Search PubMed⌕ Search

Biomedical subjects

E Thorsen

Publications and source records attributed to E Thorsen.

At least 19 recordsLinked to original sources
PubMed2006

No changes in lung function after a saturation dive to 2.5 MPa with intermittent reduction in Po2 during decompression.

Decompression stress and exposure to hyperoxia may cause a reduction in transfer factor of the lung for carbon monoxide and in maximal aerobic capacity after deep saturation dives. In this study lung function and exercise capacity were assessed before and after a helium-oxygen saturation dive to a pressure of 2.5 MPa where the decompression rate was reduced compared with previous deep dives, and the hyperoxic exposure was reduced by administering oxygen intermittently at pressures of 50 and 30 kPa during decompression. Eight experienced divers of median age 41 years (range 29-48) participated in the dive. The incidence of venous gas microemboli was low compared with previous deep dives. Except for one subject having treatment for decompression sickness, no changes in lung function or angiotensin converting enzyme, a marker of pulmonary endothelial cell damage, were demonstrated. The modified diving procedures with respect to decompression rate and hyperoxic exposure may have contributed to the lack of changes in lung function in this dive compared with previous deep saturation dives.

Adult↗
PubMed2004

Venous gas embolism in chamber attendants after hyperbaric exposure.

An initial occupational survey (OS) was initiated to investigate the prevalence of venous gas embolism (VGE) in chamber attendants assisting hyperbaric oxygen (HBO2) treatments. Nine female subjects were exposed for three consecutive days to the routine hospital procedure of compressed air exposure to 240 kPa for approximately 115 min with 12 min of terminal oxygen (O2) breathing. VGE was monitored with ultrasound Doppler in 15 min intervals for 2h after the first and third exposure. A follow-up experimental study was completed to investigate whether changed breathing gases and decompression would affect the high incidence of VGE observed in the OS. Ten female subjects were randomly exposed to the routine or revised profile (12 and 24 min of terminal O2 breathing respectively), and a Nitrox profile (breathing gas 40.5% O2 in Nitrogen during 90 min of the isobaric phase). VGE was monitored with transthoracic ultrasound scanner and Doppler. In the OS precordial VGE grade III (Doppler) was observed in five subjects, but median resting precordial VGE was Grade 0 both days and VGE score at all sites were equal Days 1 and 3. In the experimental study, median resting precordial VGE was Grade 0 (Doppler) and Grade 1 (Scanner). VGE Grade III (Doppler) was observed in all series, but VGE scores were not significantly different between the series. We conclude that chamber attendants assisting HBO2 treatment at 240 kPa for approximately 115 min are exposed to a significant decompression stress using the profiles tested in the present study.

Adult↗
PubMed2002

Effects of normobaric hyperoxia on water content in different organs in rats.

Pulmonary oxygen toxicity is a dose-dependent effect on alveolar epithelial and endothelial cells resulting in pulmonary oedema. Any concomitant effects on systemic capillary endothelium would be expected to result in capillary leakage and an increase in the tissues' water content. Total tissue water (TTW) in different organs was therefore studied in freely moving rats exposed to 100% O2 at normobaric pressure for 24 or 48 h, and compared to air-breathing control rats. The TTW for the following tissues was measured: Trachea, left bronchus, left lung, left and right ventricle, left kidney, skin (left paw-hindlimb), skin (back of the rat), left brain, left eye and thigh muscle left side. There was a significant increase in TTW of the lung accompanied by pleural effusion after 48 h of oxygen exposure as expected in all exposed animals. There was a small increase in TTW of the paw only, and a small decrease or no change in other tissues after 24 and 48 h of exposure. We conclude that there is no evidence of systemic capillary dysfunction as measured by tissue water content after exposure to hyperoxia in a dosage causing pulmonary oedema.

Animals↗
PubMed2002

Lung function over six years among professional divers.

