You quote a new animal study, where they drove the subjects to death with a direct ascent, found bubbles as expected post-mortem. But adds nothing to any of your points above. (8 ATA, 45 mins, direct ascent).
Do you have any science that properly identifies (or refutes) extra vascular bubble growth, under normal safe decompression condition, that then some how transport themselves to the intra vascular system?
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In an argument from ignorance, you seem to be suggesting that because, at present, there is not technology that can measure extra-vascular bubble formation in the course of a "normal" dive, that it doesn't happen. Since it is approximately the one year anniversary of having this same argument here:
Diving too carefully? - Page 40
I will repost the evidence that existed then, before the paper Simon just cited. None of these are "normal" dives although for the pig study, the profile (45 min O2 pre breathe / 4 atm air / 2 hr / no stop) was not particularly severe as it resulted in VGE grade 1 or less in 2/3rd of the animals
ARTICLES | Journal of Applied Physiology
There is limited evidence, but on the balance of the available evidence, yes, extravascular and venous bubbles are the same thing. The available evidence suggests that bubbles form in the extravascular tissue and then break through the walls of the blood vessels and into the blood.
First of all, we have the photomicrographs of exactly this happening (Bennett,P.B. Fine Structure of decompression sickness. In; Schilling CW, Beckett MW eds. Underwater Physiology VI. Bethesda (MB): FASED, 1978. pp595-9), which has already been cited and the figure reproduced on this thread.
Second, there is considerable evidence that bubbles do not form readily in blood, or inside blood vessels. The key paper, and one that summarizes the earlier evidence, is Lee YC, Wu YC, Gerth WA, Vann RD. Absence of intravascular bubble nucleation in dead rats. Undersea Hyperb Med 1993;20:289-96. In these experiments, dead rats were opened up and the inferior vena cava, a large vein that returns blood to the heart, was exposed. Two ligatures (loops of thread pulled tight to squeeze the vessel closed at each point) were put on the vena cava to isolate a section of this vessel and the blood inside it from the rest of the circulatory system. The rats where then exposed to high hyperbaric air pressure for many hours so that the blood and extravascular tissues take up gas by diffusion (in the same manner as the gel experiments that underlie VPM), and then decompressed. No bubbles form in the sections of vena cava isolated from the rest of the circulatory system. (Several related experiments were performed that demonstrate that the isolated sections of vena cava can produce bubbles if gas nuclei are added, but not in the native blood.) However, bubbles form profusely in the blood-filled sections of vena cava that are outside the ligatures and still connected to the tissue microcirculation. The tissue microcirculation is comprised of the small blood vessels (principally capillaries) that are inside, and considered part of, the tissue. So the bubbles come from the tissue. One possible location of the bubble formation is inside the tissue microcirculation, but that requires the assumption that the environment inside tissue microcirculation is different to that inside the large veins. Occam's Razor (which has also already been invoked on this thread) leads to the conclusion with fewer assumptions, favoured by the authors, that the bubbles form in the extravascular tissue, and rupture into the microcirculation.
In summary, the available evidence in the scientific literature suggests intravascular bubbles arise in the extravascular part of the tissue - they are the same thing. However, it is plausible that bubbles do form inside, and at the venous end of, the tissue microcirculation, and one day evidence may arise to support this possibility (we do see gas bubbles inside the microcirculation, and such a picture has been posted on this thread, but it is not clear if the bubbles formed there or migrated in from the tissue). However, as has been pointed out on several occasions, if bubbles do form inside the tissue microcirculation, they form in response to the same tissue supersaturation that exists less than a bubble diameter away on the other side of the blood vessel walls. Most decompression models / algorithms have compartments as their basic structure. These compartments represent the extravascular tissue and the blood in the microcirculation, precisely because over the time course of processes relevant to decompression, there are not important gradients of gas partial pressures across the regions represented by a compartment. Thus, if bubbles form separately in the extravascular and intravascular parts of the tissue, their dynamics will be closely linked - perhaps not identical, because of different physical properties of the blood and extravascular tissue, but linked. For instance, there are probably more nucleation sites in extravascular tissue than in blood, and therefore more bubbles might form in extravascular tissue than in blood, but the dynamics will be linked. Evidence for this linkage is provided by a paper already cited on this thread (Swan JG, Wilbur JC, Moodie KL, Kane SA, Knaus DA, Phillips SD et al. Microbubbles are detected prior to larger bubbles following decompression. J Appl Physiol 2014;116:790-6) These authors used a dual-frequency ultrasound (DFU) technique that can be tuned to detect bubbles of particular size (1-4 microns in this study), is capable of detecting smaller bubbles than those detected by the B-mode ultrasound used to detect VGE, and can be used to detect bubbles both in the blood and in extravascular tissues. This paper showed that, in pigs, following decompression from hyperbaric air exposures, the number of DFU-detected microbubbles of a particular size rises and then falls before larger VGE are detected. A reasonable interpretation is that the DFU-detected microbubbles are the precursors of the B-mode-detectable VGE - i.e. the number of DFU-detected microbubbles decreases as they grow (by diffusion and coalescence) larger than the size for which the DFU is tuned to detect, eventually getting large enough to be detected by B-mode ultrasound. Importantly, the authors made simultaneous DFU measurements inside veins and in extravascular tissue, and the dynamics of the intravascular and extravascular microbubbles were the same - i.e. the number of DFU-detected microbubbles in the extravascular part of the tissue and in the venous blood rise and fall at the same time - demonstrating a linkage between the magnitude and time course of extravascular and intravascular bubble formation.
I doubt there is a single scientist working in the area of decompression research who does not believe that the sizes and profusions of intravascular and extravascular bubbles are proportional, and that a decompression procedure that results in many VGE also results in many extravascular bubbles.
David Doolette
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