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  1. Book ; Thesis: Immunzytochemischer und immunchemischer Nachweis von Proteinkinasen im Nucleus suprachiasmaticus, dem zirkadianen Schrittmacher der Ratte

    Revermann, Marc

    2002  

    Author's details vorgelegt von Marc Revermann
    Language German
    Size III, 122 S. : Ill., graph. Darst.
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Frankfurt (Main), Univ., Diss., 2003
    HBZ-ID HT013718473
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2003 D 1277 order for loan Magazin

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  2. Article ; Online: Pharmacological inhibition of the soluble epoxide hydrolase-from mouse to man.

    Revermann, Marc

    Current opinion in pharmacology

    2010  Volume 10, Issue 2, Page(s) 173–178

    Abstract: Epoxyeicosatrienoic acids (EETs) build a family consisting of four arachidonic acid derived regioisomers that are generated by P450 epoxygenases. In the past years, growing interest in influencing EET level arose since EETs possess numerous beneficial ... ...

    Abstract Epoxyeicosatrienoic acids (EETs) build a family consisting of four arachidonic acid derived regioisomers that are generated by P450 epoxygenases. In the past years, growing interest in influencing EET level arose since EETs possess numerous beneficial effects in the cardiovascular system, for example, vasodilation, anti-inflammation and elicit renal and myocardial protection. Because EETs are primarily metabolized by the soluble epoxide hydrolase (sEH) and potent inhibitors of this enzyme are currently available, pharmacological sEH inhibition seems to be a feasible approach to elevate EET level in vivo. Hence, first clinical trials on sEH inhibition in man have begun. This review focuses on sEH inhibition as a novel pharmacological cardiovascular protective strategy with special regard to in vivo investigations.
    MeSH term(s) 8,11,14-Eicosatrienoic Acid/analogs & derivatives ; 8,11,14-Eicosatrienoic Acid/metabolism ; Animals ; Arachidonic Acids/chemistry ; Arachidonic Acids/metabolism ; Cardiovascular Diseases/drug therapy ; Cardiovascular Diseases/metabolism ; Cardiovascular System/drug effects ; Cardiovascular System/metabolism ; Enzyme Inhibitors/adverse effects ; Enzyme Inhibitors/pharmacology ; Enzyme Inhibitors/therapeutic use ; Epoxide Hydrolases/antagonists & inhibitors ; Epoxide Hydrolases/metabolism ; Humans ; Isomerism ; Models, Biological
    Chemical Substances Arachidonic Acids ; Enzyme Inhibitors ; 8,11,14-Eicosatrienoic Acid (7324-41-6) ; Epoxide Hydrolases (EC 3.3.2.-)
    Language English
    Publishing date 2010-04
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2037057-X
    ISSN 1471-4973 ; 1471-4892
    ISSN (online) 1471-4973
    ISSN 1471-4892
    DOI 10.1016/j.coph.2009.12.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Response to Sympathoinhibitory effect of diltiazem and prevention of aneurysm formation.

    Mieth, Anja / Revermann, Marc / Babelova, Andrea / Weigert, Andreas / Schermuly, Ralph T / Brandes, Ralf P

    Hypertension (Dallas, Tex. : 1979)

    2014  Volume 63, Issue 3, Page(s) e13

    MeSH term(s) Animals ; Anti-Inflammatory Agents/pharmacology ; Aortic Aneurysm/prevention & control ; Blood Pressure/drug effects ; Calcium Channel Blockers/pharmacology ; Diltiazem/pharmacology ; Male
    Chemical Substances Anti-Inflammatory Agents ; Calcium Channel Blockers ; Diltiazem (EE92BBP03H)
    Language English
    Publishing date 2014-01-31
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/hypertensionaha.113.02849
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  4. Article ; Online: Inhalation of the BK(Ca)-opener NS1619 attenuates right ventricular pressure and improves oxygenation in the rat monocrotaline model of pulmonary hypertension.

