一氧化氮（NO）和內皮源性超極化因子（EDHFs）是內皮衍生的血管舒張因子兩大類。 EETs是構成EDHFs的主要類型，這是由花生四烯酸通過細胞色素P450 （CYP）表氧化酶的催化活性得到。雖然這兩個EET和NO誘導血管舒張，從而降低血壓，許多報告表明，NO對EET引起的血管舒張起抑製作用。然而，不管它的重要性，有關一氧化氮對EETs的抑制作用的機理尚未完全了解。 / 在本研究中，我調查了一氧化氮對EET的負調控。通過膜電位和動脈張力測量，我們發現， 11,12-EET可引起內皮剝脫豬冠狀動脈平滑肌細胞膜超極化和血管舒張。該反應被S-亞硝基-N-乙酰青黴胺（SNAP）和8-Br-cGMP，一個NO的供體和cGMP的膜穿透物類似物，分別抑制。 SNAP和8-Br-cGMP對11,12-EET引起的細胞膜超極化和血管舒張的抑製作用被羥鈷胺，一氧化氮清除劑; ODQ ，鳥苷酸環化酶抑製劑;和KT5823 ，蛋白激酶G（PKG）抑製劑逆轉。 SNAP和8-Br-cGMP對EET反應的抑製作用也被過度供應外源性激酶底物， TAT-TRPC1S¹⁷²和TAT -TRPC1T³¹³廢除。羥鈷胺，ODQ， KT5823， TAT -TRPC1，和TAT -scrambled獨自使用不影響11,12-EET引起的細胞膜超極化和血管舒張作用。然而，獨自使用14，15-EEZE（EET的拮抗劑）抑制了11,12-EET的作用。 此外，磷酸化試驗表明， PKG可以直接在Ser172和Thr313位點磷酸化TRPC1 。此外，TRPV4 ， TRPC1 ，或KCa1.1被選擇性地抑制時，11,12-EET未能引起細胞膜超極化和血管舒張。免疫共沉澱研究表明， TRPV4 ， TRPC1和KCa1.1物理上彼此相關聯。 / 以上結果表明，NO-cGMP-PKG通路可通過TRPC1的磷酸化來抑制11,12- EETs在冠狀動脈血管平滑肌細胞上的作用。此外，TRPV4，TRPC1和KCa1.1參與11,12-EET誘導平滑肌超極化和血管舒張，他們可能互相關聯。從本研究的結果表明，NO和cGMP可通過PKG-介導的TRPC1的磷酸化，抑製EET誘導的平滑肌超極化和血管舒張。 / Nitric oxide (NO) and endothelium-derived hyperpolarizing factors (EDHFs) are two main classes of endothelium-derived vascular relaxant factors. EETs constitute a major type of EDHFs, which are derived from arachidonic acids via the catalytic activity of cytochrome P450 (CYP) epoxygenases. Although both EET and NO induce vascular relaxation, thus reduce blood pressure, numerous reports demonstrated that NO exerts an inhibitory action on EET-induced vascular relaxation. However, despite of its importance, the mechanisms related to the inhibitory effects of NO on EETs are incompletely understood. / In the present study, I investigated the scheme for negative regulation of NO on EET action. Through measurements of membrane potential and arterial tension, we showed that 11,12-EET could induce membrane hyperpolarization and vascular relaxation in endothelium-denuded porcine coronary arteries. The responses were suppressed by S-nitroso-N-acetylpenicillamine (SNAP) and 8-Br-cGMP, a NO donor and a membrane-permeant analogue of cGMP, respectively. The inhibitory actions of SNAP and 8-Br-cGMP on 11,12-EET-induced membrane hyperpolarization and vascular relaxation were reversed by hydroxocobalamin, a NO scavenger; ODQ, a guanylyl cyclase inhibitor; and KT5823, a protein kinase G (PKG) inhibitor. The inhibitory actions of SNAP and 8-Br-cGMP on EET responses were also abrogated by shielding TRPC1-PKG phosphorylation sites with excessive supply of exogenous PKG substrates, TAT-TRPC1S¹⁷² and TAT-TRPC1T³¹³. Hydroxocobalamin, ODQ, KT5823, TAT-TRPC1 and TAT-scrambled alone has no effect on 11,12-EET-induced membrane hyperpolarization and vascular relaxation. However, 14,15-EEZE (a selective EET antagonist) alone inhibits the action of 11,12-EET. Furthermore, phosphorylation assay was performed and it demonstrated that PKG could directly phosphorylate TRPC1 at Ser¹⁷² and Thr³¹³. In addition, 11,12-EET failed to induce membrane hyperpolarization and vascular relaxation when TRPV4, TRPC1, or KCa1.1 was selectively inhibited. Co-immunoprecipitation studies demonstrated that TRPV4, TRPC1 and KCa1.1 physically associated with each other in smooth muscle cells. / Taking together, our findings demonstrated that the NO-cGMP-PKG pathway may act through the phosphorylation of TRPC1 to inhibit the action of 11,12-EETs in coronary arterial smooth muscle cells. Furthermore, TRPV4, TRPC1 and KCa1.1 are critically involved in the 11,12-EET-induced smooth muscle hyperpolarization and relaxation and that they may physically associate with each other. The results from this study demonstrated that NO and cGMP could lead to PKG-mediated phosphorylation of TRPC1, resulting in an inhibition of EET-induced smooth muscle hyperpolarization and vascular relaxation. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Zhang, Peng. / "Ca" on title page is subscript. / Thesis (Ph.D.) Chinese University of Hong Kong, 2014. / Includes bibliographical references (leaves 115-133). / Abstracts also in Chinese.