AIMS: To analyse longitudinal changes in pulmonary function in professional divers and their relation with cumulative diving exposure. METHODS: The study included 87 men at the start of their education as professional divers. At follow up one, three, and six years later, 83, 81, and 77 divers were reexamined. The median number of compressed air dives in the 77 divers over the follow up period was 196 (range 37-2000). A group of non-smoking policemen (n = 64) were subjected to follow up examinations in parallel with the divers. Assessment of lung function included dynamic lung volumes, maximal expiratory flow rates, and transfer factor for carbon monoxide (Tl(CO)). The individual rates of change of the lung function variables were calculated by fitting linear regression lines to the data, expressed as percent change per year. RESULTS: The annual reductions in forced vital capacity (FVC) and forced expired volume in one second (FEV(1)) were 0.91 (SD 1.22) and 0.84 (SD 1.28) per cent per year in divers, which were significantly higher than the reductions in the policemen of 0.24 (SD 1.04) and 0.16 (SD 1.07) per cent per year (p < 0.001). The annual reduction in the maximal expiratory flow rates at 25% and 75% of FVC expired (FEF(25%) and FEF(75%)) were related to the log(10) transformed cumulative number of dives in a multiple regression analysis (p < 0.05). The annual reductions in Tl(CO) were 1.33 (SD 1.85) and 0.43 (SD 1.53) per cent per year in divers and policemen (p < 0.05). CONCLUSIONS: FVC, FEV(1), maximal expiratory flow rates, and Tl(CO) were significantly reduced in divers over the follow up period when compared with policemen. The contrasts within and between groups suggest that diving has contributed to the reduction in lung function.

Accidents, Occupational↗
PubMed2001

Lipid rafts exist as stable cholesterol-independent microdomains in the brush border membrane of enterocytes.

Glycosphingolipid/cholesterol-rich membranes ("rafts")can be isolated from many types of cells, but their existence as stable microdomains in the cell membrane has been elusive. Addressing this problem, we studied the distribution of galectin-4, a raft marker, and lactase, a protein excluded from rafts, on microvillar vesicles from the enterocyte brush border membrane. Magnetic beads coated with either anti-galectin-4 or anti-lactase antibodies were used for immunoisolation of vesicles followed by double immunogold labeling of the two proteins. A morphometric analysis revealed subpopulations of raft-rich and raft-poor vesicles by the following criteria: 1) the lactase/galectin-4 labeling ratio/vesicle captured by the anti-lactase beads was significantly higher (p < or = 0.01) than that of vesicles captured by anti-galectin-4 beads, 2) subpopulations of vesicles labeled by only one of the two antibodies were preferentially captured by beads coated with the respective antibody (p < or = 0.01), 3) the average diameter of "galectin-4 positive only" vesicles was smaller than that of vesicles labeled for lactase. Surprisingly, pretreatment with methyl-beta-cyclodextrin, which removed >70% of microvillar cholesterol, did not affect the microdomain localization of galectin-4. We conclude that stable, cholesterol-independent raft microdomains exist in the enterocyte brush border.

Animals↗
PubMed2001

Caveolae/lipid rafts in fibroblast-like synoviocytes: ectopeptidase-rich membrane microdomains.

Membrane peptidases play important roles in cell activation, proliferation and communication. Human fibroblast-like synoviocytes express considerable amounts of aminopeptidase N/CD13, dipeptidyl peptidase IV/CD26, and neprilysin/CD10, transmembrane proteins previously proposed to be involved in the regulation of intra-articular levels of neuropeptides and chemotactic mediators as well as in adhesion and cell-cell interactions. Here, we report these peptidases in synoviocytes to be localized predominantly in glycolipid- and cholesterol-rich membrane microdomains known as 'rafts'. At the ultrastructural level, aminopeptidase N/CD13 and dipeptidyl peptidase IV/CD26 were found in caveolae, in particular in intracellular yet surface-connected vesicle-like structures and 'rosettes' made up of several caveolae. In addition, clusters of peptidases were seen at the cell surface in flat patches ranging in size from about 60 to 160 nm. Cholesterol depletion of synoviocytes by methyl-beta-cyclodextrin disrupted >90% of the caveolae and reduced the raft localization of aminopeptidase N/CD13 without affecting Ala-p-nitroanilide-cleaving activity of confluent cell cultures. In co-culture experiments with T-lymphocytes, cholesterol depletion of synoviocytes greatly reduced their capability to induce an early lymphocytic expression of aminopeptidase N/CD13. We propose caveolae/rafts to be peptidase-rich 'hot-spot' regions of the synoviocyte plasma membrane required for functional cell-cell interactions with lymphocytes. The peptidases may act in concert with other types of proteins such as receptors and signal transducers localized in these specialized membrane domains.

