Skip header and navigation

Refine By

178 records – page 1 of 18.

1H-NMR metabolomic biomarkers of poor outcome after hemorrhagic shock are absent in hibernators.

https://arctichealth.org/en/permalink/ahliterature267428
Source
PLoS One. 2014;9(9):e107493
Publication Type
Article
Date
2014
Author
Lori K Bogren
Carl J Murphy
Erin L Johnston
Neeraj Sinha
Natalie J Serkova
Kelly L Drew
Source
PLoS One. 2014;9(9):e107493
Date
2014
Language
English
Publication Type
Article
Keywords
Animals
Biological Markers - blood
Hibernation
Lipids - blood
Magnetic Resonance Spectroscopy
Male
Metabolome
Rats, Sprague-Dawley
Reperfusion Injury - blood - prevention & control
Sciuridae
Shock, Hemorrhagic - blood - therapy
Treatment Outcome
Abstract
Hemorrhagic shock (HS) following trauma is a leading cause of death among persons under the age of 40. During HS the body undergoes systemic warm ischemia followed by reperfusion during medical intervention. Ischemia/reperfusion (I/R) results in a disruption of cellular metabolic processes that ultimately lead to tissue and organ dysfunction or failure. Resistance to I/R injury is a characteristic of hibernating mammals. The present study sought to identify circulating metabolites in the rat as biomarkers for metabolic alterations associated with poor outcome after HS. Arctic ground squirrels (AGS), a hibernating species that resists I/R injury independent of decreased body temperature (warm I/R), was used as a negative control.
Male Sprague-Dawley rats and AGS were subject to HS by withdrawing blood to a mean arterial pressure (MAP) of 35 mmHg and maintaining the low MAP for 20 min before reperfusing with Ringers. The animals' temperature was maintained at 37 ? 0.5 ?C for the duration of the experiment. Plasma samples were taken immediately before hemorrhage and three hours after reperfusion. Hydrophilic and lipid metabolites from plasma were then analyzed via 1H-NMR from unprocessed plasma and lipid extracts, respectively. Rats, susceptible to I/R injury, had a qualitative shift in their hydrophilic metabolic fingerprint including differential activation of glucose and anaerobic metabolism and had alterations in several metabolites during I/R indicative of metabolic adjustments and organ damage. In contrast, I/R injury resistant AGS, regardless of season or body temperature, maintained a stable metabolic homeostasis revealed by a qualitative 1H-NMR metabolic profile with few changes in quantified metabolites during HS-induced global I/R.
An increase in circulating metabolites indicative of anaerobic metabolism and activation of glycolytic pathways is associated with poor prognosis after HS in rats. These same biomarkers are absent in AGS after HS with warm I/R.
Notes
Cites: Am J Physiol Regul Integr Comp Physiol. 2010 Feb;298(2):R329-4019923364
Cites: Gerontology. 2010;56(2):220-3019602865
Cites: Am J Physiol Regul Integr Comp Physiol. 2011 Nov;301(5):R1440-5221865542
Cites: Transplantation. 2011 Dec 15;92(11):1215-2122082817
Cites: Am J Respir Crit Care Med. 2011 Sep 15;184(6):647-5521680948
Cites: Pharmacol Ther. 2012 Feb;133(2):230-5522138603
Cites: Bioanalysis. 2012 Feb;4(3):321-4122303835
Cites: Resuscitation. 2012 Feb;83(2):253-821864484