Hipertensão do avental branco significa uma elevação persistente da pressão arterial no consultório médico ou clínica, com pressão normal em quaisquer outras circunstâncias. Existem diversos questionamentos a respeito da origem, significado clínico, prognóstico e tratamento desta manifestação. Em relação à etiologia, nossa hipótese é que uma alteração endotelial, resultando em deficiência na produção ou utilização de óxido nítrico endógeno, constitua um fator primário para a ocorrência da hipertensão do avental branco. Este estudo, desenvolvido entre moradores do município de Dumont - São Paulo, Brasil, teve como objetivos caracterizar os participantes em relação a fatores demográficos, alterações fisiológicas e metabólicas para posteriormente identificar e comparar os níveis plasmáticos de nitrato - produto da degradação do óxido nítrico ? entre os sujeitos da pesquisa. De uma amostra de 441 voluntários, selecionamos 109 indivíduos, que foram divididos em três grupos: normotensão (no=58), hipertensão essencial (no=33) e hipertensão do avental branco (no=18), após medidas de pressão arterial com aparelho oscilométrico e exame de Monitorização Ambulatorial da Pressão Arterial. Realizamos entrevista, mensuração de dados e coleta de exames laboratoriais para comparação das variáveis encontradas entre os grupos. Para o tratamento estatístico, foram utilizados os testes ANOVA e Tukey. Os resultados foram expressos como médias ± erros padrões das médias. As diferenças foram consideradas estatisticamente significativas para p<0,05. A prevalência de hipertensão do avental branco foi de 34,1%, com predominância do sexo feminino (83,3%), média de idade de 45,28 anos, sendo a maioria natural do Estado de São Paulo (66,7%), de cor branca (88,9%), alfabetizada (33,3%), casada (72,2%), com histórico familiar para doenças cardiovasculares (72,2%). A análise da quantificação de nitrato plasmático apontou diferença significativa entre os grupos hipertensão do avental branco e normotensão em comparação aos hipertensos, com elevação dos níveis de nitrato sérico em portadores de hipertensão essencial. Também encontramos diferença estatisticamente significativa para índice de massa corporal, relação cintura/quadril, glicemia e creatinina plasmáticas, na comparação entre hipertensos do avental branco e normotensos. As distinções observadas entre os grupos e a presença de variações clínicas, demográficas e bioquímicas possibilitam inferir que a hipertensão do avental branco é uma condição que deve ser analisada de maneira distinta em relação a indivíduos normotensos e portadores de hipertensão essencial. / The white coat hypertension is understood as a persistent increase in arterial pressure in the medical office or clinic, while normal blood pressure is observed in any other circumstances. There are several issues regarding the origin, clinical meaning, prognosis and treatment of this condition. Concerning the etiology, our hypothesis is that an endothelial alteration, leading to deficiency either in the production or utilization of endogenous nitric oxide, may constitute a primary factor for the occurrence of white coat hypertension. This study, developed with the population of the city of Dumont São Paulo, Brazil, aims to characterize the participants in relation to demographical factors and metabolic and physiological changes to afterwards identify and compare plasma levels of nitrate product of nitric oxide degradation among the researchs subjects. We selected 109 individuals, from a sample of 441, who were divided in three groups: normotensive (n=58), essential hypertension (n=33) and white coat hypertension (n=18), following arterial pressure measures with oscilometric