Chronic hyperbaric exposure activates proinflammatory mediators in humans.
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Decompression illness (DCI) is an illness affecting divers subjected to reductions in ambient pressure. Besides a mechanical explanation to DCI, an inflammatory mechanism has been suggested. In this study, levels of interleukin (IL)-8, IL-6, IL-1 receptor antagonist (IL-1ra), secretory leukocyte protease inhibitor (SLPI), and neutrophil gelatinase-associated lipocalcin (NGAL) were measured in divers before and after a 2-mo period of daily diving. The divers were military conscripts and completed their diving period with no clinical symptoms of DCI. We found no change in IL-6 and IL1-ra but did find an increase in IL-8 and NGAL together with a decrease in SLPI levels. The findings suggest an inflammatory activation. This activation is not severe because no changes in IL-6 or IL-1ra were found. The increase in NGAL and IL-8 levels were interpreted as a sign of leukocyte activation. The decreased SLPI levels suggest an influence on the inflammatory defense mechanism. All in all, the findings of this study show a compensated activation of the inflammatory defense mechanism without loss of homeostasis of the inflammatory system. (+info)
Gas bubbles in rats after heliox saturation and different decompression steps and rates.
(50/437)
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. (+info)
Chronic carbon monoxide enhanced IbTx-sensitive currents in rat resistance pulmonary artery smooth muscle cells.
(51/437)
Exogenous carbon monoxide (CO) can induce pulmonary vasodilation by acting directly on pulmonary artery (PA) smooth muscle cells. We investigated the contribution of K+ channels to the regulation of resistance PA resting membrane potential on control (PAC) rats and rats exposed to CO for 3 wk at 530 parts/million, labeled as PACO rats. Whole cell patch-clamp experiments revealed that the resting membrane potential of PACO cells was more negative than that of PAC cells. This was associated with a decrease of membrane resistance in PACO cells. Additional analysis showed that outward current density in PACO cells was higher (50% at +60 mV) than in PAC cells. This was linked to an increase of iberiotoxin (IbTx)-sensitive current. Chronic CO hyperpolarized membrane of pressurized PA from -46.9 +/- 1.2 to -56.4 +/- 2.6 mV. Additionally, IbTx significantly depolarized membrane of smooth muscle cells from PACO arteries but not from PAC arteries. The present study provides initial evidence of an increase of Ca2+-activated K+ current in smooth muscle cells from PA of rats exposed to chronic CO. (+info)
Weather, Chinook, and stroke occurrence.
(52/437)
BACKGROUND: Changes in weather and season have been linked to stroke occurrence. However, the association has been inconsistent across stroke types. Calgary is a city in the Chinook belt and is subject to high variability in weather conditions. METHODS: We obtained hourly weather data over a 5-year period from 1996 to 2000; Chinook events were identified according to the accepted definition. We reviewed administrative data to determine stroke occurrence and defined stroke types to maximize specificity of diagnosis. To examine the hypothesis that weather affected the number of strokes occurring in a given day, we compared average daily stroke occurrence on Chinook days and non-Chinook days; we compared mean daily temperature, relative humidity, barometric pressure, and wind speed by the number of strokes occurring on any given day. RESULTS: Annual variation in stroke frequency was observed. No seasonal, monthly, or weekly variation in overall stroke occurrence or occurrence by type was evident. No relationship with changes in weather parameters was observed. CONCLUSIONS: We found no association between weather changes and stroke occurrence. A cause-and-effect relationship between weather and stroke occurrence is dubious because of a lack of consistency across studies. (+info)
Does shoot water status limit leaf expansion of nitrogen-deprived barley?
(53/437)
The role of shoot water status in mediating the decline in leaf elongation rate of nitrogen (N)-deprived barley plants was assessed. Plants were grown at two levels of N supply, with or without the application of pneumatic pressure to the roots. Applying enough pressure (balancing pressure) to keep xylem sap continuously bleeding from the cut surface of a leaf allowed the plants to remain at full turgor throughout the experiments. Plants from which N was withheld required a greater balancing pressure during both day and night. This difference in balancing pressure was greater at high (2.0 kPa) than low (1.2 kPa) atmospheric vapour pressure deficit (VPD). Pressurizing the roots did not prevent the decline in leaf elongation rate induced by withholding N at either high or low VPD. Thus low shoot water status did not limit leaf growth of N-deprived plants. (+info)
Evidence for protection of nitrogenase from O(2) by colony structure in the aerobic diazotroph Gluconacetobacter diazotrophicus.
