cerebral DCS, an inflammatory reaction?

[anton115]

Hi Dr Deco,

There is much literature that suggests that cerebral DCS is a consequence of venous bubbles shunting into the arterial system and embolising in the brain. some article then suggest that the bubbles then block the arterioles and capillary bed resulting in ischemia and this causes the deterioration seen in DCS muck like a stroke. I have however not found any evidence to suggest that bubbles would lodge in the capillaries rather than just pass through them. There are other articles that suggest that the bubbles pass through but damage the endothelium resulting in an inflammatory response that causes the deterioration seen in DCS. I was wondering what your thoughts were on the matter and if there was any evidence that bubble do get stuck in the vasculature for any period of time?If so I was wondering why the bubbles get stuck and are not able to deform and pass through the vasculature?


Many Thanks
Anton

 

[Dr Deco]

Hello anton115:

“Sticky” Capillary Bubbles

The earliest evidence of which I am aware for bubbles sticking in the capillaries [of muscle,anyway] is from my work using ultrasound and decompressed rats.

[MRPowell. Leg pain and gas bubbles in the rat following decompression from pressure: monitoring by ultrasound: Aerospace Med., 43, 168-172 (1972); ​

I found that a persistent signal decrease [from gas bubbles in muscle capillaries] came after bubbles were found in the arterial system. [These bubbles came from arterialization of venous bubbles.] It seemed that only a small number of bubbles would not stick and produce this blockage of the U/S signal. A large number were required for blockade.


Brain Bubbles

In a later study using implanted Doppler U/S probes, Dr Merrill Spencer and I found that bubbles in the venous system could overload the lung capillary filter and enter the arterial system. These bubbles could first be found in the carotid artery [a large artery to the brain] and within a few seconds, they could be heard with a U/S probe over the sagittal sinus [a large vein draining the brain].

MRPowell and MP Spencer. The Pathophysiology of Decompression Sickness and Doppler-detectable Gas Bubbles. Final Technical Report, O.N.R., Contract #N00014-73-C-0094, (1980).​

It appears that gas bubbles do not necessarily lodge in the capillaries of the brain when only a few are present. How many are “a few” is not known. Dr. Des Gorman in Australia performed studies examining the brain capillaries with a microscope.

Gorman,D. F. and D. M. Browning (1986). Cerebral vasoreactivity and arterial gas embolism. Undersea Biomed. Res., 13,(3), 317;
Gorman,D. F.; D. M. Browning and D. W. Parsons (1987). Redistribution of cerebral gas emboli: a comparison of treatment regimens. In: Proceedings of the Ninth Symposium on Underwater Physiology,Bethesda, MD.] ​

Blockage depended on the number of bubbles. In very small vessels [50 to 200 microns; actually bigger than a capillary] gas bubbles would always block if the gas embolus was longer than 5,000 microns in the vessel. Between 500 < Vessel Length < 5000 microns, bubbles would often pass within three minutes. Smaller emboli volumes would always pass. Therefore, some bubbles in the brain&#8217;s arterial system will not always produce adverse clinical effects.

Stickiness migh tbe related to some micro biological effect, also. Possibly the lining of the capillary is different in different individuals, and bubble-vessel adhesion might be thus affected.

One group hypothesized that the adhesion force leading to bubble arrest within the microvasculature results from interactions between blood-borne macromolecules adsorbed to the bubble surface and the vessel endothelial surface. Proteins are known to adsorb to gas-liquid interfaces.

Suzuki A, Eckmann DM. Embolism bubble adhesion force in excised perfused microvessels. Anesthesiology. 2003 Aug; 99(2):400-8​

Gas bubbles provide interfacial surface area for adsorption of circulating molecules. Biomacromolecules present in blood can bind to gas-liquid interfaces through hydrophobic [water-repelling] interactions. The specificity of this process is currently poorly understood. Adsorbed protein surface layers have mechanical implications for direct surface-surface adhesion interactions within the vasculature. The pressure for the breakaway of the bubble and the surface [vessel wall] is called the disjunction pressure and is a function of electrostatic and Van der Waals forces. This is complicated with many variables, all of which can vary from diver to diver.

There is a good possibility that damage occurs to the endothelium of the capillary wall. Bubble adhesion might be influence by this damage so that bubbles arriving later become lodged more easily - creating a very bad day for the diver.

Dr Deco :doctor:

 

[anton115]

thanks for you reply. It was very interesting. I had thought that the vascular bubbles produced on decompression were significantly smaller in volume than the volume required to fill an arteriole 50 micros in diameter for a length of 500 microns. Is this the case?
Thanks Anton