Vascular dysfunction following breath-hold diving

Abstract

The pathogenesis of predominantly neurological decompression sickness (DCS) is multifactorial. In SCUBA diving, besides gas bubbles, DCS has been linked to microparticle release, impaired endothelial function, and platelet activation. This study focused on vascular damage and its potential role in the genesis of DCS in breath-hold diving. Eleven breath-hold divers participated in a field study comprising eight deep breath-hold dives with short surface periods and repetitive breath-hold dives lasting for 6 h. Endothelium-dependent vasodilation of the brachial artery, via flow-mediated dilation (FMD), and the number of microparticles (MPs) were assessed before and after each protocol. All measures were analyzed by two-way within-subject ANOVA (2 × 2 ANOVA; factors: time and protocol). Absolute FMD was reduced following both diving protocols (p < 0.001), with no interaction (p = 0.288) or main effect of protocol (p = 0.151). There was a significant difference in the total number of circulating MPs between protocols (p = 0.007), where both increased post-dive (p = 0.012). The number of CD31+/CD41– and CD66b+ MP subtypes, although different between protocols (p < 0.001), also increased by 41.0% ± 56.6% (p = 0.050) and 60.0% ± 53.2% (p = 0.045) following deep and repetitive breath-hold dives, respectively. Both deep and repetitive breath-hold diving lead to endothelial dysfunction that may play an important role in the genesis of neurological DCS.

Decompression Illness in Repetitive Breath-Hold Diving: Why Ischemic Lesions Involve the Brain?

“…The diver's BMI was 24, which is similar to Ama divers' (Lemaître et al, 2014). In another recent echocardiography study, Barak et al (2020) recorded the "lowest" venous bubbles in six out of 11 BH divers for 15 min after dives at rest or after provocation. Interestingly, the results were similar after eight dives to 35 m for 1 h and after 6 h of competitive dives to depths between 15 and 40 m.…”

“…The neuroimaging studies show considerably large ischemic lesions in the external watershed areas and the territories of perforating arteries, a pattern seen in embolic brain injuries. However, VGEs after BH diving are detected rarely and in small quantities (Spencer and Okino, 1972;Lemaître et al, 2014;Barak et al, 2020). Thus, we believe that VGE need not be detectable to initiate processes resulting in cerebral ischemic lesions.…”

“…Gas embolization alone may not be sufficient to cause DCI. Repeated bubble insults and involvement of other processes may be necessary (Thalmann, 2003;Balestra et al, 2019;Barak et al, 2020).…”

“…In compressed-air diving, other factors like vascular dysfunction, microparticles, and neutrophil activation have been identified as potential contributors (Thom et al, 2015). Recently, Barak et al (2020) have also described in BH diving that microparticles play an essential role in endothelial dysfunction of the brain. Although, the circulating microparticles could induce cerebral small vessel disease, the microparticle theory may not completely explain the differences in clinical characteristics of DCI between compressed-air and BH diving, nor the number and location of the large cerebral lesions.…”

“…However, clinical presentation and imaging in BHDND is different. Endothelial dysfunction has been observed after BH diving (Nossum et al, 2002;Theunissen et al, 2013;Barak et al, 2020), which may stimulate aggregation of blood components and form thrombi in vessels (Francis and Mitchell, 2003). However, acute neuroradiological findings in BHDND indicate the absence of multiple small cortical infarcts (Kohshi et al, 1998(Kohshi et al, , 2000(Kohshi et al, , 2020Tamaki et al, 2010b;Matsuo et al, 2012), which suggest a typical shower of thrombotic emboli (Wityk et al, 2001).…”