    Revermann, Marc / Neofitidou, Skevi / Kirschning, Thomas / Schloss, Manuel / Brandes, Ralf P / Hofstetter, Christian

    PloS one

    2014  Volume 9, Issue 1, Page(s) e86636

    Abstract: Background: Right heart failure is a fatal consequence of chronic pulmonary hypertension (PH). The development of PH is characterized by increased proliferation of vascular cells, in particular pulmonary artery smooth muscle cells (PASMCs) and pulmonary ...

    Abstract Background: Right heart failure is a fatal consequence of chronic pulmonary hypertension (PH). The development of PH is characterized by increased proliferation of vascular cells, in particular pulmonary artery smooth muscle cells (PASMCs) and pulmonary artery endothelial cells. In the course of PH, an escalated right ventricular (RV) afterload occurs, which leads to increased perioperative morbidity and mortality. BK(Ca) channels are ubiquitously expressed in vascular smooth muscle cells and their opening induces cell membrane hyperpolarization followed by vasodilation. Moreover, BK activation induces anti-proliferative effects in a multitude of cell types. On this basis, we hypothesized that treatment with the nebulized BK channel opener NS1619 might be a therapy option for pulmonary hypertension and tested this in rats.
    Methods: (1) Rats received monocrotaline injection for PH induction. Twenty-four days later, rats were anesthetized and NS1619 or the solvent was administered by inhalation. Systemic hemodynamic parameters, RV hemodynamic parameters, and blood gas analyses were measured before as well as 30 and 120 minutes after inhalation. (2) Rat PASMCs were stimulated with PDGF-BB in the presence and absence of NS1619. AKT, ERK1 and ERK2 activation were investigated by western blot analyses, and relative cell number was determined 48 hours after stimulation.
    Results: Inhalation of a 12 µM and 100 µM NS1619 solution significantly reduced RV pressure without affecting systemic arterial pressure. Blood gas analyses demonstrated significantly reduced carbon dioxide and improved oxygenation in NS1619-treated animals pointing towards a considerable pulmonary shunt-reducing effect. In PASMC's, NS1619 (100 µM) significantly attenuated PASMC proliferation by a pathway independent of AKT and ERK1/2 activation.
    Conclusion: NS1619 inhalation reduces RV pressure and improves oxygen supply and its application inhibits PASMC proliferation in vitro. Hence, BK opening might be a novel option for the treatment of pulmonary hypertension.
    MeSH term(s) Administration, Inhalation ; Animals ; Becaplermin ; Benzimidazoles/administration & dosage ; Benzimidazoles/pharmacology ; Blotting, Western ; Cell Proliferation/drug effects ; Cells, Cultured ; Hemodynamics/drug effects ; Hypertension, Pulmonary/chemically induced ; Hypertension, Pulmonary/physiopathology ; Hypertension, Pulmonary/prevention & control ; Large-Conductance Calcium-Activated Potassium Channels/metabolism ; Male ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; Monocrotaline ; Myocytes, Smooth Muscle/drug effects ; Myocytes, Smooth Muscle/metabolism ; Oxygen/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Proto-Oncogene Proteins c-sis/pharmacology ; Pulmonary Artery/cytology ; Rats ; Rats, Sprague-Dawley ; Ventricular Dysfunction, Right/physiopathology ; Ventricular Dysfunction, Right/prevention & control ; Ventricular Pressure/drug effects
    Chemical Substances Benzimidazoles ; Large-Conductance Calcium-Activated Potassium Channels ; Proto-Oncogene Proteins c-sis ; NS 1619 (153587-01-0) ; Becaplermin (1B56C968OA) ; Monocrotaline (73077K8HYV) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 3 (EC 2.7.11.24) ; Oxygen (S88TT14065)
    Language English
    Publishing date 2014-01-31
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0086636
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: L-type calcium channel inhibitor diltiazem prevents aneurysm formation by blood pressure-independent anti-inflammatory effects.

    Mieth, Anja / Revermann, Marc / Babelova, Andrea / Weigert, Andreas / Schermuly, Ralph T / Brandes, Ralf P

    Hypertension (Dallas, Tex. : 1979)

    2013  Volume 62, Issue 6, Page(s) 1098–1104

    Abstract: Formation of abdominal aortic aneurysms is a progressive inflammatory process that involves infiltration and differentiation of monocytes in the vessel wall, proliferation and migration of smooth muscle cells, and eventually the degradation of the ... ...