Cites: Comp Biochem Physiol B Biochem Mol Biol. 2012 May;162(1-3):1-922326449
Cites: Nucleic Acids Res. 2012 Jul;40(Web Server issue):W127-3322553367
Cites: Physiol Genomics. 2012 Jul 15;44(14):717-2722643061
Cites: Resuscitation. 2012 Sep;83(9):1166-7222353638
Cites: Exp Biol Med (Maywood). 2013 May;238(5):539-4823856905
Cites: J Surg Res. 2014 Jan;186(1):338-4524124975
Cites: PLoS One. 2014;9(4):e9422524728042
Cites: Jpn J Pharmacol. 2001 Oct;87(2):143-5011700013
Cites: Am J Surg. 2001 Nov;182(5):481-511754855
Cites: J Comp Physiol B. 2010 Apr;180(4):599-61719967378
Cites: J Trauma. 2010 Jul;69(1):31-4020622576
Cites: J Surg Res. 2010 Nov;164(1):e131-920855081
Cites: Shock. 2010 Dec;34(6):565-7220386494
Cites: Comp Biochem Physiol Part D Genomics Proteomics. 2010 Dec;5(4):265-7320728417
Cites: Am J Physiol Lung Cell Mol Physiol. 2011 Jan;300(1):L4-L1120889676
Cites: J Exp Biol. 2011 Apr 15;214(Pt 8):1300-621430207
Cites: Physiol Genomics. 2011 Jul 14;43(13):799-80721540299
Cites: PLoS One. 2011;6(10):e2702122046435
Cites: Jpn J Pharmacol. 2002 May;89(1):36-4312083741
Cites: Horm Behav. 2003 Feb;43(2):318-2612694642
Cites: J Emerg Med. 2003 May;24(4):413-2212745044
Cites: Surgery. 2003 Aug;134(2):267-7412947328
Cites: Biol Reprod. 1988 Apr;38(3):616-223378074
Cites: J Comp Physiol B. 1988;158(1):25-373385059
Cites: Science. 1989 Jun 30;244(4912):1593-52740905
Cites: J Lipid Res. 1993 Jun;34(6):1009-198354948
Cites: J Cereb Blood Flow Metab. 1994 Mar;14(2):193-2058113316
Cites: Anal Chem. 1995 Mar 1;67(5):793-8117762816
Cites: J Cereb Blood Flow Metab. 1998 Feb;18(2):168-759469159
Cites: Kidney Int. 2005 Mar;67(3):1142-5115698456
Cites: Physiol Rev. 2003 Oct;83(4):1153-8114506303
Cites: Annu Rev Physiol. 2004;66:239-7414977403
Cites: Am J Physiol Gastrointest Liver Physiol. 2005 Mar;288(3):G473-8015701622
Cites: Chem Res Toxicol. 2005 Apr;18(4):639-5415833024
Cites: Annu Rev Nutr. 2005;25:469-9716011475
Cites: Anesth Analg. 2005 Dec;101(6):1577-8316301222
Cites: J Hepatol. 2006 May;44(5):956-6216223541
Cites: Stroke. 2006 May;37(5):1261-516574920
Cites: Surgery. 2006 Sep;140(3):404-1216934602
Cites: Am J Physiol Gastrointest Liver Physiol. 2006 Nov;291(5):G895-90116751173
Cites: J Surg Res. 2007 Jan;137(1):96-10217064732
Cites: JPEN J Parenter Enteral Nutr. 2007 Mar-Apr;31(2):94-10017308249
Cites: Bioessays. 2007 May;29(5):431-4017450592
Cites: Acta Cardiol. 2007 Aug;62(4):381-917824299
Cites: Physiol Genomics. 2007 Sep 19;31(1):15-2417536023
Cites: J Cereb Blood Flow Metab. 2008 Jul;28(7):1307-1918398417
Cites: J Neural Transm (Vienna). 2008 Jul;115(7):1011-718478178
Cites: Am J Physiol Regul Integr Comp Physiol. 2008 Jul;295(1):R316-2818434441
Cites: Allergol Int. 2008 Sep;57(3):211-718566550
Cites: Crit Care. 2008;12(4):21818638356
Cites: Shock. 2009 Jan;31(1):40-918497709
Cites: Am J Physiol Regul Integr Comp Physiol. 2009 Feb;296(2):R383-9319052316
Cites: Conf Proc IEEE Eng Med Biol Soc. 2008;2008:4891-419163813
Cites: Brain Res Rev. 2009 Mar;59(2):293-31518845187
Cites: Nucleic Acids Res. 2009 Jul;37(Web Server issue):W652-6019429898
Cites: J Neurochem. 2009 Aug;110(4):1170-919493168
Cites: Exp Biol Med (Maywood). 2009 Sep;234(9):1011-919546346
Cites: Mol Biosyst. 2010 Jan;6(1):215-2420024083
PubMed ID
25211248 View in PubMed
Less detail