device and Arterial Pressure Monitoring Exam. Interviews, data measures and laboratory exams were accomplished as to enable the comparison of the variables found between groups. For the statistical treatment, ANOVA and Tukeys test were used. Results were expressed in terms of means ± means standard deviations. The significance level adopted was p<0,05. White coat hypertension prevalence was of 34,1% with predominance of the feminine gender (83,3%), mean age 45,28, most of the participants original from the state of São Paulo (66,7%), white (88,9%), alphabetized (33,3%), married (72,2%) and with family history of cardiovascular diseases (72,2%). Quantification of plasma nitrate showed significant difference between the white coat hypertension group and the normotensive group in comparison to hypertensive patients, with increased levels of serum nitrate in essential hypertension patients. We also found statistically significant difference for corporal mass index, hip/waist ratio, plasma glucose and creatinine, in the comparison between white coat hypertensive and normotensive patients. The distinctions observed between groups and the presence of clinical, demographical and biochemical variations allow us to suggest that the white coat hypertension is a condition which must be analyzed in a distinct way in relation to normotensive and essential hypertension patients.

Many illnesses and infections are exacerbated and/or caused by biofilms. Neisseria gonorrhoeae, the etiologic agent of gonorrhea, is frequently asymptomatic in women, which can lead to persistent infection. Persistent infection can result in pelvic inflammatory disease, tubo-ovarian abscesses, infertility, and ectopic pregnancy. N. gonorrhoeae has been shown to form biofilms over glass, primary and immortalized cervical cells, and during natural cervical infection. Asymptomatic infection occurs in only 1% of infected males, and the infection site is subject to periodic rapid fluid flow, which may limit biofilm formation. Thus, biofilm formation may specifically play an important role in the infection of women and could contribute to the infrequent occurrence of symptoms. Prior to work presented in this dissertation, little was known about biofilm formation by N. gonorrhoeae. Therefore, we elected to compare the transcriptional profiles of biofilms to their planktonic counterparts, to identify genetic pathways involved in biofilm formation and maintenance. We found that 3.8% of the genome was differentially regulated, and that genes involved in anaerobic metabolism and oxidative stress tolerance were up-regulated in biofilm, while genes involved in aerobic metabolism were down-regulated. We determined that expression of aniA , ccp, and norB is required for robust biofilm formation over glass and human cervical cells, and anaerobic respiration occurs in the substratum of gonococcal biofilms. Disruption of the norB gene resulted in severe attenuation of biofilm formation. We determined that the accumulation of nitric oxide (NO) contributes to the phenotype of a norB mutant and can retard biofilm formation when present at sublethal concentrations. However, higher concentrations of NO can enhance biofilm formation in the absence of nitrite. NO enhances biofilm formation in an aniA mutant, but cannot completely restore biofilm formation, suggesting that NO can support anaerobic growth, although nitrite is preferred. We determined that the majority of the genes involved in gonococcal oxidative stress tolerance are required for normal biofilm formation, as mutations in the following genes resulted in biofilm attenuation over cervical cells and/or glass: oxyR, gor, prx, mntABC, trxB, and estD. Overall, biofilm formation may represent an adaptation for coping with the stresses present in the female genitourinary tract.