    Abstract Formation of abdominal aortic aneurysms is a progressive inflammatory process that involves infiltration and differentiation of monocytes in the vessel wall, proliferation and migration of smooth muscle cells, and eventually the degradation of the internal elastic lamina, which leads to outward vascular remodeling and distension of the vessel. Because calcium channel blockers exert multiple beneficial effects on the vascular system, we investigated the effect of the benzothiazepine-type calcium channel blocker diltiazem on aneurysm formation in a mouse model. Angiotensin II infusion induced massive suprarenal aortic aneurysm formation in male apolipoprotein E-deficient mice that was blocked by cotreatment with diltiazem even if the blood pressure was controlled by coinfusion of phenylephrine. Diltiazem prevented the angiotensin II-mediated induction of proinflammatory cytokines after 7 days of angiotensin II treatment in the aortic arch attributable to a reduction in the amount of locally infiltrating macrophages. To identify the underlying mechanism, vascular segments and cultured vascular cells as well as monocytes were studied. Diltiazem failed to reduce the angiotensin II-induced expression of proinflammatory chemokines and cytokines in isolated mouse thoracic aortic segments in organ culture. Furthermore, diltiazem did not affect the recruitment of proinflammatory Ly6C(+) monocytes in vivo pointing toward an effect of the compound on gene expression in monocytes/macrophages. Indeed, diltiazem prevented the interleukin-6-induced mRNA expression of interleukin-1β and the monocyte chemoattractant protein CCL12 in peritoneal macrophages and RAW264.7 cells independent of the intracellular calcium concentration. Thus, diltiazem limits aortic aneurysm formation in mice by a blood pressure-independent anti-inflammatory effect on monocytic cells.
    MeSH term(s) Angiotensin II ; Animals ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Aorta/drug effects ; Aorta/metabolism ; Aortic Aneurysm/chemically induced ; Aortic Aneurysm/drug therapy ; Aortic Aneurysm/prevention & control ; Apolipoproteins E/genetics ; Apolipoproteins E/metabolism ; Blood Pressure/drug effects ; Calcium Channel Blockers/pharmacology ; Calcium Channels, L-Type/metabolism ; Cell Line ; Diltiazem/pharmacology ; Diltiazem/therapeutic use ; Disease Models, Animal ; Interleukin-6/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Transcription Factor AP-1/metabolism
    Chemical Substances Anti-Inflammatory Agents ; Apolipoproteins E ; Calcium Channel Blockers ; Calcium Channels, L-Type ; Interleukin-6 ; Transcription Factor AP-1 ; Angiotensin II (11128-99-7) ; Diltiazem (EE92BBP03H)
    Language English
    Publishing date 2013-12
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/HYPERTENSIONAHA.113.01986
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    Zs.A 1488: Show issues Location:
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  6. Article: Protein kinase G I immunoreaction is colocalized with arginine-vasopressin immunoreaction in the rat suprachiasmatic nucleus.

    Revermann, Marc / Maronde, Erik / Ruth, Peter / Korf, Horst-Werner

    Neuroscience letters

    2002  Volume 334, Issue 2, Page(s) 119–122

    Abstract: The suprachiasmatic nucleus (SCN) contains the primary mammalian circadian clock. This clock is entrained to environmental rhythms by external stimuli called zeitgebers. This entrainment is accomplished by the activation of specific, interacting signal ... ...

