Darko Duplančić

A single air dive reduces arterial endothelial function in man

During and after decompression from dives, gas bubbles are regularly observed in the right ventricular outflow tract. A number of studies have documented that these bubbles can lead to endothelial dysfunction in the pulmonary artery but no data exist on the effect of diving on arterial endothelial function. The present study investigated if diving or oxygen breathing would influence endothelial arterial function in man. A total of 21 divers participated in this study. Nine healthy experienced male divers with a mean age of 31 ± 5 years were compressed in a hyperbaric chamber to 280 kPa at a rate of 100 kPa min−1 breathing air and remaining at pressure for 80 min. The ascent rate during decompression was 9 kPa min−1 with a 7 min stop at 130 kPa (US Navy procedure). Another group of five experienced male divers (31 ± 6 years) breathed 60% oxygen (corresponding to the oxygen tension of air at 280 kPa) for 80 min. Before and after exposure, endothelial function was assessed in both groups as flow‐mediated dilatation (FMD) by ultrasound in the brachial artery. The results were compared to data obtained from a group of seven healthy individuals of the same age who had never dived. The dive produced few vascular bubbles, but a significant arterial diameter increase from 4.5 ± 0.7 to 4.8 ± 0.8 mm (mean ±s.d.) and a significant reduction of FMD from 9.2 ± 6.9 to 5.0 ± 6.7% were observed as an indication of reduced endothelial function. In the group breathing oxygen, arterial diameter increased significantly from 4.4 ± 0.3 mm to 4.7 ± 0.3 mm, while FMD showed an insignificant decrease. Oxygen breathing did not decrease nitroglycerine‐induced dilatation significantly. In the normal controls the arterial diameter and FMD were 4.1 ± 0.4 mm and 7.7 ± 0.2.8%, respectively. This study shows that diving can lead to acute arterial endothelial dysfunction in man and that oxygen breathing will increase arterial diameter after return to breathing air. Further studies are needed to determine if these mechanisms are involved in tissue injury following diving.

Aerobic exercise before diving reduces venous gas bubble formation in humans

We have previously shown in a rat model that a single bout of high‐intensity aerobic exercise 20h before a simulated dive reduces bubble formation and after the dive protects from lethal decompression sickness. The present study investigated the importance of these findings in man. Twelve healthy male divers were compressed in a hyperbaric chamber to 280kPa at a rate of 100kPamin−1 breathing air and remaining at pressure for 80min. The ascent rate was 9mmin−1 with a 7min stop at 130kPa. Each diver underwent two randomly assigned simulated dives, with or without preceding exercise. A single interval exercise performed 24h before the dive consisted of treadmill running at 90% of maximum heart rate for 3min, followed by exercise at 50% of maximum heart rate for 2min; this was repeated eight times for a total exercise period of 40min. Venous gas bubbles were monitored with an ultrasonic scanner every 20min for 80min after reaching surface pressure. The study demonstrated that a single bout of strenuous exercise 24h before a dive to 18 m of seawater significantly reduced the average number of bubbles in the pulmonary artery from 0.98 to 0.22 bubbles cm−2(P= 0.006) compared to dives without preceding exercise. The maximum bubble grade was decreased from 3 to 1.5 (P= 0.002) by pre‐dive exercise, thereby increasing safety. This is the first report to indicate that pre‐dive exercise may form the basis for a new way of preventing serious decompression sickness.

The influence of selective vitamin D receptor activator paricalcitol on cardiovascular system and cardiorenal protection

The ubiquitous distribution of vitamin D receptors in the human body is responsible for the pleiotropic effects of vitamin D-receptor activation. We discuss the possible beneficial effects of a selective activator of vitamin D receptor, paricalcitol, on the cardiovascular system in chronic heart failure patients and chronic kidney patients, in light of new trials. Paricalcitol should provide additional clinical benefits over the standard treatment for chronic kidney and heart failure, especially in cases of cardiorenal syndrome.

Influence of haemodialysis on early markers of atherosclerosis

Introduction:  End‐stage renal disease (ESRD) patients treated by haemodialysis (HD) have impaired endothelium‐dependent vasodilatation and increased intima‐media thickness (IMT) of the carotid artery The aim of the study was to analyse the relationships between parameters of chronic HD treatment and non‐invasive assessments of preclinical atherosclerosis (endothelial dysfunction and carotid IMT) in ESRD patients on HD.

Acute application of antioxidants protects against hyperoxia-induced reduction of plasma nitrite concentration.