Accurate knowledge of heat transfer to materials in recombining plasmas is needed to improve heat shield designs. A lack of understanding of the chemical component of surface heating motivates the use of conservative assumptions with regards to surface catalysis in the design of thermal protection systems (TPS) that detrimentally impact payload capability. Chemical heating is the release of potential energy from recombining reactive species on the surface to form molecules. For a stable surface interacting with partially-dissociated air, the chemical heating component is due to surface-catalyzed recombination reactions of atomic O and N to produce molecular O2, N2, and NO. Unfortunately, heat flux measurements provide no fundamental information about the surface recombination pathways involved, or how the energy reaches the surface. Rather, they give a total heating rate. This work has taken steps to advance the current poor understanding about the chemical energy transport to and from material surfaces in high-temperature, recombining plasmas. A combination of spatially resolved laser-based diagnostics and emission spectroscopy was used to measure the number densities and gradients of the reactants (N, O), the products (NO, N2) and the energy distribution of recombined molecules (NO, N2) in the boundary layer adjacent to a plasma heated material. Laser excitation can probe individual species by electronic state (atoms) and by electronic, vibrational and rotational states (molecules). Emission can probe the radiative emission for a range of species and electronic, vibrational and rotational states of both atoms and molecules. These measurements of spatial variations in species concentrations through the boundary layer are directly related to near-surface gas-phase chemistry and energy exchange and have provided experimental information that was not currently available. Results provide the initial steps to determine recombination rates and the energy deposited on the surface due to surface catalyzed recombination of atomic nitrogen and oxygen in air plasma.

共著者あり。共著者名:Hizawa Nobuyuki, Yamaguchi Etsuro, Jinushi Eisei, Nishimura Masaharu. / Hokkaido University (北海道大学) / 博士 / 医学

<p>Reduksjon av gassbobler i blodbanen: metoder for å forebygge ugunstige effekter av dekompresjon.</p><p>Når en dykker returnerer til overflaten etter dykking, kan det dannes gassbobler i kroppen som følge av overmetning av gasser. Slike gassbobler kan igjen føre til trykkfallsyke, men det gjenstår fremdeles å finne alle mekanismene bak denne sammenhengen. Gassbobler er derimot gode indikatorer på risiko for trykkfallsyke, og den gjennomgående arbeidshypotesen i denne avhandlingen har vært at gassbobler i blodbanen er den bakenforliggende årsaken til alvorlig trykkfallsyke. Det å redusere mengden gassbobler vil dermed øke sikkerheten for dykkeren.</p><p>Avhandlingen består av tre studier som på forskjellige måter forsøker å redusere boblemengden ved trykkreduksjon. Alle arbeidene er gjennomført med bruk av gris som forsøksdyr, og alle dykkene er simulert i trykk-kammer spesielt laget for slike studier. For å måle gassbobler har vi benyttet ultralydavbildning, samt at vi har tatt ut kar for å måle eventuelle funksjonelle endringer i disse i etterkant av dykkene.