    Abstract The suprachiasmatic nucleus (SCN) contains the primary mammalian circadian clock. This clock is entrained to environmental rhythms by external stimuli called zeitgebers. This entrainment is accomplished by the activation of specific, interacting signal transduction cascades. Since a cyclic guanosine monophosphate-dependent mechanism play a crucial functional role for light entrainment in the late night and for transmission of cholinergic stimuli, we examined the expression of protein kinase (PKG) in the rat SCN by means of qualitative and semi-quantitative immunocytochemistry. Immunoreaction (IR) for the isozyme protein kinase G I (PKG I) was found in the dorsomedial part of the SCN considered as an important relay in the output pathways of the clock. Within the SCN, PKG-I IR was colocalized with arginine-vasopressin-IR. The intensities of the PKG-I-IR did not vary between day and night.
    MeSH term(s) Animals ; Arginine Vasopressin/metabolism ; Circadian Rhythm/physiology ; Cyclic GMP-Dependent Protein Kinases/metabolism ; Immunohistochemistry ; Male ; Neurons/metabolism ; Rats ; Rats, Wistar ; Suprachiasmatic Nucleus/metabolism
    Chemical Substances Arginine Vasopressin (113-79-1) ; Cyclic GMP-Dependent Protein Kinases (EC 2.7.11.12)
    Language English
    Publishing date 2002-12-13
    Publishing country Ireland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 194929-9
    ISSN 1872-7972 ; 0304-3940
    ISSN (online) 1872-7972
    ISSN 0304-3940
    DOI 10.1016/s0304-3940(02)01118-7
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  7. Article ; Online: Effects of intravenous and inhaled levosimendan in severe rodent sepsis.

    Scheiermann, Patrick / Ahluwalia, Devan / Hoegl, Sandra / Dolfen, Andrea / Revermann, Marc / Zwissler, Bernhard / Muhl, Heiko / Boost, Kim A / Hofstetter, Christian

    Intensive care medicine

    2009  Volume 35, Issue 8, Page(s) 1412–1419

    Abstract: Purpose: We aimed at comparing the effects of intravenous (i.v.) and inhaled (inh.) levosimendan (LEVO) on survival, inflammatory cytokines and the apoptotic mediator caspase-3 in a rat model of severe sepsis induced by cecal ligation and incision (CLI). ...

    Abstract Purpose: We aimed at comparing the effects of intravenous (i.v.) and inhaled (inh.) levosimendan (LEVO) on survival, inflammatory cytokines and the apoptotic mediator caspase-3 in a rat model of severe sepsis induced by cecal ligation and incision (CLI).
    Methods: Twenty-eight anesthetized/ventilated male Sprague-Dawley rats (body weight 528 +/- 20 g) underwent laparotomy. Cecal mobilisation served as control (SHAM, n = 7). In all other groups, severe sepsis was induced by CLI. No further intervention occurred in the CLI-group (n = 7). 180 min after CLI, 24 microg/kg i.v. LEVO was administered in the CLI + LEVO-IV-group (n = 7), and 24 microg/kg inh. LEVO was administered via jet nebulizer in the CLI + LEVO-INH-group (n = 7).
    Results: CLI induced arterial hypotension, with i.v. and inh. LEVO attenuating blood pressure decrease over 390 min [CLI 34(31/50), CLI + LEVO-IV 82(69/131)*, CLI + LEVO-INH 78(62/85)* mmHg; median(25/75% quartile), *P < 0.05]. CLI induced metabolic acidosis. I.v. and inh. LEVO avoided arterial pH [CLI 7.18(7.16/7.2), CLI + LEVO-IV 7.27(7.24/7.31)*, CLI + LEVO-INH 7.26(7.24/7.28)*] and base excess deterioration [CLI -19(-21.8/-17.9), CLI + LEVO-IV -13(-14.8/-12)*, CLI + LEVO-INH -12.7(-14/-12.2)* mmol/l]. Overall mortality in the CLI-group was 57% compared to 0%* in both LEVO-treated groups after 390 min. LEVO administration significantly attenuated the increase in proinflammatory interleukin (IL)-1beta [CLI 896(739/911), CLI + LEVO-IV 302(230/385)*, CLI + LEVO-INH 346(271/548) pg/ml] and IL-6 [CLI 35651(31413/35816), CLI + LEVO-IV 21156(18397/28026), CLI + LEVO-INH 13674(10105/24843) pg/ml] in the plasma and reduced cleaved caspase-3 expression in the spleen.
    Conclusions: In a rat model of severe sepsis induced by CLI, i.v. and inh. LEVO equally attenuated arterial hypotension, metabolic acidosis and prolonged survival. Moreover, i.v. and inh. LEVO inhibited proinflammatory mediator release and reduced splenic caspase-3 expression.
    MeSH term(s) Administration, Inhalation ; Animals ; Humans ; Hydrazones/administration & dosage ; Hydrazones/pharmacology ; Injections, Intraventricular ; Models, Animal ; Phosphodiesterase Inhibitors/administration & dosage ; Phosphodiesterase Inhibitors/pharmacology ; Pyridazines/administration & dosage ; Pyridazines/pharmacology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Rodentia ; Sepsis/diagnosis ; Sepsis/drug therapy ; Sepsis/etiology ; Severity of Illness Index ; Simendan ; Survival Analysis ; Treatment Outcome
    Chemical Substances Hydrazones ; Phosphodiesterase Inhibitors ; Pyridazines ; Simendan (349552KRHK)
    Language English
    Publishing date 2009-04-15
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80387-x
    ISSN 1432-1238 ; 0340-0964 ; 0342-4642 ; 0935-1701
    ISSN (online) 1432-1238
    ISSN 0340-0964 ; 0342-4642 ; 0935-1701
    DOI 10.1007/s00134-009-1481-9
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    Zs.A 1089: Show issues Location:
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  8. Article ; Online: Soluble epoxide hydrolase deficiency attenuates neointima formation in the femoral cuff model of hyperlipidemic mice.