Blotting, Western↗
PubMed2001

Increased lung compliance in response to a moderate hyperoxic exposure.

With deep saturation diving a reduction in vital capacity caused by oxygen toxicity may be opposed by a training effect of respiratory muscles due to increased gas density and work of breathing. We measured lung and chest wall mechanics before and after a 28-day saturation dive to a pressure of 0.25 MPa with the same profile of oxygen exposure as in a deep dive to a pressure of 3.7 MPa; 40 kPa during the isopression phase and 50 kPa during the decompression phase. Eight males aged 22-28 yr served as subjects. The measurements included dynamic lung volumes, static lung compliance, lung recoil pressure, and maximal respiratory pressures. Only one subject had decreased lung compliance and increased recoil pressure after the dive. The others had an increase in compliance and decrease in recoil pressure. There was a significant increase in inspiratory lung compliance (P = 0.041) and a trend for a decrease in lung recoil pressure (P = 0.061). We found no change in forced vital capacity, but decreases in forced expired volume in 1 s (P = 0.049) and forced midexpiratory flow rate (P = 0.009) were noted. There were no changes in maximal respiratory pressures. These findings are opposite to the classical findings associated with pulmonary oxygen toxicity. The results may reflect an increase in surfactant production and turnover as an early adaptive response to hyperoxic stress.

Adult↗
PubMed2001

Exposure to hyperoxia in diving and hyperbaric medicine--effects on blood cell counts and serum ferritin.

A reduction in hemoglobin concentration has been consistently reported after deep saturation dives, whereas reductions in thrombocyte counts and changes in biochemical parameters specific for liver function have been reported after some dives. In this study the contribution of exposure to hyperoxia to these changes were studied. Hemoglobin concentration, blood cell counts, serum ferritin, and biochemical parameters specific for liver damage were measured before and after a shallow 28-day saturation dive to a pressure of 250 kPa with the same hyperoxic exposure (40-50 kPa) as in a deep saturation dive in eight male divers. The same parameters were measured before, during, and after a standard 21-day hyperbaric oxygen (HBO2) treatment series in a selected group of 16 patients (8 male). There were significant reductions in hemoglobin concentrations of 3.8 +/- 4.7% (P = 0.023) and 10.2 +/- 5.3% (P = 0.003) after the HBO2 treatment series and dive, respectively, accompanied with reductions in red cell counts, reticulocyte counts, and hematocrit. There was an increase in ferritin concentrations of 29 +/- 21% (P = 0.002) and 107 +/- 43% (P < 0.001). In contrast to some deep dives, there were no changes in thrombocyte counts or biochemical parameters specific for liver damage. Exposure to hyperoxia contributes significantly to reduced hemoglobin and increased ferritin concentrations after saturation dives. The changes may reflect a shift of iron from synthesis of hemoglobin in the bone marrow to storage in macrophages caused by a downregulation of hemoglobin synthesis, or an increased oxidative stress. The changes are too small to be of clinical significance with respect to diving and HBO2 treatment.

Adult↗
PubMed2000

[Hyperbaric oxygen treatment for radiation reactions].