6-Hydroxycleroda-3,13-dien-15,16-olide protects neuronal cells from lipopolysaccharide-induced neurotoxicity through the inhibition of microglia-mediated inflammation.

https://arctichealth.org/en/permalink/ahliterature149311
Source
Planta Med. 2010 Feb;76(2):120-7
Publication Type
Article
Date
Feb-2010
Author
Yu-Tzu Shih
Ya-Yun Hsu
Fang-Rong Chang
Yang-Chang Wu
Yi-Ching Lo
Author Affiliation
Graduate Institute of Natural Products, Kaohsiung Medical University, Kaohsiung, Taiwan.
Source
Planta Med. 2010 Feb;76(2):120-7
Date
Feb-2010
Language
English
Publication Type
Article
Keywords
Animals
Anti-Inflammatory Agents - isolation & purification - pharmacology - therapeutic use
Cell Death - drug effects
Cell Line, Tumor
Diterpenes - isolation & purification - pharmacology - therapeutic use
Enzyme Inhibitors - pharmacology
Humans
Inflammation - prevention & control
Inflammation Mediators - metabolism
Lipopolysaccharides
Microglia - drug effects
Neurons - drug effects
Neurotoxicity Syndromes - prevention & control
Phytotherapy
Plant Extracts - chemistry - pharmacology - therapeutic use
Polyalthia - chemistry
Rats
Rats, Sprague-Dawley
Abstract
Polyalthia longifolia var. pendula is used as an antipyretic agent in indigenous systems of medicine. Microglia-mediated inflammation plays an important role in the pathway leading to neuronal cell death in a number of neurodegenerative diseases. The aim of this study was to investigate the effects of 6-hydroxycleroda-3,13-dien-15,16-olide (PL3) extracted from Polyalthia longifolia var. pendula on lipopolysaccharide(LPS)-induced inflammation in microglia-like HAPI cells and primary microglia cultures. In microglia-neuron co-cultures, LPS decreased the cell viability of neuroblastoma SH-SY5Y cells. LPS-induced cell death was attenuated by the NOS inhibitor, L-NAME, the COX-2 inhibitor, NS-398 or the NADPH oxidase inhibitor, DPI, respectively. In LPS-treated microglia cells, PL3 decreased the expression of iNOS, COX-2, gp91 (phox), and NF- kappaBp65, the degradation of I kappaB alpha, and the production of NO, PGE (2), iROS, and TNF- alpha. PL3 also enhanced the expression of HO-1, a cytoprotective and anti-inflammatory enzyme. Moreover, PL3 reduced LPS-activated microglia-induced cell death. The present results suggest that PL3 inhibits microglia-mediated inflammation and inflammation-related neuronal cell death. Therefore, PL3 has potential use for the treatment of inflammation-related neurodegenerative diseases.
PubMed ID
19653144 View in PubMed
Less detail

Acidification of the osteoclastic resorption compartment provides insight into the coupling of bone formation to bone resorption.

