Utjecaj ronjenja na komprimirani zrak i primjene vitamina C i E na izabrane funkcije ljudskog srca i endotelnu funkciju nadlaktične arterije

Abstract

After decompression from dives, bubbles are frequently observed in the right ventricular outflow tract and may lead to vascular damage, pulmonary arterial hypertension and right ventricular overload. No data exist on the effect of open sea diving on the pulmonary artery pressure (PAP). Eight professional divers performed an open sea air dive to 30 msw. Before and postdive a Doppler echocardiographic study was undertaken. Systolic pulmonary artery pressure (SPAP) was estimated from measurement of peak flow velocity of the tricuspid regurgitant jet; the ratio between pulmonary artery acceleration times (AccT) and right ventricular ejection time (RVET) was used as an estimate of the mean PAP. No evidence of either patent foramen ovale or intra-pulmonary shunt was found in any subject postdive after performing a Valsalva maneuver. SPAP increased from 2 ±3 to 33±2 mm Hg and AccT/ RVET ratio decreased from 0.44±0.04 to 0.3±0.02 20 min after the dive, respectively. Pulmonary vascular resistance increased from 1.2 ±0.1 to 1.4±0.1 Wood Units. Postdive right ventricle end-diastolic and endsystolic volumes were increased for about 19% (P = 0.001) and 33% (P = 0.001) and right ejection fraction decreased about for 6% (P = 0.001). Cardiac output decreased from 4.8±0.9 (l min1) to 4.0 ± 0.6 at 40 min postdive due to decreases in heart rate and stroke volume. This study shows that a single open sea dive may be associated with right heart overload due to increased pressure in the pulmonary artery. 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 fi eld dive.Vitamin C (2 grams) and E (400 IU) were given to subjects 2 hours before second dive (protocol 1) and in placebo-controlled crossover study design (protocol 2). Seven experienced divers performed open sea dives to 30 msw with standard decompression in non randomized protocol, and six of them participated in 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 fl ow mediated dilation (FMD) and heart function with increased mean PAP. 24 hours (h) after the control dive FMD was still reduced 37% (8.1 vs. 5.1%, p=0.005 below baseline, 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 endsystolic volume was increased by 9% and mean PAP by 5%. Acute antioxidants significantly attenuated only the reduction in FMD postdive (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 72h after the dive with pre-dive placebo, whereas for most cardiovascular parameters this occurred earlier (24-48h). 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.We have recently shown that a single air dive leads to acute arterial vasodilatation and impairment of endothelium-dependent vasodilatation in humans. Additionally we have found that predive antioxidants at the upper recommended daily allowance partially prevented some of the negative effects of the dive. in this study we prospectively evaluated the effect of long-term antioxidants at a lower RDA dose on arterial endothelial function. Methods: Eight professional male divers performed an open sea air dive to 30 msw. Brachial artery fl ow-mediated dilation (FMD) was assessed before and after diving. Results: The first dive, without antioxidants, caused significant brachial arterial diameter increase from 3.85±0.55 to 4.04±0.5 mm and a significant reduction of FMD from 7.6±2.7 to 2.8±2.1%. The second dive, with antioxidants, showed unchanged arterial diameter and significant reduction of FMD from 8.11±2.4 to 6.8±1.4%. The FMD reduction was significantly less with antioxidants. Vascular smooth muscle function, assessed by nitroglycerine(endothelium-independent dilation), was unaffected by diving. ----- Discussion: This study shows that long-term antioxidant treatment at a lower RDA dose ending 3–4 h before a dive reduces the endothelial dysfunction in divers. Since the scuba dive was of a similar depth and duration to those practiced by numerous recreational divers, this study raises the possibility of routine predive supplementation with antioxidants. We report a case of a diver that developed in tra-pulmonary (I-P) shunting of venous gas bubbles at high level of exercise after diving. The diagnosis was made with a four chamber view of the heart by echocardiography during exercise. This case is the first time that we have observed an evidence for I-P shunts recruitment during exercise after diving and this bubble grade was the highest ever seen in our laboratory. Thus, the risk for venous bubbles crossing over through I-P shunts during exercise after diving is rather low