X-Message-Number: 20012
Date: Sat, 7 Sep 2002 16:27:23 -0700 (PDT)
From: Jeff Davis <>
Subject: Re: suicide by inert gas inhalation

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In Message #20003, Fri, 6 Sep 2002 11:20:36 -0700 (PDT), Scott Badger wrote:

 ...suicide using an inert gas like Nitrogen or Helium as described at the 
 following web site.


 It appears to be quick and painless enough, but does significant brain damage 
 result from using such a procedure? 


I can't answer Scott's question above, but I'm interested in the answer.  So 
allow me to contribute a bit of info re the situation.

 As I understand it, the urge to breathe/breathing rate is provoked by CO2 
 concentration in the blood.  (I think blood pH plays a role; acidity increases 
 (pH falls)  with increased CO2 levels.)  In the alveoli, under 'normal' 
 conditions, the concentrations of the constituent gases are nitrogen=~80%, 
 O2=~16%, CO2=~4%. (This is substantially the same level as that of the blood 
 immediately adjacent across the lung-tissue/alveolar membrane, as blood and 
 alveolar gas levels equilibrate by diffusion in 1/150th of a second.) These 
 levels are maintained, of course, by the in-and-out flow--the tidal flow--of 
 breathing. Without breathing (tidal exchange) cellular respiration, which of 
 course consumes O2 and generates CO2, decreases the O2 levels and increases the
 CO2 levels away from baseline(80/16/4). 

When you exercise or hold your breath, bodily CO2 level rise.  The body senses 
the elevated CO2 levels, and prompts an increased rate of breathing.  (As well 
as the subjective feeling of urgency to breathe.)  This is the feedback system 
which compensates for the displacement of the tissue-gas concentrations from 
baseline, and drives the recovery of equilibrium conditions. 

'Tidal volume' is the volumetric fraction of the total lung volume that is 
exchanged per breath. This fraction is exhausted (exhaled) and replaced with an 
equal volume of gas (inhaled).  The inhaled volume, with concentrations 80/20/0,
mixes with the residual volume, with concentrations (slightly offset from) 
80/16/4.  This mix (briefly) raises/lowers the alveolar O2/CO2 concentrations. 
This creates the concentration gradient across the alveolar surface, which is 
equilibarated by diffusion, and results in the crucial life-sustaining exchange 
of O2 and CO2.

Now, when you breathe an inert gas, you are maintaining the in-and-out (tidal 
flow) of breathing.  This means that the CO2 is being continually flushed from 
the tissues in the usual way so that it does not become elevated.  There is no 
provocation of increased breathiing rate, no sense of breath starvation/urgency 
to breath, and no increase in blood acidity/(decrease in blood pH), at least not
from a rise in CO2 levels.   

Mike Darwin once described in admirable detail the pre-apoptotic 
sequence/cascade that results from a prolonged-duration ischemic (reduced or 
stopped blood supply) event.  My impression of such an event is that it is 
characterized by both deprivation of O2 (consumption of available supply and 
failure of replenishment) and accumulation of CO2 (produced by O2 consumption 
and then not carried away by blood flow).  Breathing of inert gas is similar to 
ischemia (blood stoppage) in that it causes a lethal stoppage of O2 
replenishment, but in contrast to stoppage of blood flow, it does not interfere 
with the carrying off of and exhausting of CO2.  (At least not so long as the 
heart continues to beat.)

Might this not be a good thing?

That is to say, phrasing it more favorably, Scott's question becomes:

What effect does the breathing of inert gases as a method of 'biological 
termination" have (or, "would one speculate is likely to have") on the apoptotic
and pre-apoptotic sequence/cascade compared to conventional ischemia?  Is it 
possible that the disposal of CO2 and the attendant prevention of increased 
blood acidity creates a situation which delays and/or slows the rate of the 
apoptotic sequence?

Best, Jeff Davis

   "My guess is that people don't yet realize how
          "handy" an indefinite lifespan will be." 
                            J Corbally 

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