https://arctichealth.org/en/permalink/ahliterature70794
Source
Am J Pathol. 2005 Feb;166(2):467-76
Publication Type
Article
Date
Feb-2005
Author
Morten A Karsdal
Kim Henriksen
Mette G Sørensen
Jeppe Gram
Sophie Schaller
Morten H Dziegiel
Anne-Marie Heegaard
Palle Christophersen
Thomas J Martin
Claus Christiansen
Jens Bollerslev
Author Affiliation
Nordic Bioscience A/S, Herlev Hovedgade 207, DK-2730 Herlev, Denmark. mk@nordicbioscience.com
Source
Am J Pathol. 2005 Feb;166(2):467-76
Date
Feb-2005
Language
English
Publication Type
Article
Keywords
Acid Phosphatase - metabolism
Adult
Animals
Bone Density
Bone resorption
Bone and Bones
Cathepsins - pharmacology
Cells, Cultured
Chloride Channels - antagonists & inhibitors - metabolism
Dose-Response Relationship, Drug
Family Health
Female
Humans
Immunohistochemistry
Indicators and Reagents - pharmacology
Isoenzymes - metabolism
Macrolides - pharmacology
Macrophage Colony-Stimulating Factor - metabolism
Macrophages - metabolism
Male
Middle Aged
Models, Biological
Mutation
Osteoclasts - metabolism
Osteopetrosis - genetics
Ovary - metabolism
Oxazines - pharmacology
Phenotype
Phenylurea Compounds - pharmacology
Rats
Rats, Sprague-Dawley
Tetrazoles - pharmacology
Time Factors
Xanthenes - pharmacology
Abstract
Patients with defective osteoclastic acidification have increased numbers of osteoclasts, with decreased resorption, but bone formation that remains unchanged. We demonstrate that osteoclast survival is increased when acidification is impaired, and that impairment of acidification results in inhibition of bone resorption without inhibition of bone formation. We investigated the role of acidification in human osteoclastic resorption and life span in vitro using inhibitors of chloride channels (NS5818/NS3696), the proton pump (bafilomycin) and cathepsin K. We found that bafilomycin and NS5818 dose dependently inhibited acidification of the osteoclastic resorption compartment and bone resorption. Inhibition of bone resorption by inhibition of acidification, but not cathepsin K inhibition, augmented osteoclast survival, which resulted in a 150 to 300% increase in osteoclasts compared to controls. We investigated the effect of inhibition of osteoclastic acidification in vivo by using the rat ovariectomy model with twice daily oral dosing of NS3696 at 50 mg/kg for 6 weeks. We observed a 60% decrease in resorption (DPYR), increased tartrate-resistant acid phosphatase levels, and no effect on bone formation evaluated by osteocalcin. We speculate that attenuated acidification inhibits dissolution of the inorganic phase of bone and results in an increased number of nonresorbing osteoclasts that are responsible for the coupling to normal bone formation. Thus, we suggest that acidification is essential for normal bone remodeling and that attenuated acidification leads to uncoupling with decreased bone resorption and unaffected bone formation.
PubMed ID
15681830 View in PubMed
Less detail

Adaptive or maladaptive response to adenoviral adrenomedullin gene transfer is context-dependent in the heart.

https://arctichealth.org/en/permalink/ahliterature92802
Source
J Gene Med. 2008 Aug;10(8):867-77
Publication Type
Article
Date
Aug-2008
Author
Leskinen Hanna
Rauma-Pinola Tanja
Szokodi István
Kerkelä Risto
Pikkarainen Sampsa
Uusimaa Paavo
Hautala Timo
Vuolteenaho Olli
Ruskoaho Heikki
Author Affiliation
Institute of Biomedicine, Department of Pharmacology and Toxicology, Biocentre Oulu, University of Oulu, Oulu, Finland.
Source
J Gene Med. 2008 Aug;10(8):867-77
Date
Aug-2008
Language
English
Publication Type
Article
Keywords
Adenoviridae - drug effects
Adrenomedullin - metabolism - pharmacology
Animals
Gene Transfer Techniques
Heart - drug effects - physiology - physiopathology
Heart Ventricles - drug effects
Hypertrophy, Left Ventricular - metabolism - physiopathology
Male
Myocardial Infarction - physiopathology
Myocardium - metabolism
RNA, Messenger - metabolism
Rats
Rats, Sprague-Dawley
Systole - drug effects
Ventricular Function, Left - drug effects
Abstract
BACKGROUND: Adrenomedullin (AM) is a potent vasodilator and natriuretic peptide produced in the heart, but controversy persists regarding its cardiac effects. We explored the potential role of AM on cardiac function and remodeling by direct recombinant adenoviral AM gene delivery into the anterior wall of the left ventricle (LV). METHODS: AM was overexpressed in healthy rat hearts and in hearts during the remodeling process in response to pressure overload and myocardial infarction. The AM effects were analysed with echocardiography and in an isolated perfused rat heart preparation. The expression of AM and the activation of underlying signaling pathways were also investigated. RESULTS: AM mRNA increased by 20.9-fold (p
PubMed ID
18615773 View in PubMed
Less detail

