Autoregulation in peripheral blood flow.

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The Iceni

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Hi Dr Deco,

In a discussion on technical diving I learned that many divers believe that keeping a high(ish) ppO2 constant can actually reduce the efficiency of decompression because it is thought that on long exposures it can narrow the capillaries and so reduce offgassing at the level of the tissues. Thus many technical divers employ air breaks and extend their in-water time as a means to reduce this effect.

I know that autoregulation in cerebral blood flow is generally accepted as a part of the aetiology of acute CNS oxygen toxicity. However, I have not seen any evidence that excessive oxygen induced vasoconstriction occurs in the peripheral circulation (or indeed in the cerebral circulation) at, constant, hyperbaric levels of inspired ppO2 of less than 1.6 bar in the presence normal partial pressures of carbon dioxide. As for many generally accepted physiological concepts in diving, I am not sure if there is any evidence from scientific studies to confirm that significant peripheral vasoconstriction actually happens in practice at these exposure levels.

This is not to be confused with pulmonary oxygen toxicity which has been proven, many times, to be a local toxic reaction being both time and dose dependent and will in time reduce pulmonary offgassing efficiency. It is hardly surprising that pulmonary effects are seen at the prolonged (many hours) exposures at well over 2 bar pp O2 in chamber treatment as the lungs are directly exposed to these toxic levels. The majority of the body's tissues are most certainly not as there is a pressure gradient in life due to the preferential metabolism of free oxygen.

Is there any evidence that keeping ppO2 constantly high (but less than 1.6 bar at the lungs with relatively normal pp CO2) can actually reduce the efficiency of decompression due to peripheral vasoconstriction in recreational technical diving?

I am genuinely interested to learn if this is phenomenon is genuine as the needless extension of an extremely boring in-water decompression stop generates its own problems, not least of which is body cooling. :confused:
 
pescador775 once bubbled...
Perhaps, also, one needs ask whether N2 is a vasodilator.
Indeed, but I think I can answer that straight away. Molecular nitrogen takes no part whatsover in any biochemical reaction.

As far as I am aware, the only physiological effect nitrogen can have is subtractive. At any partial pressure a mix containing nitrogen must contain less active gas molecules (oxygen) than a mix containing the biochemically active gas alone. (Dalton's law).

Nitrogen is absorbed and excreted unaltered.

The narcotic effects of all the inert gassese are due to their molecules' physical presence in the nerve cell membranes, and are not due to any active biochemical mechanism. I suppose it is theoretically entirely possible that nitrogen could reduce vasomotor tone by narcotic effects on afferent vasoconstrictor fibres but again I am aware of do evidence that this happens at the partial pressures of nitrogen seen during decompression, or indeed at the much higher partial pressures of nitrogen seen at depth.

I believe air breaks during accelerated decompression are actually employed solely to reduce the accumulative, and very real, risks of CNS oxygen toxicity, not to restore tissue offgassing to maximum efficiency as has been proposed.:devious: :)
 
Dear Paul:

Vasoconstriction

Oxygen-induced peripheral vasoconstriction is a real phenomenon. (It is under current investigation as the attached reference illustrates: Komori M, Takada K, Ozaki M. Effects of inspired oxygen concentration on peripheral microcirculation studied by the rabbit ear chamber method. In Vivo 2001, Jul-Aug;15(4): 303-8). There may be an influence in the inactivation of nitric oxide. This effect of NO is also suspected to play a role in exercise prior to hyperbaric expose and the mitigation of bubble formation in rats and humans.

Reversal of Vasoconstriction

On the basis of our NASA studies, nothing will speed the washout of nitrogen as well as exercise, which probably aids in reversing the oxygen-induced vasoconstriction. This is why I continue to stress in-water exercise (such as cycling maneuvers) while at the in-water stop and continues activity while in the surface interval. This is not theoretical and the result of the “EFFECTIVE HALF TIME” versus “ACTIVITY LEVEL” (= oxygen consumption) as shown in the ATTACHMENT . The blood flow to the muscles (and tendons) is increased and results in effectively fastter halftimes for the clearance of nitrogen. These are measured effects in the laboratory, not hypothetical.

