's stock went though the floor, they couldn't generate any new capital, and that was that. In a rational world they'd have tried comparing (say) HFOV with and without PLV. I am told, BTW, that HFOV works fine with PLV, so they're perfectly combatible.

If you want to look at real nuts and bolts social issues for why PLV gets little funding from drug developers (which is the seed money that provides the studies that attract federal funding), it has to do with general lack of funds for research and treatment in premature babies. It is prefectly true the premies have no money. And they are generally born to young people of very low socioeconomic class who have no money, either--- yep, that's also correct. This is not a promising market for a pharm developer. Give me a pill for rich and worried middle-aged former yuppie people, which they have to take every day for the rest of their lives. Crestor. If you think there's any comparitive incentive to develop liquid ventilation fluids which require the same drug approval process, considering how and in whom they will be used, think it out again. And yes, the Leftists are right about this. The Left can't be wrong ALL the time. SBHarris 22:50, 10 August 2006 (UTC)

[edit] Comments and Suggestions For Revision

It is interesting to see an article that is pretty factually accurate, but really misses the point in almost all the critical areas. I hate editing Wikipedia pieces (but don't mind writing the first one). If anyone is interested in "fixing" this piece, let me know - meanwhile here are some corrections and comments:

First, there is one critical missed point that renders much of the discussion and speculation about diving and space-flight applications moot. The major problem with TLV isn't simply the density of PFCs, but rather the fundamental physics of fluid flow. While different PFCs have differing viscosities, on average PFC is 80 times more viscous than air. Whether it is a mouse, a dog, or cat, if you look at the literature you will notice that 5-7 breaths a minute is the maximum achieveable (Shaffer T H, Forman DL, et al. Physiological effects of ventilation with liquid fluorocarbon at controlled temperatures. Undersea Biomed Res. 1984 Sep;11(3):287-98.). You cannot do more than 5-7 breaths a minute because the liquid is too viscous compared to air. Now, it would be possible to avoid the limitation on BPMs with PFCs in an animal thats use a flow-through system for respiration, such as fish, or birds. But,not in most vertebrates.

In 1976, Miyamoto and Mikami (Maximum capacity of ventilation and efficiency of gas exchange during liquid breathing in guinea pigs. Jpn J Physiol. 1976;26(6):603-18.) calculated that the resting man normally produces 192 mL/min of CO2 (S.T.P.). This level of CO2 production would require TLV (PFC) ventilation volumes of about 4 L/min (or about 70 mL/kg/min). Although this is ~70% of the normal gas ventilatory flow for a resting adult, it is near the upper limit of flows that can be accomplished at normal pressures in TLV (Kylstra, 1974). The higher peak and mean ventilating pressures necessary to move the amount of liquid required for CO2 exchange in TLV would expose the lungs to an increased risk of barotrauma (pressure injury) and volu-trauma (over-distention injury).

During higher than normal CO2 production rates, such as physical exertion or illness, TLV would clearly not be adequate for CO2 removal. Some examples of high CO2 (hypercapnic) states are, 1) increased metabolic states (e.g. cancer, infection, burns), 2) states of physiologic stress (e.g. hyperthermia, agitation), 3) post-ischemic conditions where substantial metabolic debt has been incurred, and 4) physical exertion (such as swimming and diving). Under all these conditions the need to rapidly unload CO22 and deliver large amounts of O2 is essential. Such hypercapnic/hypercarbic states are also frequently present in shock due to sepsis or trauma, and thought to be due to both an increased production of CO2, and decreased elimination of CO2 due to low blood flow or pulmonary edema.

In anesthetized, paralyzed, normothermic dogs, TLV is capable of maintaining steady-state gas exchange with adequate O2 delivery and CO2 removal. However, TLV is not cannot deliver steady-state CO2 removal under basal metabolic conditions in smaller animals with higher specific metabolic rates, such as guinea pigs. As Matthews and co-workers document (Matthews WH, Balzer RH, et al. Steady-state gas exchange in normothermic, anesthetized, liquid-ventilated dogs. Undersea Biomed Res. 1978 Dec;5(4):341-54), the parameters for maintaining normocapnia in anesthetized beagles are narrow, even under basal normothermic metabolic conditions. In this study, as TLV rates were increased from 2.8 to 5.6 liquid breaths per minute, and alveolar ventilation was increased from 574 to 600 mL/min/animal (an increase of 4%), the pa CO2 continued to increase until dangerous hypercapnia occurred. The authors suggested that this increase was due to a 2% drop in liquid-alveolar ventilation, however using their own formulas and data, it easy to show by calculation that the dogs receiving higher ventilation rates actually have higher rates of alveolar ventilation (dVa/dt). These results would seem paradoxical until consideration is given to the inverse relationship of pa CO2 to alveolar ventilation, a relationship which holds only under equilibrium conditions. From a practical standpoint, this means TLV cannot be used in situations where humans or other mammals exert themselves. Under conditions of stress or exertion, respiratory rate increases dramatically. If a person or animal is running, or even engaging in normal activities, metabolic demands and CO2 generation will increase beyond the capability of TLV to provide adequate gas exchange.