</p><p>Den første studien demonstrer en ny metode for å redusere gassbobledannelsen ved dekompresjon. Ved kortvarig å øke trykket under pågående trykkreduksjon kan boblemengden signifikant reduseres, resultatene viser at en modell som tar hensyn til bobledannelse beskriver resultatene bedre enn en tradisjonell modell som bare tar hensyn til overmetningen. I den andre studien har vi for første gang vist at gassbobler i blodbanen kan påvirkes medikamentelt også hos store dyr under dekompresjon fra metning. Ved å gi nitrater umiddelbart før dekompresjonen startet, ble mengden gassbobler signifikant redusert sammenlignet med kontrollene som ikke fikk tilført nitrater. Studien åpner veien for videre studier av biokjemiske prosesser involvert i både dannelsen av og effektene av gassbobler. I den siste studien undersøkte vi om en behandlingsprosedyre for trykkfallsyke til bruk når et trykk-kammer ikke er tilgjengelig ville være effektiv om behandlingstrykket ble redusert fra 190 kPa til 160 kPa med pusting av ren oksygen. Vi viste her at trykket var tilstrekkelig for å fjerne boblene etter dykket, men vi forhindret ikke skader på blodkarene.</p><p>Kandidat: Andreas Møllerløkken</p><p>Institutt: Institutt for sirkulasjon og bildediagnostikk</p><p>Veileder: Professor Alf O. Brubakk</p><p>Finansieringskilder: Statoil, Norsk Hydro, Phillips Petroleum Company Norway og Petroleumstilsynet gjennom programmet forskning og utvikling innen dykking, kontraktsnr. 4600002328 med Norsk Undervannsintervensjon (NUI).</p><p>Ovennevnte avhandling er funnet verdig til å forsvares offentlig</p><p>for graden Philosophia Doctor i medisinsk teknologi</p><p>Disputas finner sted i Auditoriet, Medisinsk teknisk forskningssenter</p><p>Tirsdag 15.01.08 , kl. 12.15</p>

Context: Several recovery strategies have been used, with limited effectiveness, to reduce the muscle discomfort or pain and the diminished muscle performance following a bout of unaccustomed physical activity, a condition known as delayed onset of muscle soreness (DOMS). Muscle damage in this condition is associated with mechanical disruption of the muscle and connective tissue and inflammation and increased oxidative stress. Low frequency, low intensity, whole body periodic acceleration (WBPA) that increases nitric oxide (NO) release from vascular endothelium into the circulation through increased pulsatile shear stress offers a potential solution. This is because endothelial derived nitric oxide has anti-inflammatory, antioxidant and anti-nociceptive properties. Objective: The purpose of this study was to examine the effects of WBPA on the pain and diminished muscle performance associated with DOMS induced by unaccustomed eccentric arm exercise in young male subjects. Design: Longitudinal. Setting: University Exercise Physiology Laboratory. Participants: Seventeen active men, 23.4 +/- 4.6 yr of age. Intervention: Subjects made six visits to the research facility over a two-week period. On day one, the subject performed a 1RM elbow flexion test and was then randomly assigned to the WBPA or control group. Criterion measurements were taken on Day 2, prior to and immediately following performance of the eccentric exercise protocol (10 sets of 10 repetitions using 120% of 1RM) and after the recovery period. During all subsequent sessions (24, 48, 72, and 96 h) these data were collected before the WBPA or passive recovery was provided. Main Outcome Measures: Isometric strength (MVC), blood markers (CPK, MYO, IL-6, TNF-alpha and Uric Acid), soreness, pain, circumference, and range of motion (ROM). Results: Significantly higher MVC values were seen for the WBPA group across the entire 96 h recovery period. Additionally, within group differences were seen in CPK, MYO, IL-6, soreness, pain, circumference, and ROM showing a smaller impact and more rapid recovery by the WBPA group. Conclusion: Application of WBPA hastens recovery from DOMS after eccentric exercise. Given the lack of other potential mechanisms, these effects appear to be mediated by the increased NO release with WBPA.