BACKGROUND: A national hyperbaric centre was established in 1994 at Haukeland Hospital with responsibility for all hyperbaric oxygen (HBO) treatment in Norway. In hypoxic tissues with symptomatic radiation reactions, hyperbaric oxygen induces the formation of collagen and angiogenesis resulting in permanently improved local microcirculation. MATERIAL AND METHODS: 234 patients received elective HBO treatment at Haukeland Hospital in 1997 with a total of 4,048 treatments. All 47 patients treated for radiation reactions in the pelvic area in 1997 received a questionnaire 3-15 months after HBO therapy; 81% responded. RESULTS: Rectal bleeding and haematuria were reported as much improved in 61% and 55% respectively, while bladder incontinence was much improved in 46%. INTERPRETATION: This treatment modality may be an alternative in symptomatic radiation reactions of the urinary bladder and the bowel when conventional treatment has given unsatisfactory results.

Hematuria↗
PubMed2000

Cholesterol depletion of enterocytes. Effect on the Golgi complex and apical membrane trafficking.

Intestinal brush border enzymes, including aminopeptidase N and sucrase-isomaltase, are associated with "rafts" (membrane microdomains rich in cholesterol and sphingoglycolipids). To assess the functional role of rafts in the present work, we studied the effect of cholesterol depletion on apical membrane trafficking in enterocytes. Cultured mucosal explants of pig small intestine were treated for 2 h with the cholesterol sequestering agent methyl-beta-cyclodextrin and lovastatin, an inhibitor of hydroxymethylglutaryl-coenzyme A reductase. The treatment reduced the cholesterol content >50%. Morphologically, the Golgi complex/trans-Golgi network was partially transformed into numerous 100-200 nm vesicles. By immunogold electron microscopy, aminopeptidase N was localized in these Golgi-derived vesicles as well as at the basolateral cell surface, indicating a partial missorting. Biochemically, the rates of the Golgi-associated complex glycosylation and association with rafts of newly synthesized aminopeptidase N were reduced, and less of the enzyme had reached the brush border membrane after 2 h of labeling. In contrast, the basolateral Na(+)/K(+)-ATPase was neither missorted nor raft-associated. Our results implicate the Golgi complex/trans-Golgi network in raft formation and suggest a close relationship between this event and apical membrane trafficking.

Animals↗
PubMed2000

Lung function over the first 3 years of a professional diving career.

OBJECTIVES: To characterise diving exposure and pulmonary function in professional divers at the start of their formal education and during the first 3 years of their professional career. METHODS: The study included 87 men at the start of their education as professional divers. At follow up 1 and 3 years after the school 83 and 81 divers respectively were re-examined. Assessment of lung function included dynamic lung volumes and flows and transfer factor for carbon monoxide (Tl(CO)). RESULTS: 69 Divers had preschool SCUBA diving experience and had a median number of 70 dives (range 2-3000) to a median maximal depth of 40 (range 10-73) metres. During the 15 week introductory diving course, they had 44 dives (range 38-50) in the depth range 10-50 metres. The median number of dives over the follow up period was 95 (range 0-722) to a maximal median depth of 38 (range 0-98) metres. At the start of the diving course there were no differences in forced vital capacity (FVC), forced expired volume in 1 second (FEV(1)), and in Tl(CO) between the 69 pre-exposed divers and the 18 never exposed divers. The FVC was significantly larger than predicted in both groups. At follow up at 3 years there was a significant reduction in mean (SD) FEV(1) of 1.8% (6.5), in forced mid-expiratory flow rate (FEF(25-75%)) of 6.5% (11.7) and in forced expiratory flow at 75% of FVC expired (FEF(75%)) of 10.4% (16. 8). There was no change in FVC. The Tl(CO) was significantly decreased by 4.6% (8.8). No significant effects were found of cumulative diving exposure, including the number of dives, on the relative changes of any of the lung function variables. CONCLUSIONS: The results indicate that divers initially belong to a selected group with large FVC. Exposure to diving may contribute to changes in pulmonary function, mostly affecting small airways conductance.

Adult↗
PubMed1999

Glutathione in the cellular defense of human lung cells exposed to hyperoxia and high pressure.