(54/437)
Gluconacetobacter diazotrophicus is an endophytic diazotroph of sugarcane which exhibits nitrogenase activity when growing in colonies on solid media. Nitrogenase activity of G. diazotrophicus colonies can adapt to changes in atmospheric partial pressure of oxygen (pO(2)). This paper investigates whether colony structure and the position of G. diazotrophicus cells in the colonies are components of the bacterium's ability to maintain nitrogenase activity at a variety of atmospheric pO(2) values. Colonies of G. diazotrophicus were grown on solid medium at atmospheric pO(2) of 2 and 20 kPa. Imaging of live, intact colonies by confocal laser scanning microscopy and of fixed, sectioned colonies by light microscopy revealed that at 2 kPa O(2) the uppermost bacteria in the colony were very near the upper surface of the colony, while the uppermost bacteria of colonies cultured at 20 kPa O(2) were positioned deeper in the mucilaginous matrix of the colony. Disruption of colony structure by physical manipulation or due to 'slumping' associated with colony development resulted in significant declines in nitrogenase activity. These results support the hypothesis that G. diazotrophicus utilizes the path-length of colony mucilage between the atmosphere and the bacteria to achieve a flux of O(2) that maintains aerobic respiration while not inhibiting nitrogenase activity. (+info)
Effect of hypobaric hypoxia on blood gases in patients with restrictive lung disease.
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Several publications have reported effects of hypobaric conditions in patients with chronic obstructive pulmonary disease. To the current authors' knowledge, similar studies concerning patients with restrictive lung disease have not been published. The effect of simulated air travel in a hypobaric chamber on arterial blood gases, blood pressure, and cardiac frequency during rest and 20 W exercise, and the response to supplementary oxygen in 17 patients with chronic restrictive ventilatory impairment has been investigated. Resting oxygen tension in arterial blood (Pa,O2) decreased from 10.4+/-1.6 kPa at sea level to 6.5+/-1.1 kPa at 2,438 m simulated altitude, and decreased further during light exercise in all patients (5.1+/-0.9 kPa). Pa,O2 at this altitude correlated positively with sea-level Pa,O2 and transfer factor of the lung for carbon monoxide (TL,CO), and negatively with carbon dioxide tension in arterial blood (Pa,CO2). Pa,O2 increased to acceptable levels with an O2 supply of 2 L x min(-1) at rest and 4 L x min(-1) during 20 W exercise. In conclusion, most of the patients with restrictive ventilatory impairment developed hypoxaemia below the recommended levels of in-flight oxygen tension in arterial blood during simulated air travel. Light exercise aggravated the hypoxaemia. Acceptable levels of oxygen tension in arterial blood, with only a minor increase in carbon dioxide tension in arterial blood, were obtained by supplementary oxygen. (+info)
Modulation of decompression sickness risk in pigs with caffeine during H(2) biochemical decompression.
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In H(2) biochemical decompression, H(2)-metabolizing intestinal microbes remove gas stored in tissues of animals breathing hyperbaric H(2), thereby reducing decompression sickness (DCS) risk. We hypothesized that increasing intestinal perfusion in pigs would increase the activity of intestinal Methanobrevibacter smithii, lowering DCS incidence further. Pigs (Sus scrofa, 17-23 kg, n = 20) that ingested caffeine (5 mg/kg) increased O(2) consumption rate in 1 atm air by ~20% for at least 3 h. Pigs were given caffeine alone or caffeine plus injections of M. smithii. Animals were compressed to 24 atm (20.5-23.1 atm H(2), 0.3-0.5 atm O(2)) for 3 h, then decompressed and observed for signs of DCS. In previous studies, DCS incidence in animals without caffeine treatment was significantly (P < 0.05) lower with M. smithii injections (7/16) than in controls (9/10). However, contrary to our hypothesis, DCS incidence was marginally higher (P = 0.057) in animals that received caffeine and M. smithii (9/10) than in animals that received caffeine but no M. smithii (4/10). More information on gas kinetics is needed before extending H(2) biochemical decompression to humans. (+info)