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>From: shelps@ac*.ma*.ad*.ed*.au* (Prime Rat) > >>Prime Rat writes: >>> Blocking of brain arterioles or capillaries by bubbles produced during >>> decompression or directly injected into the arterial circulation is only >>> seen when the heart stops beating, ie (as is well known) after death. If we >>> perform a craniotomy on a rabbit and produce intra-artial bubbling by >>> decompression or direct injection of air into the arterial circulation the >>> bubbles are seen to pass though the arterioles and disappear. They can in >>> fact, be detected in the saggital sinus (using ultrasonic Doppler) exiting >>> the brain vascular bed. Conclusion? Bubbles do not block the capillaries. > >>Can you provide a little more detail here. I'm not clear after >>several readings of this how you conclude that bubbles do not block >>the capillaries. > >They are not seen to. Blood flow is not affected for at least 45 minutes >after the bubbles have been seen to enter the brain circulation. > >>If they don't block the capillaries, what do they block? Why wouldn't > >They block nothing. > Would the following summarise the damage mechanism ? Bubbles appear in the circulatory system and begin to cause platelet agregation around themselves (complement system ?). These bubbles pass into capilliary beds and cause damage to the linings of the capilliaries via the accumulated platelets scraping against them. The bubbles continue to pass through the circulatory system until dissolved and eliminated through the lungs. Meanwhile, the damaged capilliaries in turn collect platelets which actually cause the blockages which are observed to develop. The damage is not seen for an extended period due to the need for many tiny infarcts to occur (as the bubbles circulate through the system) before sufficient damage is done to produce symptoms. (Does this mean that a significant portion of bubbles actually do pass through the lung filter and re-enter the arterial circulation ?) Hence it would be possible for damage to occur after the bubbles are eliminated as the blood clotting process continues. Could one therefore assume that any time there were any "silent bubbles" present, that damage is occuring, but simply is insufficient to produce symptoms ? (sort of akin to cutting a finger versus severing it!) That last thought is kind of scary! On the effects of Hyperbaric treatment: I assume it has two impacts. 1) Reduce the size of bubbles and aid in their elimination on the first treatment. 2) HBO aiding the bodies repair process by improving the supply of oxygen to damaged tissues. I assume therefore that after the initial treatment, there should be no remaining bubbles and that the subsequent treatments are simply aiding the repair of damaged tissue in the same way that HBO can be used for gangrene, etc. Have experimental studies confirmed that there are no bubbles detectable after the initial hyperbaric treatment ? Comments anyone ? I find this discussion very interesting. Regards, David. (Electrical engineer NOT a doctor!) ______________________________________________________________________________ David Giddy, | Voice: +61 3 253 6388 Telstra Corporation, | Fax: +61 3 253 6144 P.O. Box 249, Rosebank MDC, 3169, AUSTRALIA | Internet: d.giddy@tr*.oz*.au* ------------------------------------------------------------------------------
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