We hypothesized that the interaction between tumor necrosis factor alpha(TNF)/nuclear factor-kappaB (NFkB) via activation of IKK may amplify one anotherresulting in the evolution of vascular disease and insulin resistance associated withdiabetes. The interaction between TNFa and monocyte chemoattractant protein-1 (MCP-1) may contribute to the evolution of vascular inflammation and endothelial dysfunctionin coronary arterioles in type 2 diabetes. To test this hypothesis, endothelium-dependent(ACh) and –independent (SNP) vasodilation of isolated, pressurized coronary arterioles(40-100 μm) from mLeprdb (heterozygote, normal), Leprdb (homozygote, diabetic) andLeprdb mice null for TNF (dbTNF-/dbTNF-) were examined. Although dilation of vesselsto SNP was not different between Leprdb and mLeprdb mice, dilation to ACh was reducedin Leprdb mice. The NFkB antagonist, MG-132, IKK inhibitor, sodium salicylate(NaSal), or Anti-MCP-1 partially restored endothelium-dependent coronary arteriolardilation in Leprdb mice. Protein expression of IKK and IKK were higher in Leprdb thanin mLeprdb mice. The expression of IKK, but not the expression of IKK was increasedin dbTNF-/dbTNF- mice. Leprdb mice showed increased insulin resistance, but NaSal improved insulin sensitivity. Protein expression of TNFa, NFkB, phosphorylation ofIKK and JNK were greater in Leprdb mice, but NaSal attenuated protein expression ofthem in Leprdb mice. The ratio of phosphorylated IRS-1 at Ser307 (pIRS-1)/IRS-1protein expression was elevated in Leprdb mice; both NaSal and JNK inhibitor SP600125reduced pIRS-1/IRS-1 in Leprdb mice. MG-132 or neutralization of TNF reducedsuperoxide production in Leprdb mice. Anti-MCP-1 attenuated superoxide productionand protein expression of nitrotyrosine (N-Tyr), which is an indicator of peroxynitriteproduction, in isolated coronary arterioles of Leprdb mice. Immunostaining resultsshowed that expression of MCP-1 and vascular cellular adhesion molecule-1 (VCAM) isco-localized with endothelial cells and macrophages. Anti-TNFa or anti-MCP-1markedly reduced macrophage infiltration and the number of MCP-1 positive cells.Neutralization of TNFa or anti-MCP-1 reduced the expression of adhesion molecules. Inconclusion, our results indicate that the interaction between NFkB and TNFa signalinginduces activation of IKKb. In addition, TNFa and TNFa-related signaling, includingthe expression of MCP-1 and adhesion molecules, further exacerbates oxidative stressleading to endothelial dysfunction in type 2 diabetes.

Melanophores are dark brown pigment cells located in the skin of fish, amphibia, reptiles, and many invertebrates. The color of the animal can change via rearrangement of pigment granules, melanosomes, in the cells. The dark melanophores can either hide colorful cells so that the animal appears dark, or let through colors from underneath. The animal regulates its colors and patterns via communicating nerve cells and hormones in the blood stream. It is nowadays well established that melatonin-stimulation of melanophores results in aggregation of melanosomes to the cell center and that the evident outcome is more transparent cells. It has previously been shown that the activity of serine and threonine kinases as well as phosphatases regulates the distribution of melanosomes in the cells. We wanted to study if tyrosine phosphorylations were involved in the regulation of melanosome aggregation. Melatonin-stimulated signaling in the African clawed frog, Xenopus laevis, melanophores was examined. Melansome aggregation was accompanied by tyrosine phosphorylation as shown by immunoblots. Inhibition of tyrosine phosphorylation reduced melanosome aggregation by melatonin, and the phosphorylation most likely regulated pigment aggregation. Tyrosine phosphorylation of the protein was mediated via a Gi/o protein coupled receptor, probably the melatonin receptor Mel1c. The phosphorylation was most likely not a result of the classical Gi/o protein pathway, as Src-kinase and mitogen-activated protein kinase seemed required for phosphorylation and melanosome aggregation. Two candidates for the phosphorylated protein were presented, talin and β-spectrin. The possible involvement of nitric oxide in melanosome aggregation by melatonin was investigated. Nitric oxide appeared to be necessary for melanosome aggregation. The effect of nitric oxide synthase inhibition on melanosome aggregation was not mediated via changes in the tyrosine-phosphorylated protein. We speculated that nitric oxide could affect melanosome distribution via modifications of the actin cytoskeleton. The use of recombinant melanophores as a biosensor has also been examined. A human G protein coupled receptor, opioid receptor 3, was inserted into melanophores by electroporation. The transfected melanophores responded dose-dependently to opioids and an inhibitor of opioid receptors reduced the aggregation response. Future melanophore biosensors migh detect a variety of substances, such as narcotics, pheromones, odors, and tastes.

