Diving May Damage Blood Vessels

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DandyDon

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Nitrox allegedly does more damage.

From Medical News: EuroPRevent: Diving May Damage Blood Vessels - in Meeting Coverage, EuroPRevent from MedPage Today
GENEVA -- Repeat scuba dives appear to harm the endothelium, particularly when breathing the mix of gases popular with recreational divers, according to a small study.

With the low-nitrogen air mix called nitrox, endothelial function as measured by flow mediated dilation dropped significantly after each dive -- and didn't fully recover between dives, Emeline Van Craenenbroeck, MD, PhD, of Antwerp University Hospital in Antwerp, Belgium, and colleagues reported.

Endothelial repair mechanisms appeared activated as well in their study of 10 divers, presented here at the European Society of Cardiology's EuroPRevent meeting.
Action Points

Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered to be preliminary until published in a peer-reviewed journal.


Explain that repeat scuba dives appear to harm the endothelium, particularly when breathing the mix of gases known as nitrox that is popular with recreational divers.

Based on the results of this small study, Van Craenenbroeck told MedPage Today that in his opinion the use of regular compressed air was safer for vessels.

Nitrox is popular because its lower nitrogen content allows divers to stay down longer and return to the surface faster with less decompression time needed, she explained.

But in the study, each dive with standard air reduced endothelial function by roughly 2 percentage points from around 5% flow mediated dilation at baseline (P=NS), whereas it dropped roughly 4 percentage points on the initial dive with nitrox and then, without returning to baseline, fell more than 2 percentage points on a subsequent dive two days later (both P<0.05).

"We already knew diving was bad for the endothelium," Van Craenenbroeck told MedPage Today, noting that one prior study suggested that endothelial function didn't return to baseline more than six days after just a single dive.

What effect these repeated dings to blood vessels function and repair mechanisms for frequent divers, such as military and professional divers, have on cardiovascular outcomes isn't known.

"There's no data on it," Van Craenenbroeck cautioned.

But she noted that it might be expected to lead to more atherosclerosis and coronary artery disease.

Still, divers have a choice in the gas mix they use and could attempt to protect their vessels by a preconditioning jog before going down into the water, since this method boosts oxygenation in soccer players and stimulates endothelial progenitor cells in healthy individuals, she suggested.

Her group studied a group of 10 experienced military divers who dove in the open sea with regular compressed air once a day for three days with measurements immediately before and after the dives on day one and three, and then repeated the experiment with nitrox after 15 days of rest.

All the dives were to a depth of 18 m (59 feet) with 47 minutes spent at the bottom. No cases of decompression sickness occurred.

The acute effect of a single dive pooled across the 36 dives was a decrease in endothelial progenitor cells (which differentiate into endothelial cells) circulating in the peripheral blood and an increase in circulating angiogenic cells (which contribute to re-endothelialization by stimulating mature endothelial cells to proliferate).

Together, the two factors seem to indicate an uptick in endothelial repair, the researchers suggested.

But the effects were significant only with nitrox use, they noted.

"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."
 
Can't say as that pleases me much, DonDonaldo, but thanks for posting.

It's consistent with this earlier work that I posted somewhere or another:

“J Physiol. 2005 Aug 1;566(Pt 3):901-6. Epub 2005 Jun 16.

A single air dive reduces arterial endothelial function in man.
Brubakk AO, Duplancic D, Valic Z, Palada I, Obad A, Bakovic D, Wisloff U, Dujic Z.

Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway. alfb@ntnu.no

Abstract

During and after decompression from dives, gas bubbles are regularly observed in the right ventricular outflow tract. A number of studies have documented that these bubbles can lead to endothelial dysfunction in the pulmonary artery but no data exist on the effect of diving on arterial endothelial function. The present study investigated if diving or oxygen breathing would influence endothelial arterial function in man. A total of 21 divers participated in this study. Nine healthy experienced male divers with a mean age of 31 +/- 5 years were compressed in a hyperbaric chamber to 280 kPa at a rate of 100 kPa min(-1) breathing air and remaining at pressure for 80 min. The ascent rate during decompression was 9 kPa min(-1) with a 7 min stop at 130 kPa (US Navy procedure). Another group of five experienced male divers (31 +/- 6 years) breathed 60% oxygen (corresponding to the oxygen tension of air at 280 kPa) for 80 min. Before and after exposure, endothelial function was assessed in both groups as flow-mediated dilatation (FMD) by ultrasound in the brachial artery. The results were compared to data obtained from a group of seven healthy individuals of the same age who had never dived. The dive produced few vascular bubbles, but a significant arterial diameter increase from 4.5 +/- 0.7 to 4.8 +/- 0.8 mm (mean +/- s.d.) and a significant reduction of FMD from 9.2 +/- 6.9 to 5.0 +/- 6.7% were observed as an indication of reduced endothelial function. In the group breathing oxygen, arterial diameter increased significantly from 4.4 +/- 0.3 mm to 4.7 +/- 0.3 mm, while FMD showed an insignificant decrease. Oxygen breathing did not decrease nitroglycerine-induced dilatation significantly. In the normal controls the arterial diameter and FMD were 4.1 +/- 0.4 mm and 7.7 +/- 0.2.8%, respectively. This study shows that diving can lead to acute arterial endothelial dysfunction in man and that oxygen breathing will increase arterial diameter after return to breathing air. Further studies are needed to determine if these mechanisms are involved in tissue injury following diving
 
Since the study was not peer reviewed I am hesitant to put any weight behind it. In other word "as far as I am concerned it is total crap" until the paper is put through the proper quality control measures.

If it does turn out to be good science (doing a press release before publishing is a bad sign) then this could be an issue.
 