The statement, “As in Kylstra's studies, Clark had problems due to the size of the animals' airways. The tiny size limited the amount of liquid that could get into the lungs. For that and other reasons, carbon dioxide tended to build up in the system and could not be removed fast enough," is incorrect. The “small size" of mouse airways is irrelevant to liquid distribution and to limitations on liquid breath rate. The small airways in a mouse are the same size as the small airways in a human or an elephant. PFCs have incredible spreading co-efficients and extraordinarily low surface tensions. They will get into almost any space, or through almost any hole. Indeed, they are used for leak-detection. The real limiting factor is that alveoli in both mice and men are scaled pretty much the same because of the physics of gas exchange. The same is true of capillaries in all mammals because of the physics of mass exchange and diffusion (Dawson, T. H. (1991). Engineering Design of the Cardiovascular System of Mammals. Prentice Hall Biophysics and Bioengineering Series (ed. A. Noordergraaf). Englewood Cliffs, NJ: Prentice Hall). A capillary in a mouse is the same size as that in an elephant. Consequently, blood pressure, mean arterial pressure, and capillary opening pressure, are about the same for all mammals (giraffe's have their own issues). Resting blood pressure in a mouse and a man is virtually the same (Gregg, D. E., Eckstein, R. W. and Fineberg, M. H. (1937). Pressure pulses and blood pressure values in unanesthetized dogs, Am. J. Physiol. 118,399-410, and Woodbury, R. A. and Hamilton, W. F. (1937). Blood pressure studies in small animals. Am. J. Physiol. 119,663 -674.).

Lungs were injured by many PFCs used in early liquid ventilation studies, because the vapor pressure was too high, and PFC that gets trapped in alveoli, or gets into the lung parenchyma, turns into gas. This PFC gas is not eliminated rapidly enough to avoid serious injury. If you inject 1 ml of FC-75 (vapor pressure of 30 torr at STP) into a mouse's peritoneum, the mouse inflates to about the size of a golf ball over a time course of several hours. A few days to a week later, the animal dies from starvation because its abdominal viscera are compressed (there is no fat on the animal at necropsy, and its organs are shrunken from starvation). Perflubron (perfluorooctylbromide) is the only molecularly consistent PFC. All others contain different chain lengths of the constituent perflurochemical. For example, the 3M Fluorinert compounds which were often used for early liquid ventilation experiments such as FC-75 (perfluoro(butyltetrahydrofuran), as previously noted, has a vapor pressure of 30 torr at STP and FC-77 (perfluorooctane) has a vapor pressure of 85 torr. Thus, the vapor pressure for a given PFC is the average of the molecular species present. As a consequence, even a little high vapor pressure PFC will cause lung injury. By contrast, the vapor pressure for perflubron which is the only PFC so far approved for clinical trials, is 11 torr and that is the “true” vapor pressure of perflubron since all molecules are of the same chain length.

These claims are largely incorrect and unsubstantiated:

"Profound expertise is mandatory to perform and maintain filling of the lung with perfluorocarbon to functional residual capacity (FRC). Disruption of PLV immediately deteriorates gas exchange. Incomplete filling of the lung has been shown to be less effective than filling the lung to functional residual capacity volume. Severe adverse events affecting gas exchange and pulmonary circulation limit the use of PLV."

First it is easy to maintain filling to FRC, and Alliance Pharmaceuticals had developed systems to measure the amount of PFC vaporized in real time, as well as to condense vaporized perflubron, measure it, and collect it for return the patient.

