Publications
415 results found
Bernareggi M, Mitchell JA, Barnes PJ, et al., 1997, Dual action of nitric oxide on airway plasma leakage, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 155, Pages: 869-874, ISSN: 1073-449X
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- Citations: 61
BishopBailey D, Pepper JR, Larkin S, et al., 1997, Cyclo-oxygenase-2 accounts for the sustained release of prostaglandin E(2) from cytokine stimulated human vascular smooth muscle cells, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 120, Pages: P73-P73, ISSN: 0007-1188
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- Citations: 7
Saunders MA, Mitchell JA, Seldon PM, et al., 1997, Release of granulocyte-macrophage colony stimulating factor by human cultured airway smooth muscle cells: Suppression by dexamethasone, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 120, Pages: 545-546, ISSN: 0007-1188
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- Citations: 108
Chabot F, Mitchell JA, Quinlan G, et al., 1996, Peroxynitrite is a vasodilator of rat pulmonary arteries at concetrations that do not cause endothelial dysfunction, Thorax, Vol: 51, ISSN: 0040-6376
Under physiological conditions, the potent dilator gas, nitric oxide (NO) is continuously released by endothelial cells to maintain organ blood flow. Endothelial derived NO is catalysed by endothelial NO synthase (eNOS), which my virtue of its calcium dependency, forms discreet quanta of NO. Under inflammatory conditions, such as occur in septic shock, a calcium-independent isoform of NOS is expressed (iNOS) that produces copious amounts of NO, a process which is thought to contribute to the fall in blood pressure seen in clinical sepsis. In sepsis the presence of large amounts of activated leukocytes results in elevated levels of superoxide anions (O2-) which are known to react rapidly with NO to form the potent oxidant peroxynitrite (ONOO-). Recent reports have described ONOO- as a toxic oxidant that could contribute to endothelium dysfunction in diseases such as septic shock. Since the pulmonary vasculature represents a prime site for oxidant formation, we have characterised the effects of authentic ONOO- on vascular tone in isolated rat pulmonary arteries. Pulmonary arteries were cut into rings and mounted in 2 ml organ baths containing warmed (37°C) and gassed (95%O2:5%oCO2) Krebs' buffer. ONOO- (1×10-6-1×10-4M) had no effect on resting tone but caused concentration-dependent vasodilatation in vessels pre-contracted (1 g) with the thomboxane mimetic, U46619 (1×10-6M). Similarly both acetylcholine (endothelium-dependant) and sodium nitroprusside (endothelium-independent) caused relaxation of pre-contracted pulmonary arteries. In separate experiments we found that pre-incubation of pulmonary arteries with ONOO-, had no effect on subsequent responses to acetylcholine or sodium nitroprusside. Thus, ONOO- is a vasodilator of rat pulmonary arteries at concentrations that do not cause vascular dysfunction. These observations detract from ONOO- being a toxic species in the pulmonary vasculature. ONOO- causes relaxation in the μM range whereas N
Chabot F, Mitchell JA, Quinlan G, et al., 1996, Role of poly-ADP ribosyltransferase in the vasodilator actions of peroxynitrite, Thorax, Vol: 51, ISSN: 0040-6376