Every body reacts in a different way to the same external factors. That's true, for example to Nitrogen narcosis. How ever, decompresion algoritms installed in dive computers consider that every body reacts the same way.
I'm a new diver. Only 62 logged dives. Should I worry with this statement ?
The owner of the dive school where I took my OWD course has 5000+ dives. Is he worried ?
 
Well, extrapolating from short-term effects to long-term effects is fairly risky. For example, hyperoxia creates oxidative stress and affects endothelial function . . . but hyperbaric oxygen is now routinely used to encourage healing in chronic wounds. Sometimes exciting reparative functions leads to long-term BETTER condition. I think the best you can say is that exposure to elevated ppO2s affects endothelial function, and the higher the ppO2, the more effect appears to occur. What the long-term implications are is anybody's guess at this point.

I am not aware of anything indicating a higher incidence of vascular disease in long-term divers. Dysbaric osteonecrosis, yes; coronary artery disease or peripheral vascular disease, no.
 
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Since the study was not peer reviewed I am hesitant to put any weight behind it. In other word "as far as I am concerned it is total crap" until the paper is put through the proper quality control measures. If it does turn out to be good science (doing a press release before publishing is a bad sign) then this could be an issue.

Hi Hashime,

Your statement strikes me as rather not fully considered as well as somewhat mean-spirited.

This isn't identifiable as a "press release." Medical news sites such as MedPageToday, Medscape and kindred media organs often develop an interest in a topic presented at a medical/scientific conference (as is the case with this work; to wit, European Society of Cardiology's EuroPRevent) and do a piece on their own that either precedes or roughly coincides with formal publication of a research study. This in and of itself shouldn't damn a work in any manner.

As well as the study being apparently consistent with the earlier Brubakk, et al abstract I posted above, the primary author, Emeline Van Craenenbroeck, MD, PhD, has a very credible bibliography with numerous publications related to cardiac and cardiovascular topics in recognized, respected, peer-reviewed medical journals. She didn't just crawl out of the scientific woodwork. I have very little doubt but that this work soon will appear in a form acceptable to your exacting "standards."

Regards,

DocVikingo
 
Hi Hashime,

Your statement strikes me as rather not fully considered as well as somewhat mean-spirited.

This isn't identifiable as a "press release." Medical news sites such as MedPageToday, Medscape and kindred media organs often develop an interest in a topic presented at a medical/scientific conference (as is the case with this work; to wit, European Society of Cardiology's EuroPRevent) and do a piece on their own that either precedes or roughly coincides with formal publication of a research study. This in and of itself shouldn't damn a work in any manner.

As well as the study being apparently consistent with the earlier Brubakk, et al abstract I posted above, the primary author, Emeline Van Craenenbroeck, MD, PhD, has a very credible bibliography with numerous publications related to cardiac and cardiovascular topics in recognized, respected, peer-reviewed medical journals. She didn't just crawl out of the scientific woodwork. I have very little doubt but that this work soon will appear in a form acceptable to your exacting "standards."

Regards,

DocVikingo

When the paper does reach my "standards" I will gladly take the information it presents seriously. 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. If a "revolutionary" discovery is found through bad science and released to the public before being properly checked it can have serious consequences even after that research has been proven flawed.
 
Medical News: EuroPRevent: Diving May Damage Blood Vessels - in Meeting Coverage, EuroPRevent from MedPage Today

"Based on the results of this small study, Van Craenenbroeck told MedPage Today that in his opinion the use of regular compressed air was safer for vessels.

Nitrox is popular because its lower nitrogen content allows divers to stay down longer and return to the surface faster with less decompression time needed, she explained.

But in the study, each dive with standard air reduced endothelial function by roughly 2 percentage points from around 5% flow mediated dilation at baseline (P=NS), whereas it dropped roughly 4 percentage points on the initial dive with nitrox and then, without returning to baseline, fell more than 2 percentage points on a subsequent dive two days later (both P<0.05).

"We already knew diving was bad for the endothelium," Van Craenenbroeck told MedPage Today, noting that one prior study suggested that endothelial function didn't return to baseline more than six days after just a single dive."

More: Medical News: EuroPRevent: Diving May Damage Blood Vessels - in Meeting Coverage, EuroPRevent from MedPage Today
 
Interesting. I wouldn't draw too many conclusions yet though. I enjoyed the read and it was well done for what it was. My research brain kicked in though.

Two points:

1. This was a VERY small sample for a CV study. It needs to be repeated with a larger N.

2. This was NOT a representative sample. These were buff military divers.

3. Until such tissue level data is tied to events or lack thereof, it won't have much practical application.

Thanks very much for posting, it was very interesting.
 
Why does the media report science that has yet to be subjected to the peer review process?

Many abstracts are written up with preliminary data just so that scientists can obtain funding to travel to/register for a conference. Abstracts tend to be presented in the form of a multi-panel poster at the conference. Conference participants walk around at various poster sessions and talk to the principal investigators/post docs/grad students about their work. There's a great deal of back-and-forth discussion about the limits/pros/cons of the study. It's a great time to meet interesting people, talk about science, and set up new collaborations. Scientists understand that nothing is considered "for sure" until it's published in a peer-reviewed journal.

lulubelle makes some very good points.
With regard to point #3 asking for tissue level data, the linked article contained this paragraph:
But in the study, each dive with standard air reduced endothelial function by roughly 2 percentage points from around 5% flow mediated dilation at baseline (P=NS), whereas it dropped roughly 4 percentage points on the initial dive with nitrox and then, without returning to baseline, fell more than 2 percentage points on a subsequent dive two days later (both P<0.05).
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.
 
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