Dr Deco :doctor:
 
Many thanks, Dr Deco,

I knew you'd have the answer. I will have do do some reading!

Dr Deco once bubbled...
. . .

Reversal of Vasoconstriction

On the basis of our NASA studies, nothing will speed the washout of nitrogen as well as exercise, which probably aids in reversing the oxygen-induced vasoconstriction. This is why I continue to stress in-water exercise (such as cycling maneuvers) while at the in-water stop and continues activity while in the surface interval. This is not theoretical .

Dr Deco :doctor:
I take this to mean that such exercise during a stop is greatly to be preferred to any air break - at least with regard to the effects of oxygen induced vasoconstirction on offgassing.

Kind Regards,
 
Dear Paul:

The exercise is to be preferred to the air break for off gassing. However, air breaks are advisable [possibly even necessary] to thwart the deleterious effects of oxygen on the pulmonary system. The individual should stop exercising about ten minutes before the air break to minimize the reverse process of accelerated nitrogen uptake by tissues with hyperemic flow. It works both ways.:boom:

Dr Deco :doctor:
 
While undertaking this research which Dr Deco referred to, I hope someone is checking blood PH. I suspect that simple skip breathing on O2 may take care of the alleged problem. The minor increase in acid level should counter any alkalosis and resulting vasoconstriction. Exercise may do the same. Just another theory of mine.
 
pescador775 once bubbled...
. . I hope someone is checking blood PH. I suspect that simple skip breathing on O2 may take care of the alleged problem.
Too many variables unaccounterd for pescador!

It takes quite a lot to alter the body's normal pH balance. In general it is buffered pretty well. Agreed CO2 retention due to breath holding will result in acidosis but I do not believe that any of the above discussion mentioned "skip breathing" .

As I read it all that was done is the divers were breathing either high dose oxygen or air, in which case there will be no change to CO2 excretion which will remain just as efficient :wink:
 
I still have this image in the back of my head of divers hanging off, waving their arms, switching off O2 and back to air and trying to figure decompression schedules based on all this. Reminds me of my stay in the chamber but I had highly paid helpers to manage the variables in a controlled situation. No sea state, weather, boat fire, drunk captain, leaky tank or dragging anchor to worry about. Then too, there is the well known guru who claims that he is so vascularized from exercise that he doesn't worry about decompression, much. We'll leave that one aside.

So what's the problem? We hear that O2 is bad because it constricts circulation and impairs offgassing of N2. Also, that prolonged O2 breathing is bad for the lungs. Well, the lung thing is an extreme case but stuff happens and so, follow the guidelines. As to the vascular constriction I still believe that there is a simpler answer worthy of consideration by the worthy experimenters.

In their place, I would propose that the drug Viagra be tested for countering the circulation problem imputed to the breathing of pure oxygen. Viagra causes a rise in circulating nitric oxide which is a vasodilator. Of course, there is the issue of side effects but that's all about risk management.
 
Dr Deco once bubbled...
Dear Paul:

This is why I continue to stress in-water exercise (such as cycling maneuvers) while at the in-water stop and continues activity while in the surface interval. This is not theoretical and the result of the “EFFECTIVE HALF TIME” versus “ACTIVITY LEVEL” (= oxygen consumption) as shown in the ATTACHMENT . The blood flow to the muscles (and tendons) is increased and results in effectively fastter halftimes for the clearance of nitrogen. These are measured effects in the laboratory, not hypothetical.



I am a bit :eek:ff:
Exercise introduces 'micronuclei' in the divers body. These nuclei are thought to play a great role in development of bends. Does the off gassing compensate the negative effect of nuclei generation?

:hmmm:
 
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