    Revermann, Marc / Schloss, Manuel / Barbosa-Sicard, Eduardo / Mieth, Anja / Liebner, Stefan / Morisseau, Christophe / Geisslinger, Gerd / Schermuly, Ralph T / Fleming, Ingrid / Hammock, Bruce D / Brandes, Ralf P

    Arteriosclerosis, thrombosis, and vascular biology

    2010  Volume 30, Issue 5, Page(s) 909–914

    Abstract: Objective: Epoxyeicosatrienoic acids (EETs) have antiinflammatory effects and are required for normal endothelial function. The soluble epoxide hydrolase (sEH) metabolizes EETs to their less active diols. We hypothesized that knockout and inhibition of ... ...

    Abstract Objective: Epoxyeicosatrienoic acids (EETs) have antiinflammatory effects and are required for normal endothelial function. The soluble epoxide hydrolase (sEH) metabolizes EETs to their less active diols. We hypothesized that knockout and inhibition of sEH prevents neointima formation in hyperlipidemic ApoE(-/-) mice.
    Methods and results: Inhibition of sEH by 12-(3-adamantan-1-yl-ureido) dodecanoic acid or knockout of the enzyme significantly increased plasma EET levels. sEH activity was detectable in femoral and carotid arteries. sEH knockout or inhibition resulted in a significant reduction of neointima formation in the femoral artery cuff model but not following carotid artery ligation. Although macrophage infiltration occurred abundantly at the site of cuff placement in both sEH(+/+) and sEH(-/-), the expression of proinflammatory genes was significantly reduced in femoral arteries from sEH(-/-) mice. Moreover, an in vivo 5-bromo-2'-deoxyuridine assay revealed that smooth muscle cell proliferation at the site of cuff placement was attenuated in sEH knockout and sEH inhibitor-treated animals.
    Conclusion: These observations suggest that inhibition of sEH prevents vascular remodeling in an inflammatory model but not in a blood flow-dependent model of neointima formation.
    MeSH term(s) Adamantane/analogs & derivatives ; Adamantane/pharmacology ; Animals ; Apolipoproteins E/deficiency ; Apolipoproteins E/genetics ; Arachidonic Acids/metabolism ; Atherosclerosis/enzymology ; Atherosclerosis/etiology ; Atherosclerosis/genetics ; Atherosclerosis/pathology ; Atherosclerosis/prevention & control ; Carotid Artery Diseases/enzymology ; Carotid Artery Diseases/pathology ; Carotid Artery Diseases/prevention & control ; Carotid Artery, Common/drug effects ; Carotid Artery, Common/enzymology ; Carotid Artery, Common/pathology ; Cell Proliferation/drug effects ; Disease Models, Animal ; Enzyme Inhibitors/pharmacology ; Epoxide Hydrolases/antagonists & inhibitors ; Epoxide Hydrolases/deficiency ; Epoxide Hydrolases/genetics ; Epoxide Hydrolases/metabolism ; Femoral Artery/drug effects ; Femoral Artery/enzymology ; Femoral Artery/injuries ; Femoral Artery/pathology ; Hyperlipidemias/complications ; Hyperlipidemias/enzymology ; Hyperlipidemias/genetics ; Hyperplasia ; Inflammation Mediators/metabolism ; Lauric Acids/pharmacology ; Macrophages/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle, Smooth, Vascular/drug effects ; Muscle, Smooth, Vascular/enzymology ; Muscle, Smooth, Vascular/injuries ; Muscle, Smooth, Vascular/pathology ; Tunica Intima/drug effects ; Tunica Intima/enzymology ; Tunica Intima/injuries ; Tunica Intima/pathology
    Chemical Substances 12-(3-adamantan-1-ylureido)dodecanoic acid ; Apolipoproteins E ; Arachidonic Acids ; Enzyme Inhibitors ; Inflammation Mediators ; Lauric Acids ; Epoxide Hydrolases (EC 3.3.2.-) ; Adamantane (PJY633525U)
    Language English
    Publishing date 2010-03-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1221433-4
    ISSN 1524-4636 ; 1079-5642
    ISSN (online) 1524-4636
    ISSN 1079-5642
    DOI 10.1161/ATVBAHA.110.204099
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1705: Show issues Location:
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  9. Article: Inhibition of the soluble epoxide hydrolase attenuates monocrotaline-induced pulmonary hypertension in rats.

