Diving May Damage Blood Vessels

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lulubelle makes some very good points.
With regard to point #3 asking for tissue level data, the linked article contained this paragraph:

It does appear that the authors have some physiological evidence for endothelial dysfunction. The group observed significant deficits in flow-mediated dilation. I don't know if the investigators used adenosine or acetylcholine in their protocols to induce vascular dilation -- that's what is normally used by cardiologists BTW. On a side note, I'm not sure whether ultrasound-based techniques of measuring bloodflow might be complicated by post-dive bubbling. I'm sure other people in the field have addressed this. Not my field, so I don't know.

I'm curious about the method used for counting endothelial progenitors and "angiogenic" cells. I know that some people do flow cytometric sorting of cells by cell surface markers (CD34, CD133, VEGF receptor 2), whereas others assay for endothelial cell-colony forming units (basically, plate them out, grow them up, and count them). The former method can be problematic since hematopoetic stem/progenitor cells share some of those same markers.

I like the fact that this work calls into question the safety of nitrox use on a cellular/tissue level. This study, and other studies like it, should keep us on our toes when it comes to mitigating various risks in scuba diving.

This little study really only gets to the question. Not the answer. But that is a start.

I specifically pointed out the need for tissue level data connected to CV events Ultimately, nothing will change until the study is repeated, on a larger scale, with a more typical study population, and is tied to events/outcomes. But that will be a long time coming.

I have to say that I am a little bit irritated at the author's conclusion that compressed air is safer. That is more than a little bit premature.
 
The quote I found interesting was at the end of the article: "Diving with nitrox generates less bubbles during decompression, but elicits more hyperoxia," she told attendees. "We know that the hyperoxia during diving elicits oxidative stress and subsequent endothelial dysfunction."

I wish that the, "we know that," had been referenced.
 
This little study really only gets to the question. Not the answer. But that is a start.
I agree.
I specifically pointed out the need for tissue level data connected to CV events Ultimately, nothing will change until the study is repeated, on a larger scale, with a more typical study population, and is tied to events/outcomes. But that will be a long time coming.
I think I'm missing something here. I thought that investigating whether blood vessels can dilate properly in vivo is tissue level data that looks at cardiovascular function in a fairly direct way. I don't know the specific location of the blood vessels measured by the authors. My guess is that they used acetylcholine to induce dilation and then measured blood flow by ultrasound in a large artery somewhere.

It sounds like you know more about this CV stuff than I do. I'd really appreciate your insight on this.
I have to say that I am a little bit irritated at the author's conclusion that compressed air is safer. That is more than a little bit premature.
Perhaps. I think she's basing that statement, at least in part, on the flow mediated dilation data.
 
Well I'm gona say it...Oh Well..I'm gona suck air till I die!!!!

VEVA DIVERS!!!
 
I think I'm missing something here. I thought that investigating whether blood vessels can dilate properly in vivo is tissue level data that looks at cardiovascular function in a fairly direct way. I don't know the specific location of the blood vessels measured by the authors. My guess is that they used acetylcholine to induce dilation and then measured blood flow by ultrasound in a large artery somewhere.

It sounds like you know more about this CV stuff than I do. I'd really appreciate your insight on this.

Now don't be silly, we both know that I do not.

I'm assuming that the endothelial dysfunction observed in these otherwise healthy military divers might have been temporary. So what should that mean to me? What should change?

I'm talking about clinical events related to long term endothelial dysfunction such as heart attack, heart failure, and stroke. Should anyone ever be able to tie diving with nitrox to clinical events, I suspect that it would change a LOT.
 
Now don't be silly, we both know that I do not.
Meh. My knowledge of the CV system is very basic. :)

I'm assuming that the endothelial dysfunction observed in these otherwise healthy military divers might have been temporary. So what should that mean to me? What should change?
Wait a second. Are you trying to tell me that those boots aren't connected to a burly military diver?
I'm talking about clinical events related to long term endothelial dysfunction such as heart attack, heart failure, and stroke. Should anyone ever be able to tie diving with nitrox to clinical events, I suspect that it would change a LOT.
Ah. We're talking about temporary effects vs. long-term clinical outcome (morbidity, [-]morality[/-] mortality rates of cardiovascular-related events). OK. Got it. Yup. You're right.
 
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Meh. My knowledge of the CV system is very basic. :)


Wait a second. Are you trying to tell me that those boots aren't connected to a burly military diver?

Ah. We're talking about temporary effects vs. long-term clinical outcome (morbidity, morality rates of cardiovascular-related events). OK. Got it. Yup. You're right.


Boots are definitely not connected to a burly military diver.
 
Ah. We're talking about ..........morality rates .....

No study needed there, I am already sure that they are dangerously low.
 
The author may be a credible scientist but she may have made a mistake somewhere in her research. This is why the peer review system exists, it is not perfect, but there needs to be quality control and assurances on these papers.

I couldn't agree more, Hashime. In general, I much prefer my science/medicine from recognized, respected, peer-reviewed journals.

What I was objecting to was your pejoratively and incorrectly terming the MedPageToday item a "press release" and your intemperate language in calling the work "...total crap."

Regards,

DocVikingo
 
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We know quite a bit more about the effects of SCUBA-related bubbling and oxidative stress on endothelial dysfunction and damage than has been discussed in this thread thus far.

The following entertaining piece by a couple of recognized researchers in the area contains some fascinating science and speculation on a broad coverage of the issues, including possible preventative measures such as antioxidant preconditioning as well as lots of useful references for those who wish to delve deeper (many of them from recognized, respected, peer-reviewed journals :wink:). It also highlights that DCI very likely is a multifactorial pathophysiological process and one which remains incompletely understood.

Medical Hypotheses 72 (2009) 389–392

Gas bubbles may not be the underlying cause of decompression illness – The
at-depth endothelial dysfunction hypothesis

(http://membership.uhms.org/resource/resmgr/dcs-age_journal_watch/madden_gas_bubbles_med_hypot.pdf)

Regards,

DocVikingo
 
https://www.shearwater.com/products/swift/

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