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Schirato et al. | Journal of Clinical and Translational Research 2024; 10(5): 269-282 277
Table 5. MPO and microparticle levels for the deep decompression speculated that such reduction was due to platelet activation
profile and aggregation.
Parameter Pre‑dive Post‑dive P Activated platelets release MPs (CD41 + MPs) that are involved
MPO+ (%) 2.448±0.830 2.549±0.888 0.758 in intercellular (endogenous) signaling by inducing immune
MPO (MFI) 576.796±171.399 526.565±137.525 0.472 responses in distant sites [44]. In vitro studies revealed that CD41
CD66b+ 0.28±0.07 0.27±0.06 0.207 + MPs facilitate leukocyte–leukocyte interactions and the binding
CD31+ 0.06±0.03 0.17±0.08 0.022 of P-selectin/P-selectin glycoprotein ligand-1 [45], increasing
CD41+ 24.50±5.64 35.80±4.92 0.027 leukocyte accumulation at injury sites and on activated
Note: Data are presented as mean±standard error. endothelium. In addition, platelet shedding of MPs positively
Abbreviation: MFI: Mean fluorescence intensity; MPO: Myeloperoxidase. correlates with increased vascular permeability [46]. The
results obtained in this study suggest an increase in circulating
Table 6. MPO and microparticle levels for the shallow decompression CD41+ MPs after decompression in the deep decompression
profile profile, which aligns with the observed reduction in circulating
Parameter Pre‑dive Post‑dive P platelets. This is likely due to platelet activation and recruitment
MPO+ (%) 2.61±1.17 2.32±1.16 0.15 to inflammation sites. The release of platelet, endothelial, and
MPO (MFI) 314.95±31.93 291.05±28.29 0.07 leukocyte MPs is increased during inflammatory conditions [13].
CD66b+ 0.21±0.04 0.40±0.12 0.000 Oxidative stress is known to induce the release of CD31+ MPs,
CD31+ 0.35±0.21 0.16±0.08 0.199 which attract leukocytes to the inflammatory site by adhesion
CD41+ 49.80±6.80 53.46±6.96 0.186 molecules, such as vascular cell adhesion molecule-1, a key
Note: Data are presented as mean±standard error. factor endothelial dysfunction [28,37].
Abbreviation: MFI: Mean fluorescence intensity; MPO: Myeloperoxidase. Our results demonstrated a post-dive increase in platelet- and
endothelial-derived MPs (CD41+ and CD31+ MPs, respectively)
in the deep decompression profile (Figure 9). Similarly, the
shallow decompression profile displayed a marked increase in
neutrophil-derived MPs (Figure 9).
A decrease in red blood cells and hemoglobin was observed in
the deep decompression profile (Figures 4 and 5, respectively),
likely due to eryptosis [47,48], a form of programmed cell death
in erythrocytes. Eryptosis, triggered by oxidative stress, involves
the activation of caspases expressed by erythrocytes, resulting
in their recognition and engulfment by circulating macrophages.
Since erythrocyte membranes are highly vulnerable to
oxidative damage and cannot repair damaged proteins by re-
synthesis, they are particularly sensitive to oxidative stress [49].
Eryptosis of young red blood cells is often reported in subjects
returning from high altitudes or space flights [47], and its
putative mechanism is related to changes in the erythropoietin
Figure 10. Clusters identified by the clustering algorithm. Cluster 1: sensitivity of the cells. Therefore, the observed change in red
Shallow decompression profile; Cluster 2: Deep decompression profile blood cell and hemoglobin counts might be related to a stressful
decompression profile.
was observed in the deep decompression profile. Platelets The shallow and deep decompression profiles can also be
are regarded as effectors of hemostasis, essential for vascular distinguished by indicators of immune system activation and
integrity [38,39]. Recent understanding has clarified that inflammation. The shallow decompression profile increases
they are key effectors in inflammation, immune responses, peripheral blood neutrophil count and its corresponding MPs,
and signaling, with the potential to orchestrate complex without affecting platelet count and its MPs, as well as in
endothelial MPs. Conversely, the deep decompression profile
immune and inflammatory events [39,40]. Three different exhibited an increase in the platelet- and endothelial-derived
studies by the same research team investigated platelet MPs and a decrease in platelet count, with no variations in
count and its association with decompression sickness in neutrophil count and its MPs.
mice models and with bubble formation in humans [41-43]. Neutrophils are widely recognized for their role in promoting
Their results indicate that higher bubble counts in humans inflammatory responses at the initial stages of these processes.
correlate with a greater reduction in platelet count, even in Increased neutrophil count is associated with various pathologies
the absence of decompression sickness after decompression. (e.g., bacterial infections, hypertension, and certain types of
Conversely, in mice suffering from decompression sickness cancer [50-54]) and non-pathological conditions (e.g., after
after provocative decompression, a regression model linked exercising) [55]. Their activation might also promote platelet
platelet reduction to symptom severity. In both cases, they activation [13,44] and even endothelial damage [13,56], then

DOI: https://doi.org/10.36922/jctr.24.00021