Adoptive transfer of allergic airway responses with sensitized lymphocytes in BN rats.

https://arctichealth.org/en/permalink/ahliterature57674
Source
Am J Respir Crit Care Med. 1995 Jul;152(1):64-70
Publication Type
Article
Date
Jul-1995
Author
A. Watanabe
P. Rossi
P M Renzi
L J Xu
R D Guttmann
J G Martin
Author Affiliation
Meakins-Christie Laboratories, McGill University, Royal Victoria Hospital, Montreal, Quebec, Canada.
Source
Am J Respir Crit Care Med. 1995 Jul;152(1):64-70
Date
Jul-1995
Language
English
Publication Type
Article
Keywords
Animals
Bronchial Hyperreactivity - immunology - physiopathology
Bronchial Provocation Tests
Bronchoalveolar Lavage Fluid - cytology
Eosinophils - immunology
Immunoglobulin E - immunology
Immunotherapy, Adoptive
Male
Ovalbumin - immunology
Passive Cutaneous Anaphylaxis - immunology
Rats
Rats, Inbred BN
Rats, Sprague-Dawley
Research Support, Non-U.S. Gov't
Respiratory Hypersensitivity - immunology - physiopathology
Serum Albumin, Bovine - immunology
T-Lymphocytes - immunology
Abstract
To evaluate the role of lymphocytes in the pathogenesis of allergic bronchoconstriction, we investigated whether allergic airway responses are adoptively transferred by antigen-primed lymphocytes in Brown Norway (BN) rats. Animals were actively sensitized to ovalbumin (OA) or sham sensitized, and 14 d later mononuclear cells (MNCs) were isolated from intrathoracic lymph nodes, passed through a nylon wool column, and transferred to naive syngeneic rats. Recipients were challenged with aerosolized OA or bovine serum albumin (BSA) (5% wt/vol) and analyzed for changes in lung resistance (RL), airway responsiveness to inhaled methacholine (MCh), and bronchoalveolar lavage (BAL) cells. Recipients of MNCs from sensitized rats responded to OA inhalation and exhibited sustained increases in RL throughout the 8-h observation period, but without usual early airway responses. Recipients of sham-sensitized MNCs or BSA-challenged recipients failed to respond to antigen challenge. At 32 h after OA exposure, airway responsiveness to MCh was increased in four of seven rats that had received sensitized MNCs (p = 0.035). BAL eosinophils increased at 32 h in the recipients of both sensitized and sham-sensitized MNCs. However, eosinophil numbers in BAL were inversely correlated with airway responsiveness in the recipients of sensitized MNCs (r = -0.788, p = 0.036). OA-specific immunoglobulin E (IgE) was undetectable by enzyme-linked immunosorbent assay (ELISA) or passive cutaneous anaphylaxis (PCA) in recipient rats following adoptive transfer. In conclusion, allergic late airway responses (LAR) and cholinergic airway hyperresponsiveness, but not antigen-specific IgE and early responses, were adoptively transferred by antigen-primed lymphocytes in BN rats.(ABSTRACT TRUNCATED AT 250 WORDS)
PubMed ID
7599864 View in PubMed
Less detail

Adoptive transfer of alveolar macrophages abrogates bronchial hyperresponsiveness.