Reduksjon av gassbobler i blodbanen: metoder for å forebygge ugunstige effekter av dekompresjon. Når en dykker returnerer til overflaten etter dykking, kan det dannes gassbobler i kroppen som følge av overmetning av gasser. Slike gassbobler kan igjen føre til trykkfallsyke, men det gjenstår fremdeles å finne alle mekanismene bak denne sammenhengen. Gassbobler er derimot gode indikatorer på risiko for trykkfallsyke, og den gjennomgående arbeidshypotesen i denne avhandlingen har vært at gassbobler i blodbanen er den bakenforliggende årsaken til alvorlig trykkfallsyke. Det å redusere mengden gassbobler vil dermed øke sikkerheten for dykkeren. Avhandlingen består av tre studier som på forskjellige måter forsøker å redusere boblemengden ved trykkreduksjon. Alle arbeidene er gjennomført med bruk av gris som forsøksdyr, og alle dykkene er simulert i trykk-kammer spesielt laget for slike studier. For å måle gassbobler har vi benyttet ultralydavbildning, samt at vi har tatt ut kar for å måle eventuelle funksjonelle endringer i disse i etterkant av dykkene. Den første studien demonstrer en ny metode for å redusere gassbobledannelsen ved dekompresjon. Ved kortvarig å øke trykket under pågående trykkreduksjon kan boblemengden signifikant reduseres, resultatene viser at en modell som tar hensyn til bobledannelse beskriver resultatene bedre enn en tradisjonell modell som bare tar hensyn til overmetningen. I den andre studien har vi for første gang vist at gassbobler i blodbanen kan påvirkes medikamentelt også hos store dyr under dekompresjon fra metning. Ved å gi nitrater umiddelbart før dekompresjonen startet, ble mengden gassbobler signifikant redusert sammenlignet med kontrollene som ikke fikk tilført nitrater. Studien åpner veien for videre studier av biokjemiske prosesser involvert i både dannelsen av og effektene av gassbobler. I den siste studien undersøkte vi om en behandlingsprosedyre for trykkfallsyke til bruk når et trykk-kammer ikke er tilgjengelig ville være effektiv om behandlingstrykket ble redusert fra 190 kPa til 160 kPa med pusting av ren oksygen. Vi viste her at trykket var tilstrekkelig for å fjerne boblene etter dykket, men vi forhindret ikke skader på blodkarene. Kandidat: Andreas Møllerløkken Institutt: Institutt for sirkulasjon og bildediagnostikk Veileder: Professor Alf O. Brubakk Finansieringskilder: Statoil, Norsk Hydro, Phillips Petroleum Company Norway og Petroleumstilsynet gjennom programmet forskning og utvikling innen dykking, kontraktsnr. 4600002328 med Norsk Undervannsintervensjon (NUI). Ovennevnte avhandling er funnet verdig til å forsvares offentlig for graden Philosophia Doctor i medisinsk teknologi Disputas finner sted i Auditoriet, Medisinsk teknisk forskningssenter Tirsdag 15.01.08 , kl. 12.15