Role of haematological testing: ratio values of circulating platelet aggregates in visual field loss associated with pseudoexfoliation glaucoma.

The aim of the work is to examine the role of circulating platelet aggregates (CPAs) in association with pseudoexfoliation glaucoma (PXG) and searching for visual field (VF) progression. The impact of CPAs in association with PXG and ischaemic events related to optic nerve damage and VF progression has not been so far sufficiently explained. The examination included 80 patients, of whom 35 (44 %) were men with average age of 68.3 +/- 7.0 and 45 (56 %) were women with average age of 65.7 +/- 7.0 (t = 1.66; p = 0.101). Forty of them suffered from primary open-angle glaucoma (POAG) and were included into a control (healthy) group, and 40 patients suffered from pseudoexfoliative glaucoma (PXG) and were included into the experimental group. All the examinees underwent complete ophthalmologic examination of visual acuity, ocular fundus, intraocular pressure and anterior eye segment by biomicroscopy and gonioscopy. In addition, VF examination was performed three times in six-month intervals. Laboratory testing of CPA proportion values was performed by means of Wu an Hoak method. The obtained decreased values of CPA proportion were caused by hypercoagulability of blood in PXG group resulting finally in ischaemia and hypoxia helping the progression of visual field. In conclusion, our study shows that CPA examination improves the assessment of the vascular role and PXG prognosis (Tab. 3, Ref. 30).

Diving-induced venous gas emboli do not increase pulmonary artery pressure.

Venous gas emboli are frequently observed in divers even if proper decompression procedures are followed. This study was initiated to determine if pulmonary artery pressure increases in asymptomatic divers, which could increase the risk of arterial embolization due to passage of venous gas emboli from the right to the left side of the heart. Recordings of venous gas emboli and estimation of pulmonary artery pressure by non-invasive transthoracic echocardiography were applied in 10 recreational scuba diving volunteers before and 20, 40, 60, and 80 min after simulated dives to 18 m (80 min bottom time) in a hyperbaric chamber. The ratio between pulmonary artery acceleration time and right ventricular ejection time was used as an estimate of pulmonary artery pressure. None of investigated divers had signs of decompression sickness. Despite the post-dive presence of the venous gas emboli, measured in the region of the pulmonary valve annulus (mean=1.71 bubbles.cm-2, 40 min after dive), the ratio between pulmonary artery acceleration time and right ventricular ejection time did not decrease, but actually increased (from 0.43+/-0.06 to 0.49+/-0.06, 40 min after dive; p<0.05), suggesting a decrease in pulmonary artery pressure after the dive. We conclude that diving-induced venous gas bubbles do not cause significant changes in the central circulation which could increase the risk of arterial embolization.

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.