https://arctichealth.org/en/permalink/ahliterature15196
Source
Am J Respir Cell Mol Biol. 2004 Jul;31(1):22-7
Publication Type
Article
Date
Jul-2004
Author
Eric Careau
Elyse Y Bissonnette
Author Affiliation
Centre de Recherche, Hôpital Laval, Institut universitaire de Cardiologie et de Pneumologie de l'Université Laval, Québec, Canada. eric.careau@crhl.ulaval.ca
Source
Am J Respir Cell Mol Biol. 2004 Jul;31(1):22-7
Date
Jul-2004
Language
English
Publication Type
Article
Keywords
Adoptive Transfer
Animals
Asthma - physiopathology
Bronchi - drug effects - immunology - physiopathology
Bronchial Hyperreactivity - genetics - physiopathology - therapy
Bronchial Provocation Tests
Clodronic Acid
Disease Models, Animal
Dose-Response Relationship, Drug
Drug Resistance - physiology
Genetic Predisposition to Disease - genetics
Immunoglobulin E - blood
Immunoglobulin G - blood
Liposomes
Macrophages, Alveolar - drug effects - immunology - transplantation
Male
Methacholine Chloride - pharmacology
Ovalbumin - immunology
Rats
Rats, Sprague-Dawley
Reaction Time - drug effects - physiology
Research Support, Non-U.S. Gov't
Abstract
Increasing evidence suggests that alveolar macrophages (AM) are involved in asthma pathogenesis. To better understand the role that these cells play, we investigated the capacity of AM from allergy-resistant rat, Sprague Dawley (SD), to modulate airway hyperresponsiveness of allergy-susceptible rat, Brown Norway (BN). AM of ovalbumin (OVA)-sensitized BN rats were eliminated by intratracheal instillation of liposomes containing clodronate. AM from OVA-sensitized SD rats were transferred into AM-depleted BN rats 24 h before allergen challenge. Airway responsiveness to methacholine was measured the following day. Instillation of liposomes containing clodronate in BN rats eliminated 85% AM after 3 d compared with saline liposomes. Methacholine concentration needed to increase lung resistance by 200% (EC200RL) was significantly lower in OVA-challenged BN rats (27.9 +/- 2.8 mg/ml) compared with SD rats (63.9 +/- 8.6 mg/ml). However, when AM from SD rats were transferred into AM-depleted BN rats, airway responsiveness (64.0 +/- 11.3 mg/ml) was reduced to the level of naïve rats (54.4 +/- 3.7 mg/ml) in a dose-dependent manner. Interestingly, transfer of AM from BN rats into SD rats did not modulate airway responsiveness. To our knowledge, this is the first direct evidence showing that AM may protect against the development of airway hyperresponsiveness.
Notes
Comment In: Am J Respir Cell Mol Biol. 2004 Jul;31(1):1-215208095
Comment In: Am J Respir Cell Mol Biol. 2004 Jul;31(1):3-715208096
PubMed ID
14962974 View in PubMed
Less detail

Adrenomedullin gene expression in the rat heart is stimulated by acute pressure overload: blunted effect in experimental hypertension.

https://arctichealth.org/en/permalink/ahliterature54511
Source
Endocrinology. 1997 Jun;138(6):2636-9
Publication Type
Article
Date
Jun-1997
Author
H. Romppanen
M. Marttila
J. Magga
O. Vuolteenaho
P. Kinnunen
I. Szokodi
H. Ruskoaho
Author Affiliation
Department of Pharmacology and Toxicology, University of Oulu, Finland.
Source
Endocrinology. 1997 Jun;138(6):2636-9
Date
Jun-1997
Language
English
Publication Type
Article
Keywords
Animals
Argipressin - pharmacology
Atrial Natriuretic Factor - biosynthesis
Blood Pressure - drug effects
Heart - physiology - physiopathology
Heart Failure, Congestive - metabolism
Heart Ventricles
Humans
Hypertension - metabolism - physiopathology
Male
Myocardium - metabolism
Natriuretic Peptide, Brain
Peptide Biosynthesis
Peptides
RNA, Messenger - biosynthesis
Rats
Rats, Inbred Strains
Rats, Sprague-Dawley
Research Support, Non-U.S. Gov't
Time Factors
Transcription, Genetic - drug effects
Abstract
The levels of adrenomedullin (ADM), a newly discovered vasodilating and natriuretic peptide, are elevated in plasma and ventricular myocardium in human congestive heart failure suggesting that cardiac synthesis may contribute to the plasma concentrations of ADM. To examine the time course of induction and mechanisms regulating cardiac ADM gene expression, we determined the effect of acute and short-term cardiac overload on ventricular ADM mRNA and immunoreactive ADM (ir-ADM) levels in conscious rats. Acute pressure overload was produced by infusion of arginine8-vasopressin (AVP, 0.05 microg/kg/min, i.v.) for 2 h into 12-week-old hypertensive TGR(mREN-2)27 rats and normotensive Sprague-Dawley (SD) rats. Hypertension and marked left ventricular hypertrophy were associated with 2.2-times higher ir-ADM levels in the left ventricular epicardial layer (178 +/- 36 vs. 81 +/- 23 fmol/g, P
PubMed ID
9165059 View in PubMed
Less detail