Saturation diving involves exposure to elevated partial pressure of oxygen (Po2) and high pressure. The present work demonstrated that hyperoxic exposure for up to 72 h had significant effects on human lung fibroblasts. Forty to sixty kPa Po2 had severe acute toxic effects, and 60 kPa O2 reduced plating efficiency approximately 96% and completely inhibited cell proliferation. Long-term toxic effects were observed as a persistent reduction of cell growth rate after 24 h exposure to 60 kPa O2 in helium, suggesting genetic effects or induction of cellular senescence. No effect of high pressure per se was observed in this respect. Cellular glutathione was increased up to a plateau 40-50% above control level after an initial decrease, which may indicate toxic effects during the GSH depletion period. The glutathione egress increased even more than the intracellular level after exposure to these conditions. The effects on glutathione were growth state specific with the highest response in exponentially growing cells. Slight protective effects of high pressure were noted in a cell growth assay, correlating with a reduced response on the glutathione level. The results support previous studies indicating that hyperoxia is the main contributor to the adverse effects of exposure to high Po2 and high pressure and point to the involvement of glutathione in the cellular detoxification of reactive oxygen species under these conditions.

Cell Division↗
PubMed1999

Subacute effects of inspiratory resistive loading and head-out water immersion on pulmonary function.

Extrathoracic airways obstruction and scuba diving may induce pulmonary edema, probably because of increased hydrostatic transmural capillary pressure in the lung. This study was designed to examine the subacute pulmonary effects of the combined exposure to inspiratory resistive loading and immersion, as in scuba diving. Two groups each of eight healthy men were exposed to head-out water immersion in thermoneutral water for 40 min with or without an added inspiratory resistive load. At flows of 0.5 and 1.0 liter x s, the measured resistances were 4.4 and 9.0 hPa x s(-1) x liter(-1), respectively. Pulmonary function, including a flow-volume loop and transfer factor of the lung for carbon monoxide (Tlco, was measured before and 60 min after the end of the exposures. Body fluid balance was restored in the first 15 min after exposure, and Tlco was always corrected to a hemoglobin concentration of 146 g x liter(-1). There was a significant reduction in Tlco of 7.3+/-5.5% (P < 0.01) after the combined exposure to head-out water immersion and inspiratory resistive load. No changes in pulmonary function were seen after exposure to head-out water immersion or inspiratory resistive loading alone. The change in Tlco was normalized within 24 h. Submersion and resistance in breathing apparatus may contribute to the changes in pulmonary function seen immediately after dives. The nature of the exposure in these experiments and the time for recovery indicate that these changes are mechanically induced, and may not contribute to the long-term effects of diving on the lung.

Adult↗
PubMed1998

Effects of a standard hyperbaric oxygen treatment protocol on pulmonary function.

The prescription of hyperbaric oxygen (HBO) therapy for disorders not related to diving is increasing. Pulmonary oxygen toxicity is well known, but the effect of the cumulative oxygen exposure corresponding to a standard HBO treatment protocol has not been quantified before. Twenty patients (10 male) had 21 HBO treatments at a partial pressure of oxygen of 240 kPa for 90 min daily. None had any previous lung disease and all had normal chest radiography and lung function at the start of the study. Dynamic lung volumes, forced expiratory flows and the transfer factor of the lung for carbon monoxide (TL,CO) were measured before the HBO treatment, on days 7, 14 and 21 during treatment and then 3-4 weeks after treatment. Four patients (one male) reported nonproductive coughing during the last week of treatment. There was a progressive reduction in forced expiratory volume in one second (FEV1) (p<0.001), mean forced mid-expiratory flow rate (FEF25-75%) (p<0.001) and forced expiratory flows at 50 and 75% of forced vital capacity (FVC) expired during HBO treatment. The reduction in FEV1 on day 21 was 4.4+/-1.7% and in FEF25-75% 10.3+/-6.1%. Four weeks after treatment there was a partial normalization. There were no changes in FVC or peak expiratory flow (PEF). TL,CO was slightly reduced on day 21 of treatment only (p<0.01) and fully normalized 1 month later. A reduction in small airways conductance is consistent with other studies where total oxygen exposures have been below the limit causing toxic pulmonary effects traditionally measured as a reduction in vital capacity. This effect is not considered to be of any clinical significance for patients treated with hyperbaric oxygen unless repeated treatment series are to be given.