    Revermann, Marc / Barbosa-Sicard, Eduardo / Dony, Eva / Schermuly, Ralph T / Morisseau, Christophe / Geisslinger, Gerd / Fleming, Ingrid / Hammock, Bruce D / Brandes, Ralf P

    Journal of hypertension

    2009  Volume 27, Issue 2, Page(s) 322–331

    Abstract: Objectives: The soluble epoxide hydrolase (sEH) metabolizes epoxyeicosatrienoic acids (EETs) to their less active dihydroxy derivatives. Because EETs have antiinflammatory properties, we determined whether or not inhibition of sEH attenuates disease ... ...

    Abstract Objectives: The soluble epoxide hydrolase (sEH) metabolizes epoxyeicosatrienoic acids (EETs) to their less active dihydroxy derivatives. Because EETs have antiinflammatory properties, we determined whether or not inhibition of sEH attenuates disease development in the monocrotaline model of pulmonary hypertension in rats.
    Methods: sEH inhibition was achieved using 12-(3-adamantan-1-yl-ureido)-dodecanoic acid (25 mg/l) and cis- 4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid (5 mg/l) administered via drinking water starting 3 days prior to monocrotaline injection (60 mg/kg).
    Results: Monocrotaline induced the development of progressive pulmonary hypertension. sEH inhibition increased the plasma ratio of EETs to DHETs and attenuated the monocrotaline-induced increase in pulmonary artery medial wall thickness as well as the degree of vascular muscularization. Moreover, right ventricular pressure was significantly lower in the group treated with sEH inhibitors. Pulmonary sEH protein expression and sEH activity, as well as pulmonary cytochrome P450 epoxygenase activity were all impaired in monocrotaline-treated rats as compared with control animals. sEH inhibitors, however, increased the plasma ratio of EETs to dihydroxy epoxyeicosatrienoic acids. Monocrotaline induced the proliferation of pulmonary endothelial and vascular smooth muscle cells in vivo as determined by 5-Bromo-2'-deoxy-Uridine incorporation, and this effect was significantly blunted in animals treated with sEH inhibitors. Proliferation of cultured pulmonary smooth muscle cell, however, was not affected by EETs or sEH inhibitors suggesting that the in-vivo effects are a consequence of a direct EET-mediated protection against the inflammation induced by monocrotaline.
    Conclusion: sEH inhibition reduces pulmonary vascular remodeling and the development of pulmonary hypertension in the monocrotaline model of primary pulmonary hypertension in rats.
    MeSH term(s) 8,11,14-Eicosatrienoic Acid/analogs & derivatives ; 8,11,14-Eicosatrienoic Acid/metabolism ; Animals ; Cell Proliferation ; Cells, Cultured ; Epoxide Hydrolases/antagonists & inhibitors ; Epoxide Hydrolases/metabolism ; Hypertension, Pulmonary/chemically induced ; Hypertension, Pulmonary/enzymology ; Hypertension, Pulmonary/pathology ; Male ; Monocrotaline ; Pulmonary Artery/pathology ; Rats ; Rats, Inbred WKY
    Chemical Substances Monocrotaline (73077K8HYV) ; Epoxide Hydrolases (EC 3.3.2.-) ; 8,11,14-Eicosatrienoic Acid (FC398RK06S)
    Language English
    Publishing date 2009-02-18
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 605532-1
    ISSN 1473-5598 ; 0263-6352 ; 0952-1178
    ISSN (online) 1473-5598
    ISSN 0263-6352 ; 0952-1178
    DOI 10.1097/hjh.0b013e32831aedfa
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Cecal ligation and incision: an acute onset model of severe sepsis in rats.