Adrenomedullin modulates hemodynamic and cardiac effects of angiotensin II in conscious rats.

https://arctichealth.org/en/permalink/ahliterature9538
Source
Am J Physiol Regul Integr Comp Physiol. 2004 Jun;286(6):R1085-92
Publication Type
Article
Date
Jun-2004
Author
Marja Luodonpää
Hanna Leskinen
Mika Ilves
Olli Vuolteenaho
Heikki Ruskoaho
Author Affiliation
Department of Pharmacology and Toxicology, Biocenter Ouli, University of Oulu, 90014 Oulu, Finland.
Source
Am J Physiol Regul Integr Comp Physiol. 2004 Jun;286(6):R1085-92
Date
Jun-2004
Language
English
Publication Type
Article
Keywords
Angiotensin II - antagonists & inhibitors - pharmacology
Animals
Blood Pressure - drug effects
Body Weight - drug effects
Echocardiography
Heart - drug effects
Heart Rate - drug effects
Hemodynamic Processes - drug effects
Hypertension - chemically induced - prevention & control
Hypertrophy, Left Ventricular - chemically induced - prevention & control
Intracellular Signaling Peptides and Proteins
Male
Membrane Proteins - biosynthesis - genetics
Norepinephrine - antagonists & inhibitors - pharmacology
Peptides - pharmacology
Peptidyl-Dipeptidase A - biosynthesis - genetics
Rats
Rats, Sprague-Dawley
Receptor, Angiotensin, Type 1 - biosynthesis - genetics
Receptors, Peptide - biosynthesis - genetics
Research Support, Non-U.S. Gov't
Reverse Transcriptase Polymerase Chain Reaction
Telemetry
Vasoconstrictor Agents - antagonists & inhibitors
Vasodilator Agents - pharmacology
Abstract
We examined whether adrenomedullin, a vasoactive peptide expressed in the heart, modulates the increase in blood pressure, changes in systolic and diastolic function, and left ventricular hypertrophy produced by long-term administration of ANG II or norepinephrine in rats. Subcutaneous administration of adrenomedullin (1.5 microg.kg(-1).h(-1)) for 1 wk inhibited the ANG II-induced (33.3 microg.kg(-1).h(-1) sc) increase in mean arterial pressure by 67% (P
PubMed ID
14751847 View in PubMed
Less detail

Alveolar macrophages of allergic resistant and susceptible strains of rats show distinct cytokine profiles.