Female↗
PubMed1998

Toxicity of hyperoxia and high pressure on C3H/10T1/2 cells and effects on cellular glutathione.

Saturation diving involves the exposure of humans to elevated partial pressure of oxygen (PO2) and high ambient pressure. The present study is part of a research program that focuses on how such conditions affect basal cellular functions. C3H/10T1/2 Cl 8 mouse embryo fibroblasts were exposed to 20-80 kPa O2 in a He-O2 mixture at 0.1 and 5.0 MPa ambient pressure for 24-72 h. Elevated PO2 had severe toxic effects on the cells, and there was an additional effect of high pressure on net cell growth. A persistent reduction of cell growth rate after the end of exposure to He-O2 was noted, suggesting genetic effects. We observed no effects of the ambient pressure per se in this respect. High PO2 increased the cellular glutathione level reaching a plateau approximately 100% above control at a PO2 of 60 kPa. No alteration of the glutathione redox status was observed, and high ambient pressure per se had no significant effect on the cellular glutathione content. The increased glutathione content did not completely protect the cells against toxic injury of high oxygen levels.

Analysis of Variance↗
PubMed1996

Divers' pulmonary function after open-sea bounce dives to 10 and 50 meters.

We have studied pulmonary function before and 2 h after open sea dives to 10 and 50 m and 24 h after the dive to 10 m. Nine trainee divers participated in the dive to 10 m and 17 in the dive to 50 m. Mean time in water was 53 (32-62) min for the 10-m dive and 38 (26-76) min for the 50-m dive. Assessment of lung function included dynamic lung volumes and flows and transfer factor for carbon monoxide (TlCO). There were significant reductions (P < 0.05) in forced vital capacity of 5.8% (SD = 3.9) and 1.8% (SD = 2.8), in forced expired volume in 1 s of 6.6% (SD = 3.5) and 2.7% (SD = 2.4), in forced mid-expiratory flow rate of 10.3% (SD = 7.8) and 5.2% (SD = 6.5), and in TlCO of 11.3% (SD = 7.9) and 12.8% (SD = 5.9) 2 h after the 10- and 50-m dive, respectively. Our results indicate that factors related to submersion and increased breathing resistance contribute to changes in pulmonary function in the first hours after open-sea bounce dives.

Adult↗
PubMed1995

Persistent small-airways dysfunction after exposure to hyperoxia.

To assess the contribution of hyperoxia to reduced pulmonary function after a deep saturation dive, a shallow saturation dive to a pressure of 0.25 MPa with the same profile of hyperoxic exposure as in a deep saturation dive to 3.7 MPa was conducted. The PO2 was 40 kPa, with periods of 75 kPa for 2 h every 2nd day during the first 14 days, 50 kPa the next 12 days, and a gradual fall to 21 kPa over the last 2 days in decompression. Seven submariners and one professional diver aged 22-27 yr participated. Pulmonary function, including static and dynamic lung volumes and flows and transfer factor for carbon monoxide (TLCO), were measured twice before, immediately after, 1 mo after, and 1 and 3 yr after the dive. As reported previously, there was a significant reduction in TLCO and in maximal expiratory flow rates at low lung volumes immediately after the dive. At the follow-up examinations 1 and 3 yr after, there was no recovery of the maximal expiratory flow rates. Forced midexpiratory flow rate was still reduced by 8.7 +/- 5.6% (P < 0.05) and 9.3 +/- 7.1% (P < 0.01), respectively. Forced expired volume in 1 s and forced vital capacity were not significantly reduced. There was a complete recovery of the TLCO. The findings are consistent with the studies indicating development of airway obstruction in divers, and the findings indicate that exposure to hyperoxia contributes to this effect.

Adult↗