We investigated the effects of acute intake of antioxidants on hyperoxia‐induced oxidative stress, reduction of plasma nitrite and change in arterial stiffness. Twelve healthy males randomly consumed either placebo or an oral antioxidant cocktail (vitamin C, 1000 mg; vitamin E, 600 IU; alpha‐lipoic acid, 600 mg). Every therapy was consumed once, a week apart, in a cross‐over design, 30 min before the experiment. The volunteers breathed 100% normobaric oxygen between 30th and 60th min of 1‐h study protocol. Plasma levels of nitrite, lipid peroxides (LOOH) and vitamin C, arterial stiffness (indicated by augmentation index, AIx) and arterial oxygen (PtcO2) pressure were measured before and after hyperoxia. Exposure to oxygen caused a similar increase of PtcO2 in both placebo and antioxidants groups, confirming comparable exposure to hyperoxia (438 ± 100 versus 455 ± 83 mm Hg). Vitamin C was increased in the antioxidants group confirming successful application of antioxidants (69 ± 14 versus 57 ± 15 μm). Hyperoxia resulted in increased AIx and LOOH and decreased nitrite in placebo (−32 ± 11 versus −47 ± 13%, 72 ± 7 versus 62 ± 6 μm H2O2 and 758 ± 184 versus 920 ± 191 nm, respectively), but not in the antioxidants group (−42 ± 13 versus −50 ± 13%, 64 ± 9 versus 61 ± 8 μm H2O2 and 847 ± 156 versus 936 ± 201 nm, respectively). The acute intake of selected antioxidants was effective in preserving bioavailabity of ˙NO and vascular function, against hyperoxia‐induced oxidative stress.

2D speckle tracking echocardiography of the right ventricle free wall in SCUBA divers after single open sea dive

The presence of circulating gas bubbles and their influence on pulmonary and right heart hemodynamics was reported after uncomplicated self‐contained underwater breathing apparatus (SCUBA) dive(s). Improvements in cardiac imaging have recently focused great attention on the right ventricle (RV). The aim of our study was to evaluate possible effects of a single air SCUBA dive on RV function using 2D speckle tracking echocardiography in healthy divers after single open sea dive to 18 meters of seawater, followed by bottom stay of 47 minutes with a direct ascent to the surface. Twelve experienced male divers (age 39.5 ± 10.5 years) participated in the study. Echocardiographic assessment of the right ventricular function (free wall 2 D strain, tricuspid annular planes systolic excursion [TAPSE], lateral tricuspid annular peak systolic velocity [RV s`] and fractional area change [FAC]) was performed directly prior to and 30, 60, 90 and 120 minutes after surfacing. Two‐dimensional strain of all three segments of free right ventricular wall showed a significant increase in longitudinal shortening in post‐dive period for maximally 26% (basal), 15.4% (mid) and 16.3% (apical) as well as TAPSE (11.6%), RV FAC (19.2%), RV S` (12.7%) suggesting a rise in systolic function of right heart. Mean pulmonary arterial pressure (mean PAP) increased post‐dive from 13.3 mmHg to maximally 23.5 mmHg (P = .002), indicating increased RV afterload. Our results demonstrated that single dive with significant bubble load lead to increase in systolic function and longitudinal strain of the right heart in parallel with increase in mean PAP.

CASTLEMAN'S DISEASE PRESENTING AS A TUMOROUS PARACARDIAC FORMATION.

Castlemans disease (in the literature also known as angiofollicular hyperplasia) is a rare benign lymphoproliferative disease. Clinically, it can manifest as unicentric or multicentric disease. Unicentric disease is most often diagnosed by accident or by symptomatology resulting from compression upon the adjoining anatomical structures. Considering its lymphatic origin, tumor mass can theoretically occur in any body region. We present a case of paracardiac localization of unicentric Castlemans disease in a previously healthy 24-year-old woman. In such clinical cases, the specific localization of the tumor and its radiological properties can pose a differential diagnostic dilemma. Correct diagnosis is only possible after complete surgical excision and histopathologic analysis, which is the optimal therapeutic approach in this disease.

Castelman’s disease presenting as tumorous paracardial formation

pRIKAz sLUČAJA: Prikazujemo slučaj od ranije zdrave 24-godišnje žene koja se javila na Hitni kirurški prijam Kliničkog bolničkog centra Split zbog protrahiranih bolova u leđima koji su nastali dva dana ranije kada je doživjela prometnu nezgodu. U sklopu dijagnostičke obrade urađena je rendgenska snimka torakalnih organa kojom se postavi sumnja na tumorsku tvorbu prednjeg medijastinuma. Žurna obrada se nadopuni MSCT-om prsišta i transtorakalnom ehokardiografijom koje su ukazale na postojanje moguće pseudoaneurizme lijeve klijetke (slika 1). Daljnjim dijagnostičkim postupcima (MSCT angiografija) odbaci se INTROdUCTION: Castelman’s disease is a rare benign lymphoprolipherative disease. Clinically it can manifest as unicentric or multicentric.