    Scheiermann, Patrick / Hoegl, Sandra / Revermann, Marc / Ahluwalia, Devan / Zander, Johannes / Boost, Kim A / Nguyen, Thach / Zwissler, Bernhard / Muhl, Heiko / Hofstetter, Christian

    The Journal of surgical research

    2009  Volume 151, Issue 1, Page(s) 132–137

    Abstract: Background: Sepsis is a leading cause of death among critically ill patients. Up to now, severe sepsis with acute onset in animals has been induced mainly through injection of single bacteria species or endotoxin and not through a surgical procedure, ... ...

    Abstract Background: Sepsis is a leading cause of death among critically ill patients. Up to now, severe sepsis with acute onset in animals has been induced mainly through injection of single bacteria species or endotoxin and not through a surgical procedure, which might adequately mirror the situation in septic patients. We therefore aimed to establish a surgical model of severe sepsis in rodents fulfilling international sepsis criteria.
    Materials and methods: Twenty-eight anesthetized/ventilated Sprague Dawley rats underwent laparotomy and cecal mobilization. The cecum was either replaced into the abdomen (SHAM, n = 14) or the cecum and the mesenteric blood vessels were ligated, and the cecum was opened through a 1.5 cm blade incision (cecal ligation and incision, CLI, n = 14).
    Results: Within 390 min, mortality was 0% (SHAM) and 50% (CLI), respectively. Compared with SHAM, CLI resulted in a 43% reduction of mean arterial blood pressure and in severe metabolic acidosis as measured by arterial base excess and pH. CLI led to a 15-fold increase in mononuclear cell population and to a 5-fold accumulation of nitrite in peritoneal lavage. Abdominal swabs from the Douglas cavity in CLI-animals showed gram-positive and gram-negative bacterial growth on agar compared with sterile swabs from SHAM-animals. In CLI-animals, plasma IL-1beta level was increased to 435 pg/mL (SHAM: 10 pg/mL) and plasma IL-6 level to 19718 pg/mL (SHAM: 832 pg/mL).
    Conclusions: CLI causes bacterial peritonitis with subsequent systemic inflammation and organ dysfunction. Thus, CLI mimics clinical sepsis and provides a surgical short term model of severe sepsis in rodents.
    MeSH term(s) Acidosis/physiopathology ; Acute Disease ; Animals ; Blood Pressure/physiology ; Body Temperature/physiology ; Cecum/surgery ; Disease Models, Animal ; Heart Rate/physiology ; Hydrogen-Ion Concentration ; Interleukin-1beta/blood ; Interleukin-6/blood ; Ligation ; Male ; Peritoneum/microbiology ; Peritonitis/microbiology ; Peritonitis/physiopathology ; Rats ; Rats, Sprague-Dawley ; Sepsis/microbiology ; Sepsis/physiopathology ; Tidal Volume/physiology
    Chemical Substances Interleukin-1beta ; Interleukin-6
    Language English
    Publishing date 2009-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80170-7
    ISSN 1095-8673 ; 0022-4804
    ISSN (online) 1095-8673
    ISSN 0022-4804
    DOI 10.1016/j.jss.2008.02.032
    Database MEDical Literature Analysis and Retrieval System OnLINE

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