I don't know what "disruption" of PLV means, but PLV is only initiated in the first place because gas exchange is inadequate! Of course, if you stop adding perflubron, gas exchange will deteriorate -- it will go back to about what it was before -- unless the injury has improved or resolved. It is not easy to disrupt PLV because once the liquid is in the lungs it is in there until it vaporizes. The only way to get it out would be turn the patient upside down and attempt to drain it of out of him -- and even then you will still end up with pretty near FRC in the lungs. I know this because we tried to recover as much PFC from our experimental animals as possible in order to save money as all the PFCs are very expensive. The statement "Severe adverse events affecting gas exchange and pulmonary circulation limit the use of PLV," is totally unsupported and incorrect. There are no adverse hemodynamic effects, and the worst that can be said of PLV in clinical trials is that did little better, and maybe a bit worse, than gas ventilated patients AFTER the new lung protective ventilation strategies were adopted. Nobody ever tried PLV with the lower tidal volumes and lung protective ventilation strategies because Alliance ran out of money. Nor were there any clinical studies with high frequency oscillation ventilation (where PLV absolutely shines and all the issues of baro and volutrauma from liquid moving more slowly as the lungs are inflated and deflated go away). The tragedy of therapeutic PLV for respiratory distress syndrome is that the clinical trials were so badly designed and Alliance’s handling of the technology was even more poorly managed (Reiss SG. Understanding the fundamentals of perfluorocarbons and perfluorocarbon emulsions relevant to in vivo oxygen delivery. Artif Cells Blood Substit Immobil Biotechnol. 2005;33(1):47-63).

These incorrect statements should be supported by peer-reviewed references, or deleted.

Finally, the really important thing about Gas Liquid Ventilation (GLV) cooling or warming, and the major innovation, is that it uncouples heat exchange from gas exchange. Inducing hypothermia using TLV is problematic because PFC viscosity (pressure/flow) also places a limit on the rate at which heat can be extracted from an animal or patient using TLV. In addition to the CO2 diffusion limitation, there is indirect evidence suggesting that thermal equilibrium is not reached between blood and liquid in small airways at high TLV "alveolar ventilation" rates. Thus, there appears to be a heat-diffusion limitation to TLV that is analogous to the CO2 diffusion limitation.

This phenomenon may explain why Shaffer's TLV cat studies failed to achieve concurrent increases in the rates of animal core cooling, when significantly greater PFC temperature gradients were used (Shaffer T H, Forman DL, et al. Physiological effects of ventilation with liquid fluorocarbon at controlled temperatures. Undersea Biomed Res. 1984 Sep;11(3):287-98). Shaffer found that decreasing PFC infusion temperature from approximately 20.degrees C to about 10 degrees C (from ∆T =15.degrees C to ∆T =24.degrees C), resulted in cooling rates increasing from 0.13.degrees C/min (7.8 degrees C/hr) to 0.15.degrees C/min (9.0degrees C/hr) a change of only 15%. This 15% increase occurred despite an increase of ∆T equal to 60%. These results suggest a sharp decline in the efficiency of heat extraction with increased ∆T at higher TLV ventilation rates (in this experiment, rate was increased from 4.5 to 5.3 liquid breaths/min).

In Shaffer's study, the authors calculate from PFC inspiration and expiration temperature differences, a 96% increase in heat extraction per kg from their animals at the 10degrees C PFC infusion temperature versus that calculated at 20degrees C. However, the fact is that this increase in heat extraction does not show up in the rate of body core cooling (15%), to which it should be proportional. This indicates that Shaffer's calculations of heat removal performed on the basis of integrated measurements of expired fluid temperatures must have been in error. As further evidence of this error, calculations of expected cooling rates of animals used in this study (using a reasonable 0.8 cal/g/degrees C, or kcal/kg/.degrees C average specific heat capacity for the body), indicate that up to half of the heat extraction calculated by PFC temperature differences in this experiment are unaccounted for even at the fastest cooling rates. For example, an animal with an average 0.8 kcal/kg/.degrees C specific heat capacity, cooling at the reported rate of 9.0.degree. C/hr, could theoretically give up heat at a rate no faster than (0.8 kcal/kg/C)(4184 J/kcal)(9 C/hr)=30,124 J/kg/hr. However, Shaffer's experiment reports on the basis of temperature readings of PFC infused and expired, the extraction of 65,637 J/kg/hr. It is likely that the difficult integration of [expired fluid temperature] versus (fluid volume) curve for this experiment was in error by a factor of 2.0. For examples of experiments in which integrated cooling rates calculated from PFC temperature differences match actual animal body cooling, see: Harris SB, Darwin MG, et al. Rapid (0.5 degrees C/min) minimally invasive induction of hypothermia using cold perfluorochemical lung lavage in dogs. Resuscitation. 2001 Aug;50(2):189-204. The authors found that at rapid (machine-controlled) liquid infusion and removal rates, and peak fluid temperatures do not accurately reflect volume-averaged fluid temperatures, or fluid heats.

