RESUMEN
INTRODUCTION: Diving, hyperbaric oxygen, and decompression have been described as inducers of alterations in various components of the human immune system, such as the distribution of circulating lymphocytes. Hypothetically, the monitoring of specific lymphocyte subsets during hyperbaric exposure, including T- and NK-cell subsets, can serve as biomarkers of hyperbaric stress. METHODS: Eight experienced saturation divers and eight reference subjects, naive to deep saturation diving, were examined. Peripheral blood mononuclear cells were isolated before and at different points during a 19.3-d dry heliox saturation dive to 2.64 MPa (254 msw). The NK cell cytotoxicity was estimated in a 4-h 51Cr-release assay using the NK cell sensitive tumor cell-line K562 as target cells. The major lymphocyte subpopulations, with special emphasis on the NK cell subsets, were phenotypically delineated by the use of 4-color flow cytometry. RESULTS: Although NK cell cytotoxicity increased significantly in the divers during the compression phase and the reference subjects who remained in normoxic conditions outside the chamber, the NK cell cytotoxicity was significantly higher in the divers. DISCUSSION: This finding, together with augmentation in the absolute number of circulating NK cells in the divers due to a possible activation of specific parts of the innate cellular immune system during hyperbaric exposure, suggests the monitoring of specific immune functions can be useful as biomarkers of hyperbaric-induced inflammatory stress.
Asunto(s)
Barotrauma/inmunología , Buceo/efectos adversos , Células Asesinas Naturales/metabolismo , Subgrupos Linfocitarios/metabolismo , Adulto , Biomarcadores , Citometría de Flujo , Helio , Humanos , Modelos Lineales , Masculino , Análisis Multivariante , OxígenoRESUMEN
INTRODUCTION: Saturation diving involves exposure to high pressure and elevated oxygen level. The impact of cellular defense systems like glutathione in protecting cells against oxidative DNA damage seems unclear. The aim of the present study was, therefore, to investigate whether diving conditions would affect blood cell glutathione and thus alter the mononuclear cells' (MNC) susceptibility to oxidative DNA damage. METHODS: Eight subjects participated in a simulated saturation dive to 2.6 MPa (250 msw) lasting 19.3 d (0.8 d compression, 6.6 d bottom phase, 11.9 d decompression) breathing helium-oxygen with PO2 ranging from 35 to 70 kPa (3.5-7.0 msw). Blood samples collected before compression and after decompression were analyzed for glutathione content and single-stranded DNA breaks. RESULTS: The results demonstrate for the first time that a simulated saturation dive decreased glutathione content in peripheral blood cells (32% decrease in MNC), and that the decrease was most pronounced in the erythrocytes (45%). Remarkably, no single-stranded DNA breaks could be detected in the MNC despite the low glutathione level. DISCUSSION: The results suggest that glutathione is a useful indicator of oxidative stress and that a low glutathione level represents no significant harm to the blood cells in the absence of other toxic agents. The lack of DNA strand breaks suggests that protection against oxidative DNA damage was mainly provided by mechanisms other than the glutathione system. Although previous investigations point to hyperoxia as the most plausible explanation for the present observations, the effect of high pressure cannot be excluded.
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Biomarcadores/sangre , Daño del ADN , Buceo/fisiología , Glutatión/sangre , Estrés Oxidativo/fisiología , Adulto , Análisis de Varianza , Descompresión , Humanos , Masculino , Persona de Mediana Edad , Estadísticas no ParamétricasRESUMEN
A reduction in haemoglobin concentration is consistently reported after deep saturation dives. This may be due to a downregulation of erythropoietin (EPO) concentration or to a toxic effect of the hyperoxia associated with the dives resulting in an increased destruction rate of erythrocytes. In this study haemoglobin concentration, blood cell counts, serum ferritin, bilirubin, haptoglobin and EPO concentrations were measured before, during and after a 19 day saturation dive to 240 m. The partial pressure of oxygen (PO(2)) was 35-70 kPa during the 7 day compression and bottom phase, and 30-50 kPa during the 12 day decompression phase. There was a reduction in EPO concentration from 8.4+/-1.4 (mean +/- 1SD) to 6.3 +/- 1.9 U.L(-1) on Dive day 2. On Dive days 7 and 17 EPO concentrations were not significantly different from baseline despite the continued exposure to hyperoxia. Immediately after the dive and return to a normoxic environment there was an increase in the EPO concencentration to 14.5 +/- 4.7 U.L(-1). Haemoglobin concentration, erythrocyte and reticulocyte counts were decreased at the end of the dive, and there was an increase in serum ferritin. There were no changes in bilirubin or haptoglobin concentrations indicative of haemolysis. It appears that the change in PO(2), rather than the sustained exposure to a hyperoxic environment, induces the changes in the EPO concentrations and erythropoietic activity.
Asunto(s)
Buceo/fisiología , Eritropoyetina/sangre , Hemoglobinas/metabolismo , Hiperoxia/sangre , Adulto , Bilirrubina/sangre , Recuento de Células Sanguíneas , Ferritinas/sangre , Haptoglobinas/metabolismo , Humanos , Masculino , Persona de Mediana EdadRESUMEN
Effects of pressure reduction, decompression rate, and repeated exposure on venous gas bubble formation were determined in five groups (GI, GII, GIII, GIV, and GV) of conscious and freely moving rats in a heliox atmosphere. Bubbles were recorded with a Doppler ultrasound probe implanted around the inferior caval vein. Rats were held for 16 h at 0.4 MPa (GI), 0.5 MPa (GII and GIII), 1.7 MPa (GIVa), or 1.9 MPa (GIV and GV), followed by decompression to 0.1 MPa in GI to GIII and to 1.1 MPa in GIV and GV. A greater decompression step, but at the same rate (GII vs. GI and GIVb vs. GIVa), resulted in significantly more bubbles (P < 0.01). A twofold decompression step resulted in equal amount of bubbles when decompressing to 1.1 MPa compared with 0.1 MPa. The faster decompression in GII and GVa (10.0 kPa/s) resulted in significantly more bubbles (P < 0.01) compared with GIII and GVb (2.2 kPa/s). No significant difference was observed in cumulative bubble score when comparing first and second exposure. With the present animal model, different decompression regimes may be evaluated.