Successive deep dives impair endothelial function and enhance oxidative stress in man

Abstract

The aim of this study was to assess the effects of successive deep dives on endothelial function of large conduit arteries and plasma pro-oxidant and antioxidant activity. Seven experienced divers performed six dives in six consecutive days using a compressed mixture of oxygen, helium and nitrogen (trimix) with diving depths ranging from 55 to 80 m. Before and after first, third and sixth dive, venous gas emboli formation and brachial artery function (flow-mediated dilation, FMD) was assessed by ultrasound. In addition, plasma antioxidant capacity (AOC) was measured by ferric reducing antioxidant power, and the level of oxidative stress was assessed by thiobarbituric acid-reactive substances (TBARS) method. Although the FMD was reduced to a similar extent after each dive, the comparison of predive FMD showed a reduction from 8.6% recorded before the first dive to 6.3% before the third (P = 0.03) and 5.7% before the sixth dive (P = 0.003). A gradual shift in baseline was also detected with TBARS assay, with malondialdehyde values increasing from 0.10 ± 0.02 μmol l⁻¹ before the first dive to 0.16 ± 0.03 before the sixth (P = 0.005). Predive plasma AOC values also showed a decreasing trend from 0.67 ± 0.20 mmol l⁻¹ trolox equivalents (first day) to 0.56 ± 0.12 (sixth day), although statistical significance was not reached (P = 0.08). This is the first documentation of acute endothelial dysfunction in the large conduit arteries occurring after successive deep trimix dives. Both endothelial function and plasma pro-oxidant and antioxidant activity did not return to baseline during the course of repetitive dives, indicating possible cumulative and longer lasting detrimental effects.

Reactive Oxygen Species, Mitochondria, and Endothelial Cell Death during In Vitro Simulated Dives

“…Therefore, the disorder of mitochondrial membrane physiology forms a constant feature of apoptosis induction, marking an early and irreversible step of commitment to cell death, which is also confirmed in this study. These observations are coherent with the decreased vasodilation observed after SCUBA diving (3,14,19,22) and with the postdive release of endothelial MP (7,31).…”

“…The apparently modulating relationship between oxygen partial pressure and hydrostatic pressure remains nonetheless particularly interesting. These new perspectives are in accordance with the results of human studies on diving physiology, for example, oxidative stress-induced acute endothelial dysfunction in large conduit arteries after successive deep human dives (22) or ROS-mediated decrease of FMD after breath-hold dives (30). By a novel experimental procedure, this study allowed differentiating the effects of hydrostatic pressure and individual gas partial pressures, showing that nitrogen has no effect on the function or activity of arterial endothelial cells within the range of recreational diving.…”

“…A common research approach in the physiopathology of DCS is based on the endothelial dysfunction hypothesis, which states that diving induces an alteration of endothelial cell activity, which could be a causative factor for DCS (17). In support to this, decreased vasodilation is well documented to occur in conductance arteries after diving (3,14,19,22).…”

“…These effects are linked to reactive oxygen species (ROS) since acute and long-term predive supplementation of antioxidants has been shown to protect against abnormal reduction of vascular endothelial function in humans after air dives (22)(23)(24). Furthermore, the bioavailability of nitric oxide (NO), an endothelium-derived relaxing factor, and the activity of NO synthase (NOS) are decisively determined by ROS such as superoxide, which rapidly reacts with NO to form the highly reactive intermediate peroxynitrite (10).…”

Could there be an association between chronic brucellosis and endothelial damage?

“…This inflammatory response, as well as the immunological reactions that develop against the Brucella antigens in the vessel wall, are responsible for the pathogenesis of the damage that results in the vascular system [5]. The dysfunction observed in the endothelial system is one of the first changes that occur in the pathogenesis of cardiovascular diseases, and is encountered in various clinical conditions [6]. The measurement technique of flow-mediated dilatation (FMD) has been developed in the last decade to assess the endothelium-dependent function of the vascular system following an occlusion in the brachial artery.…”