In TLV too few breaths and too little turbulence probably results in a lot of the liquid at the terminal end of the airways remaining there from one breath to the next. Heat exchange is very poor. In conclusion it is not possible to meet the gas exchange demands of a critically ill patient with TLV, nor is it possible to meet the gas exchange demands of humans under real-world conditions making TLV with currently available PFCs impossible for applications such deep sea diving or space travel. PLV remains a promising modality for the treatment of respiratory distress and for the induction of hyper- or hypothermia (Wauer RR, Gama de Abreu M. 4th European symposium on perfluorocarbon application. Eur J Med Res. 2006 Mar 16;11 Suppl 1:1-12).

Unmentioned in the Wikipedia article are potent anti-inflammatory and immune modulating properties of most PFCs, properties which undoubtedly contribute the salutary effects of PLV in the setting of lung injury (Haeberle HA, et al. Perflubron reduces lung inflammation in respiratory syncytial virus infection by inhibiting chemokine expression and nuclear factor-kappa B activation. Am J Respir Crit Care Med. 2002 May 15;165(10):1433-8, Forman MB, et al. Pharmacologic perturbation of neutrophils by Fluosol results in a sustained reduction in infarct size in the canine model of reperfusion. J Am Coll Cardiol. 1992 Jan;19(1):205-16 and Jiang L, et al. Effect of different ventilation modes with FC-77 on pulmonary inflammatory reaction in piglets after cardiopulmonary bypass. Pediatr Pulmonol. 2007 Feb;42(2):150).

Necrobiologist Necrobiologist 11:04, 3 February 2007 (UTC)

[edit] Space application not possible

I have added a paragraph about the impossibility of using liquid breathing to withstand high G-forces. Source: http://yarchive.net/med/liquid_breathe.html 17:47, 2 March 2006 User:71.247.67.39

Also, the trials by Alliance produced little results. I added the following sentence:

Unfortunately, results of the clinical trials were disappointing and Alliance is no longer pursuing partial liquid ventilation application.

-neolex 20:02, 2 March 2006 User:71.247.67.39

For the record, the space application is possible, just not with fluorocarbons. See the discussion in "Removed from Article" below. Cryobiologist 20:39, 17 January 2007 (UTC)

[edit] Removed from article

However, while simultaneous immersion of the astronaut in a fluid filled chamber AND fluid breathing would mitigate G forces, the mass penalties of filling an entire space capsule with fluid would make its gross weight much higher than that of an air filled capsule, and thus the former would be less capable of high acceleration (due to lower thrust to weight) than the latter.

Formatting is a bit odd, as is wording. Furthermore, the paragraph doesn't seem to have a point to make. Can anyone rewrite it, or comment on it? -- Ec5618 22:55, 2 June 2006 (UTC)

Yes, the idea is basically wrong. When you are floating in fluid you are no more weightless than when lying on a waterbed; you just happen to be a bit more well-supported. A watermattress which allows nearly total sinking should do almost as well as a tank, but it's not worth doing because the limiting factor to g's an astronaut can take is NOT the pressure he feels on his skin. Basically, g-load limit is due to blood pooling due to g-forces and fluid support doesn't change that. An astronaut subjected to "vertical" g's in liquid would still black out. Just as a scuba diver who has difficulty with head downward positions ala the "inversion table" will find that it's just as uncomfortable to be head downward while underwater (as I personally can testify). Again, fluid immersion is not weightlessness. Your internal organs can't tell whether you're floating in fluid or lying on a bed of nails-- it's all the same to them. 00:41, 3 June 2006 User:Sbharris

No, the idea is basically right. At high gees, there is no blood pooling in extremities without distention. And there is no distention without pressure differential. That is how anti-g suits (see g-suit) protect pilots from blacking out; they increase external pressure on lower parts of the body to counteract inreased internal pressure. A new type of anti-g suit, the Libelle Suit, actually surrounds the pilot with water, allowing pilots to remain conscious at 12g. The principle of zero-g equivalence with water suspension works, the only limitation being air cavities and tissues with density different from water. Cryobiologist 21:12, 12 December 2006 (UTC)

Okay, I admit that in the limit of suspension in an anti-acceleration fluid of the same density as blood, and with all vessels inside the body supported internally in the same way, you could take very high acceleration-- in theory all you like--- and wouldn't feel it. In practice, since blood and tissues do have different density (for example the brain would float in blood, so blood would pool at the bottom of the brain in verticle g-load), and there are some air spaces here and there, the relatively dense vessels have to be supported by bone, connective tissue, fat, etc. And the even denser bones in the same way. If you filled the lungs with a fluid of the density of blood, and the mediastenum also, you could in theory keep the aorta from tearing off the top of the heart with a big forward deceleration (as commonly happens). Fluids of near-blood different density should give some help there, but by the time you get to perfluorocarbons (PFC)s at 1.8 times the density of water, now your problem is even worse than before, since the ligaments which hold the lungs aren't designed to hold big heavy bags of PFC at high g, and their effective weight is the difference between water and PFC density, times volume.