https://arctichealth.org/en/permalink/ahliterature15450
Source
Clin Exp Immunol. 2001 Oct;126(1):9-15
Publication Type
Article
Date
Oct-2001
Author
J. Sirois
E Y Bissonnette
Author Affiliation
Département de médecine, Centre de recherche, Hôpital Laval, Institut universitaire de cardiologie et de pneumologie de l'Université Laval, Sainte-Foy, Canada.
Source
Clin Exp Immunol. 2001 Oct;126(1):9-15
Date
Oct-2001
Language
English
Publication Type
Article
Keywords
Administration, Inhalation
Animals
Asthma - immunology
Bronchoalveolar Lavage Fluid - immunology
Cells, Cultured
Comparative Study
Cytokines - biosynthesis - genetics
Hypersensitivity, Immediate - immunology
Interleukins - biosynthesis - genetics
Macrophage Inflammatory Protein-1 - biosynthesis - genetics
Macrophages, Alveolar - immunology
Nitric Oxide - biosynthesis
Ovalbumin - administration & dosage - immunology
RNA, Messenger - biosynthesis
Rats
Rats, Sprague-Dawley
Research Support, Non-U.S. Gov't
Th1 Cells - immunology
Th2 Cells - immunology
Tumor Necrosis Factor-alpha - biosynthesis - genetics
Abstract
Brown Norway rats are widely used as a model of asthma, whereas Sprague Dawley rats do not develop allergic reactions under the same conditions. Given the importance of alveolar macrophages (AM) in down-regulating cellular immune responses in the lung, we postulated that the different susceptibilities in the development of airway allergic reactions in these rat strains may be related to functional differences in their AM. We investigated the production of important mediators in asthma, namely tumour necrosis factor (TNF), interleukin-10 (IL-10), IL-12, IL-13, nitric oxide (NO) and macrophage inflammatory protein-1alpha (MIP-1alpha), by AM of unsensitized Sprague Dawley and Brown Norway rats. AM were purified by adherence and stimulated with OX8 (anti-CD8 antibody) or LPS. OX8 stimulation significantly increased the release of TNF, IL-10 and NO in both strains of rats, whereas MIP-1alpha and IL-12 release were increased in Brown Norway rats only. Interestingly, stimulated AM from Sprague Dawley rats released significantly more TNF and less IL-10, IL-12, IL-13, MIP-1alpha and NO compared with AM from Brown Norway rats. These differences were also observed at the mRNA level, except for TNF. Thus, AM from Brown Norway and Sprague Dawley rats are functionally different. Furthermore, LPS- and OX8-stimulated AM from Brown Norway rats produce more Th2 type cytokines (IL-10 and IL-13) than AM from Sprague Dawley rats, suggesting that these cells may play an important role in creating a cytokine milieu that may favour the development of allergic reactions.
PubMed ID
11678894 View in PubMed
Less detail

Anastomotic healing of small bowel with or without chronic radiation damage in protein-deficient malnourished rats.

https://arctichealth.org/en/permalink/ahliterature62018
Source
Eur J Surg. 1996 Jan;162(1):47-53
Publication Type
Article
Date
Jan-1996
Author
S. Jahnson
B. Gerdin
Author Affiliation
Department of Urology, Orebro Medical Centre, Sweden.
Source
Eur J Surg. 1996 Jan;162(1):47-53
Date
Jan-1996
Language
English
Publication Type
Article
Keywords
Anastomosis, Surgical
Animals
Biomechanics
Intestine, Small - physiopathology - surgery
Male
Protein Deficiency - complications - physiopathology
Radiation Injuries, Experimental - complications - physiopathology
Rats
Rats, Sprague-Dawley
Wound Healing
Abstract
OBJECTIVE. To assess the influence of protein malnutrition on anastomotic healing in rat small bowel with or without chronic radiation damage. DESIGN. Controlled laboratory study. SETTING. University hospital, Sweden. MATERIAL. 60 male Sprague-Dawley rats. INTERVENTION. A short segment of the distal ileum was exteriorised and irradiated (n = 30) or only exposed (n = 30), and 20 weeks later an anastomosis was made within this segment. Two weeks before anastomosis half of the animals in each group received rat chow in which the protein content had been reduced to 25%; standard rat chow was given to the remaining animals. MAIN OUTCOME MEASUREMENTS. Weight changes, anastomotic bursting strength, amount of perianastomotic hydroxyproline, and number of anastomotic complications. RESULTS. 13 animals in the irradiated group and 11 animals in the non-irradiated group died of intestinal obstruction or respiratory distress leaving 17 and 19 animals that could be evaluated. Body weight was significantly reduced in animals with protein restriction (p
PubMed ID
8679763 View in PubMed
Less detail

178 records – page 1 of 18.