Abstract
We suggested that the nanobubbles, which appear at the active hydrophobic spots (AHSs) at the luminal aspect of the blood vessels, are the gas micronuclei from which the decompression bubbles evolve and the endothelial injury during the decompression is due to the tearing off the cell membranes with the detaching bubbles. Ovine blood vessels were stretched over the polycarbonate plates or glass microscopic slides and were exposed under saline to the hyperbaric pressure (1,013 kPa, 19 h). Following decompression, the blood vessels were photographed for the identification (by bubble formation) of the AHS. Nanobubbles could not be demonstrated at the AHS by using the atomic force microscopy (AFM) because of the roughness of the surface, which disabled the close contact of the probe. In the electron microscopy, no endothelial cells were observed in the samples from the area near to the AHS, but the underlying elastin layer of the intima was observed adjacent to the media. Some intact endothelial cells were observed only in the locations far from an AHS. In the optical microscopy, no endothelial cells were observed in the blood vessels in close proximity to the AHS and in some sections, debris or a detached cluster of the endothelial cells were observed. Intact endothelial cells could be found at the sites distant from an AHS. This study supports the assumption, where the detached bubbles tear off the endothelial cells and cause the initial endothelial injury following the decompression.
Highlights
In the search for the hypothesized gas micronuclei from which the bubbles evolve during the decompression after diving, we succeeded in establishing the chain of the events (Arieli, 2017)
We aimed to observe the nanobubbles at the active hydrophobic spots (AHSs)
The main outcome is that the detached bubble at the AHS tears off the entire underlying endothelial layer
Summary
In the search for the hypothesized gas micronuclei from which the bubbles evolve during the decompression after diving, we succeeded in establishing the chain of the events (Arieli, 2017). The lung surfactant such as dipalmitoylphosphatidylcholine (DPPC) leaks into the bloodstream. The DPPC settles on the luminal aspect of the blood vessels to create an oligolamellar lining of the phospholipids (Hills, 1992). We named this site an “active hydrophobic spot” (AHS).
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