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Diving-induced acute alterations in cardiovascular function such as arterial endothelial dysfunction, increased pulmonary artery pressure (PAP) and reduced heart function have been recently reported. We tested the effects of acute antioxidants on arterial endothelial function, PAP and heart function before and after a field dive. Vitamins C (2 g) and E (400 IU) were given to subjects 2 h before a second dive (protocol 1) and in a placebo-controlled crossover study design (protocol 2). Seven experienced divers performed open sea dives to 30 msw with standard decompression in a non-randomized protocol, and six of them participated in a randomized trial. Before and after the dives ventricular volumes and function and pulmonary and brachial artery function were assessed by ultrasound. The control dive resulted in a significant reduction in flow-mediated dilatation (FMD) and heart function with increased mean PAP. Twenty-four hours after the control dive FMD was still reduced 37% below baseline (8.1 versus 5.1%, P= 0.005), while right ventricle ejection fraction (RV-EF), left ventricle EF and endocardial fractional shortening were reduced much less (∼2–3%). At the same time RV end-systolic volume was increased by 9% and mean PAP by 5%. Acute antioxidants significantly attenuated only the reduction in FMD post-dive (P < 0.001), while changes in pulmonary artery and heart function were unaffected by antioxidant ingestion. These findings were confirmed by repeating the experiments in a randomized study design. FMD returned to baseline values 72 h after the dive with pre-dive placebo, whereas for most cardiovascular parameters this occurred earlier (24–48 h). Right ventricular dysfunction and increased PAP lasted longer. Acute antioxidants attenuated arterial endothelial dysfunction after diving, while reduction in heart and pulmonary artery function were unchanged. Cardiovascular changes after diving are not fully reversed up to 3 days after a dive, suggesting longer lasting negative effects.
Recreational diving has become one of the most frequently performed types of outdoor sport activities, with millions of recreational divers worldwide. During dives with compressed air the divers are exposed to various environmental stresses that may affect haemodynamics and cardiovascular function, such as immersion-induced increase in preload, cold-induced increase in afterload, reduced filling of the left heart due to ventilation of high-density gas mixtures, hyperoxia, formation of intravascular nitrogen bubbles, exercise and psychological stress. We have shown that simulated chamber diving results in acute arterial endothelial dysfunction (Brubakk et al. 2005) and unchanged pressure in the pulmonary artery (PAP) (Valic et al. 2005), while field scuba diving is associated with increased PAP (Dujic et al. 2006a) and endothelial dysfunction (Obad et al. 2006). Four weeks of oral antioxidant supplementation with vitamins C (1 g day−1) and E (400 IU day−1) reversed acute endothelial dysfunction after diving (Obad et al. 2006). Reduction in endothelial function post-dive may also be present in the heart, as a reduction in endothelial function is an important factor in heart failure (Landmesser & Drexler, 2005). Immersion leads to an increase in thoracic blood volume, and 180–240 ml of blood is added to the heart volume with enlargement of all four chambers (Risch et al. 1978). Stroke volume is increased by about 50% after upright immersion to the neck in healthy individuals (Meyer & Bucking, 2004). This leads to an increase in right ventricular dimensions and to an increase in PAP to a degree that in some cases even can lead to pulmonary artery oedema (Pons et al. 1995). Thus, it is conceivable that immersion and hyperoxia, with the addition of gas bubble formation caused by decompression, can reduce systemic conduit as well as pulmonary artery function and cardiac endothelial–myocardial coupling, which would account for the observations.
Oxidative stress in the vessel wall and endocardium is associated with the generation of reactive oxygen and nitrogen species (ROS and RNS) by activities of several oxidases, like nitric oxide synthase (NOS), NOx oxidases, NADPH oxidases, xanthine oxidase, cytochrome-450 and cyclooxygenase, and of mitochondria (Wolin et al. 2005). The superoxide anion was shown to quench NO (Rubanyi & Vanhoutte, 1986), but it will also react with NO to generate peroxynitrate, which causes additional oxidative stress due to activation of oxidases and inactivation of antioxidant enzymes (Wolin et al. 2005). Reduction of local NO by ROS causes hyperoxic vasoconstriction and impairs NO-dependent vasodilatation (Milone et al. 1999; Zhilyaev et al. 2003). Oxidative stress has been recently implicated in different cardiovascular pathologies such as atherosclerosis (Schulz et al. 2004), hypertension (de Champlain et al. 2004), diabetes (Gonzalez-Vilchez et al. 2005), atrial fibrillation (Dudley et al. 2005) and ischaemia–reperfusion injury (Seccombe & Schaff, 1995). A variety of antioxidants, including vitamins C and E, have been shown to have a protective effect on the pulmonary endothelial function after cardiopulmonary bypass (Angdin et al. 2003), but also offer general endothelial protection (Pratico, 2005).
Thus, in the present study we wanted to determine whether acute oral antioxidants can attenuate the negative effects of diving on the function of the heart and the pulmonary and brachial artery in men performing standard dives.