The pulmonary vasculature is constantly exposed to oxygen species such as nitric oxide (NO) and superoxide anions which are usually metabolised by anti-oxidant enzymes. However, during inflammatory conditions, oxidants may be formed in excess leading to cellular damage or dysfunction. NO reacts rapidly with superoxide anions to form the putative toxic oxidant, peroxynitrite ONOO-. ONOO- has been shown to activate poly-ADP ribosyltransferase (PARS) leading to a depletion NAD+ and ATP, an event that is likely to greatly compromise energetic processes such as the maintenance of vascular tone. We have shown that ONOO- is a vasodilator of rat pulmonary arteries. Thus, we have investigated the possible contribution of PARS activation in the vasodilator properties of ONOO-. Pulmonary arteries were cut into rings and mounted in 2 ml organ baths containing warmed (37°C) and gassed (95%O2:5%CO2) Krebs' buffer. Tone (0.5 g) was induced by the addition of U46619 (1×10-6M). Under these conditions ONOO- (1×10-6-1×10-4M), acetylcholine (1×10-8-1×10-6M), and sodium nitroprusside (1×10-8-1×10-6M) caused concentration-dependent relaxation of pulmonary arteries. The NO synthase inhibitor, NG-nitro-L-arginine methyl ester (1×10-4M), inhibited the effects of acetylcholine but not ONOO- or sodium nitroprusside. Superoxide dismutase had no effect on any of the vasodilator agents. The PARS inhibitor 3-aminobenzamide (1×10-2M) significantly inhibited the relaxation caused by ONOO- but did not effect that caused by acetylcholine or sodium nitroprusside. Thus, ONOO- relaxes rat pulmonary artery directly, without causing the release of NO or superoxide. Moreover, ONOO-, unlike endogenously released NO (by acetylcholine) or nitrovasodilators appears to cause relaxation by activation of PARS. We propose that ONOO- activates PARS resulting in the depletion of cellular ATP reducing active processes of vascular smooth muscle including vaso-c
Curzen NP, Mitchell JA, Jourdan KB, et al., 1996, Endothelin-1-induced contraction of pulmonary arteries from endotoxemic rats is attenuated by the endothelin-A receptor antagonist, BQ123, CRITICAL CARE MEDICINE, Vol: 24, Pages: 2007-2013, ISSN: 0090-3493
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- Citations: 19
BishopBailey D, Larkin SW, Williams TJ, et al., 1996, Roles of nitric oxide and COX-metabolites in proliferation of rat aortic segments in organ culture, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 119, Pages: P77-P77, ISSN: 0007-1188
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- Citations: 1
Saunders MA, Belvisi MG, Corden MB, et al., 1996, Exacerbation of the release of prostaglandin E(2) by bradykinin after COX-2 induction in human airway epithelial cells, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 119, Pages: P46-P46, ISSN: 0007-1188
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- Citations: 3
Stanford SJ, Mitchell JA, BishopBailey D, et al., 1996, The dilator response to sensory nerve stimulation in the mesenteric circulation of the rat is modulated prejunctionally by nitric oxide, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 118, Pages: P83-P83, ISSN: 0007-1188
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- Citations: 1
Jourdan KB, Curzen NP, Evans TW, et al., 1996, Nitric oxide compromises the constrictor effects of the non-cyclooxygenase-derived prostanoid, 8-iso prostaglandin F-2 alpha, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 118, Pages: P85-P85, ISSN: 0007-1188
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- Citations: 1
Curzen NP, Jourdan KB, Mitchell JA, 1996, Endothelial modification of pulmonary vascular tone, INTENSIVE CARE MEDICINE, Vol: 22, Pages: 596-607, ISSN: 0342-4642
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- Citations: 8
BishopBailey D, Larkin SW, Pepper JR, et al., 1996, Comparison of the ability of human, rat and rabbit vessels to produce nitric oxide and prostanoids in response to LPS, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 117, Pages: P78-P78, ISSN: 0007-1188
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- Citations: 2
Saunders MA, Mitchell JA, HIrst SJ, et al., 1996, Characterisation of cyclo-oxygenase-2 induction in human airway smooth muscle cells, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 117, Pages: P82-P82, ISSN: 0007-1188
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- Citations: 1
