Nitrox - 1.40 or 1.60 PO2?

[Bismark]

You betchum. But I do believe in having a "bottom line" so that I'm not thinking about as the crash clock is running. Similary you need to make decisions about blood without gloves and rescue breathing without a mask, etc. Make your decisions now, not in the heat of the moment.

Okay, I will come and get you if you promise to come and get me......... I am okay with no rescue breathing though..........especially if I am still conscious.......

 

[Thalassamania]

No tongues.

 

[Papa_Bear]

Every breath you take, every move you make, I'll be watching you!

 

[Bismark]

Sounds like you got in trouble with one of the AR dolls in the past............. "honest, I thought I was doing it right"..........

 

[Anti-Hero]

One question comes to mind. There has been anecdotal evidence that suggest it may be possible to actually develop a sensitivity to high O2 PP over an extended period. Does anyone believe this could be a factor as mixed gas diving becomes more prevalent?

 

[Thalassamania]

One question comes to mind. There has been anecdotal evidence that suggest it may be possible to actually develop a sensitivity to high O2 PP over an extended period. Does anyone believe this could be a factor as mixed gas diving becomes more prevalent?

Can anyone supply a reference on that? I'd greatly appreciate it.

 

[Lee Taylor]

1.4 po2

 

[Tomeck]

1.6 pO2

 

[Anti-Hero]

Can anyone supply a reference on that? I'd greatly appreciate it.

It came out of a discussion on TDS, regarding a husband / wife cave diving team, where the wife suffered an oxtox at 1.4 ppO2, after ~20 min. On that discussion there were links to others toxing as low as 1.3. It was suggested by some that rather than building a tolerance to 02 exposure, some people actually develop a sensitivity to it.

I'll see if I can dig up the link.

 

[Thalassamania]

Hmmmm ... (granted we're not talking CNS here)

Protection from Oxygen Toxicity with Endotoxin


ROLE OF THE ENDOGENOUS ANTIOXIDANT ENZYMES OF THE LUNG


L. Frank, J. Summerville, and D. Massaro

The Pulmonary Toxicology Laboratory, Veterans Administration Hospital, Miami, Florida 33101
Calvin and Flavia Oak Asthma Research Center, University of Miami School of Medicine, Miami, Florida 33101


Abstract

Endotoxin treatment of adult rats before hyperoxic exposure significantly increases their survival rate in >95% O2 (J. Clin. Invest.61: 269, 1978). In this study, we wished to determine: (a) whether endotoxin would protect against O2 toxicity if it were administered after the animals were already in >95% O2 for 12-48 h; and (b) the relationship between the endogenous antioxidant enzymes of the lung and the protective effect of endotoxin treatment.

Our results showed that adult rats given a single 500 &#956;g/kg dose of endotoxin up to 36 h after the onset of O2 exposure had significantly increased survival rates and decreased lung fluid accumulation compared to untreated animals in O2 (P < 0.05). (Survival, 16/49 [untreated rats]; 18/20 [endotoxin at 12 h after the start of O2 exposure]; 25/26 [endotoxin-24 h]; 15/20 [endotoxin-36 h].)


Endotoxin-treated animals in O2 showed increases in pulmonary superoxide dismutase, catalase, and glutathione peroxidase activities before the usual time of onset of measurable pulmonary edema in untreated animals in O2. When diethyldithiocarbamate was used to block the superoxide dismutase enzyme rise in the endotoxin-treated rats in O2, the protective action of endotoxin against pulmonary O2 toxicity was nullified. In endotoxin-treated, O2-exposed mice, there were no lung antioxidant enzyme increases, and no protective effect from O2 toxicity was achieved.


We conclude that, in the rat, a single dose of endotoxin given even 36 h after the onset of hyperoxic exposure results in marked protection against O2-induced lung damage; and the increased lung antioxidant enzyme activity in the endotoxin-treated rats appears to be an essential component of this protective action.


link