I suppose I'm saying that the problems of liquid-breathing have to be separated from the problems of high-g acceleration, and in any case, so long as we're talking about the perfluorocarbons or any fluid much different in density from water or blood, it doesn't work to fully ameliorate g-stress whether it's in the lungs or you're floating in it. For example, an astronaut with density of water, fully immersed in PFC with specific gravity 1.8, would be squashed against the roof of his tank with a weight equivalent to 0.8 g, and this would increase by 0.8 g for every g of acceleration, so no help there. But if you let him float freely at the surface of a tank of PFC, he'd have some part of his body (45% or something) above the PFC surface (presumably in gas), and that part of him in the air would get no help at all from g-effects. His lungs, of course, would be squashed by the differential weight of PFC, whether he were floating in PFC or not. SBHarris 22:42, 13 December 2006 (UTC)

[edit] Space section is all wrong

The section on using this in space travel is based around a very common misconception. It contains this sentence, which seems to sum up the misconception:

"A person immersed in liquid of the same density as tissue has acceleration forces distributed around the body, rather than applied at a single point such as a seat or harness straps. This principle is used in the Libelle G-suit, which allows aircraft pilots to remain conscious and functioning at more than 10 G acceleration by surrounding them with water in a rigid suit."

The problem here is that a G-suit works because it applies unequal pressure to a pilots body; it squeezes the legs and lower abdomen (but not upper body) so that blood can't pool in the lower body during high-g maneuvers. If the suit applied the same pressure evenly across the pilots body, it would be useless. The particular flight suit linked to in the article is simply a regular flight suit that has a system to automatically change the pressure being applies across different parts of the pilot's body, allowing it to provide optimal support during different types of maneuvers - but it still works on the principle of applying unequal pressure to prevent blood from pooling in different parts of the body.

Being immersed in a fluid would not magically protect you from acceleration forces. For example, if a person were standing immersed in a tank of fluid and the entire tank began accelerating upward, the person’s blood would still pool in his lower body and eventually cause a blackout. His lower body would get slightly larger as it fills with blood and his upper body would get slightly smaller as the blood drains out. Since the fluid is applying pressure evenly across his entire body surface, it wouldn't do him any good.

20:39, 14 February 2007 User:128.227.142.57

The space section is correct, and is supported by an authoritative secondary source (Textbook of Medical Physiology). The reason fluid immersion prevents blood pooling is because hydrostatic pressure is NOT the same at all points on the body when g forces are applied. At one gee, water pressure increases by 0.5 psi per foot of depth. At 10 gees, water pressure increases by 5 psi per foot of depth. Under water, at 10 gees, a seated pilot's legs will experience an external pressure of 15 psi relative to the head, which exactly counterbalances internal pressures that would otherwise distend the legs and cause blood pooling. Think of a bag of water immersed in a tank of water. There's no force to change the shape of the bag regardless of gees.

The Libelle G-suit, by the way, is a purely passive device. The only "automatic" change in pressure applied to different parts of the pilot's body is due to the water bladders which experience passive hydrodrastic pressure gradients by the mechanism described above. Please see the review article Current Concepts in Acceleration Physiology Cryobiologist 23:33, 14 February 2007 (UTC)

[edit] Fiction

I remember an episode of Captain Simian and the Space Monkeys in which they crashed onto a water-planet, and were concerned with drowning until they realized they could breathe the "water" and called it "wet air." 05:48, 19 February 2007 User:75.72.21.221

[edit] Filling all air-filled cavities

I have reverted the recent edit that said reducing the physical stress of G forces requires "filling all normally air-filled body cavities with liquid." This is not necessary for the mere reduction of the stress of G forces. As the article explains, simple water immersion does reduce the stress of G forces, allowing tolerance up to 15 or 20 Gs. It is the near-elimination (as opposed to reduction) of the stress of G forces that requires both water immersion and filling of the major air-filled cavities with a similar liquid, which is where the role of liquid breathing comes in. Cryobiologist 17:18, 18 March 2007 (UTC)