Bernareggi M, Mitchell JA, Barnes PJ, et al., 1996, Dual action of nitric oxide on airway inflammation: Differential effects at different airway levels, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 117, Pages: P52-P52, ISSN: 0007-1188
Mitchell JA, Larkin S, Williams TJ, 1995, Cyclooxygenase-2: regulation and relevance in inflammation., Biochem Pharmacol, Vol: 50, Pages: 1535-1542, ISSN: 0006-2952
BELVISI M, BARNES PJ, LARKIN S, et al., 1995, NITRIC-OXIDE SYNTHASE ACTIVITY IS ELEVATED IN INFLAMMATORY LUNG-DISEASE IN HUMANS, EUROPEAN JOURNAL OF PHARMACOLOGY, Vol: 283, Pages: 255-258, ISSN: 0014-2999
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- Citations: 62
MITCHELL JA, CHESTER AH, BOARLAND AA, et al., 1995, COINDUCTION OF NITRIC-OXIDE SYNTHASE AND CYCLOOXYGENASE ACTIVITY IN HUMAN INTERNAL MAMMARY ARTERY, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 115, Pages: P78-P78, ISSN: 0007-1188
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- Citations: 2
BISHOPBAILEY D, LARKIN SW, GRIFFITHS MJD, et al., 1995, CHARACTERIZATION OF PROSTACYCLIN (PGI(2)) AND PROSTAGLANDIN E(2) (PGE(2)) RELEASE FROM HUMAN SAPHENOUS-VEIN IN RESPONSE TO BACTERIAL LPS, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 115, Pages: P136-P136, ISSN: 0007-1188
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- Citations: 2
BELVISI MG, WARD JK, MITCHELL JA, et al., 1995, NITRIC-OXIDE AS A NEUROTRANSMITTER IN HUMAN AIRWAYS, ARCHIVES INTERNATIONALES DE PHARMACODYNAMIE ET DE THERAPIE, Vol: 329, Pages: 97-110, ISSN: 0003-9780
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- Citations: 68
MITCHELL JA, BELVISI MG, AKARASEREENONT P, et al., 1994, INDUCTION OF CYCLO-OXYGENASE-2 BY CYTOKINES IN HUMAN PULMONARY EPITHELIAL-CELLS - REGULATION BY DEXAMETHASONE, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 113, Pages: 1008-1014, ISSN: 0007-1188
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- Citations: 294
MITCHELL JA, BELVISI MG, ROBBINS RA, et al., 1994, INDUCTION OF CYCLOOXYGENASE-2 IN HUMAN PULMONARY EPITHELIAL-CELLS, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 112, Pages: U41-U41, ISSN: 0007-1188
MITCHELL JA, BATCHELOR JR, CHAPEL H, et al., 1987, ERYTHROCYTE COMPLEMENT RECEPTOR TYPE-1 (CR-1) EXPRESSION AND CIRCULATING IMMUNE-COMPLEX (CIC) LEVELS IN HYDRALAZINE-INDUCED SLE, CLINICAL AND EXPERIMENTAL IMMUNOLOGY, Vol: 68, Pages: 446-456, ISSN: 0009-9104
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- Citations: 18
Kimber I, Pierce BB, Mitchell JA, et al., 1987, Depression of lymph node cell proliferation induced by oxazolone., Int Arch Allergy Appl Immunol, Vol: 84, Pages: 256-262, ISSN: 0020-5915
The influence of topical exposure to two sensitizing chemical on draining lymph node cell proliferative responses in BALB/c mice has been examined. Conventional contact sensitization with 4-ethoxymethylene-2-phenyloxazol-5-one (oxazolone) has been shown to induce a rapid and systemic suppression of subsequent proliferative responses to topically applied chemical which can be adoptively transferred to recipient mice with immune lymph node cells. In contrast to some previous reports in which such suppression was found to be largely antigen-specific in nature, we report that, at least initially, the inhibition of lymphocyte proliferation induced by skin sensitization is hapten-non-specific. The relevance of this phenomenon to the regulation of contact sensitization is discussed.
Price S, Mitchell JA, Anning PB, et al., The myocardial dysfunction of endotoxaemia is exacerbated by nitric oxide synthase inhibition, EUROPEAN HEART JOURNAL, Vol: 21, Pages: 486-486, ISSN: 0195-668X
Stanford SJ, Pepper JR, Mitchell JA, Reciprocal regulatory mechanisms exist between GM-CSF and COX-2 in human venous smooth muscle cells, EUROPEAN HEART JOURNAL, Vol: 21, Pages: 161-161, ISSN: 0195-668X
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