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• W2091940904 abstract "Just 10 years ago, who would have thought that a lethal gas that was “… found in unsavory places as cigarette smoke and smog …” and was a “… destroyer of ozone, suspected carcinogen and precursor of acid rain …”1Culotta E. Koshland Jr, D.E. NO news is good news.Science. 1992; 258: 1862-1865Crossref PubMed Scopus (696) Google Scholar would one day be recognized as playing a crucial role in mammalian physiology? Since 1987 when Palmer et al2Palmer R. Fergie A.C. Moncada S. Nitric oxide release accounts for the biological activity of endothelium derived relaxing factor.Nature. 1987; 327: 524-526Crossref PubMed Scopus (9260) Google Scholar and Ignaro et al3Ignaro L.J. Buga G.M. Wood K.S. et al.Endothelium derived relaxing factor produced and released from artery and vein in nitric oxide.Proc Natl Acad Sci USA. 1987; 84: 9261-9265Crossref Scopus (91) Google Scholar independently identified nitric oxide (NO) as the endothelium-derived relaxing factor, this gas has generated a phenomenal amount of interest.4Koshland Jr, D. Molecule of the year [editorial].Science. 1992; 258: 1861Crossref PubMed Scopus (416) Google Scholar Many excellent reviews of the biochemical, physiologic, and clinical aspects of NO have appeared,5Moncada S. Palmer R.M.J. Higgs E.A. Nitric oxide: physiology, pathophysiology, and pharmacology.Pharmacol Rev. 1991; 43: 109-142PubMed Google Scholar, 6Moncada S. Higgs A. The L-arginine-nitric oxide pathway.N Engl J Med. 1993; 329: 2002-2012Crossref PubMed Scopus (5686) Google Scholar, 7Barnes P.J. Bebisi M.G. Nitric oxide and lung disease.Thorax. 1993; 48: 1034-1043Crossref PubMed Scopus (368) Google Scholar including a review by Mitzutani and Layon8Mizutani T. Layon A.J. Clinical applications of nitric oxide. Review.Chest. 1996; 110: 506-524Abstract Full Text Full Text PDF PubMed Scopus (48) Google Scholar and an editorial by Brett and Evans9Brett S.J. Evans T.W. Endogenous nitric oxide in exhaled human breath: a new means of monitoring airway disease or another NO-NO?.Chest. 1996; 110: 873-874Abstract Full Text Full Text PDF Scopus (4) Google Scholar in recent issues of CHEST.The role of NO in human physiology can be briefly summarized as follows. NO is synthesized by the enzyme, NO synthase (Nos), from the amino acid L-arginine. The two major isoforms of constitutive Nos (cNoS) are present in the vascular endothelial cells (Nos3) and neurons (Nosl). These isoforms release NO in rapid short bursts with potent vasodilator and neurotransmitter actions. NO thus released also possesses antithrombotic properties10Schultz P.J. Roji L. Endogenously synthesized nitric oxide prevents endotoxin induced glomerular thrombosis.J Clin Invest. 1992; 90: 1718-1725Crossref PubMed Scopus (283) Google Scholar, 11Azyma H. Ishikawa M. Sekizaki S. Endothelium dependent inhibition of platelet aggregation.Br J Pharmacol. 1986; 88: 411-415Crossref Scopus (465) Google Scholar, 12Radoimski M.W. Palmer R.M. Moncada S. Endogenous nitric oxide inhibits human platelet adhesion to vascular endothelium.Lancet. 1987; : 1057-1058Abstract Scopus (1220) Google Scholar and inhibits the proliferative response of the intima to vascular injury.13Garg V.C. Haasid A. Nitric oxide generating vasodilators and 8-bronco cyclic guanosine monophosphate inhibits mitogenesis and proliferation of cultured rat smooth vacular muscle cells.J Clin Invest. 1989; 83: 1774-1777Crossref PubMed Scopus (1987) Google Scholar A second category of Nos, known as inducible (iNos), is formed de novo under the influence of cytokines released in immunologic or inflammatory reactions.5Moncada S. Palmer R.M.J. Higgs E.A. Nitric oxide: physiology, pathophysiology, and pharmacology.Pharmacol Rev. 1991; 43: 109-142PubMed Google Scholar, 6Moncada S. Higgs A. The L-arginine-nitric oxide pathway.N Engl J Med. 1993; 329: 2002-2012Crossref PubMed Scopus (5686) Google Scholar, 7Barnes P.J. Bebisi M.G. Nitric oxide and lung disease.Thorax. 1993; 48: 1034-1043Crossref PubMed Scopus (368) Google Scholar Release of NO by iNos occurs for prolonged periods and has antimicrobial, immunologic, and inflammatory activities.The lung contains all three isoforms of Nos. Nos3 is present in vascular endothelium and plays a key role in the maintenance of vascular tone through the release of NO in response to increase in intracellular calcium.14Griffith T.M. Edwards D.H. Davies R.L. et al.EDRF coordinates the behavior of vascular resistance vessels.Nature. 1987; 329: 442-445Crossref PubMed Scopus (255) Google Scholar Exercise or volume overload or biochemical mediators like thrombin, bradykinin, or adenosine diphosphate activate Nos3. NO is released and rapidly diffuses to the smooth muscles, producing relaxation. Nosl, the primary neurotransmitter, is in nonadrenergic, noncholinergic nerves,15Belvisi M.G. Ward J.K. Mitchell J.A. et al.Nitric oxide as a neurotransmitter in human airways.Arch Int Pharmacodyn Ther. 1995; 329: 97-100PubMed Google Scholar whose stimulation also leads to increased NO production. Finally, iNos (Nos2) is present in alveolar macrophages, airway cells, Clara cells, neutrophils, bronchial epithelium, and alveolar pneumocytes, and is activated in immunologic, inflammatory, or irritant reactions.16Warner R.L. Paine R III Christensen P.J. et al.Lung sources and cytokine requirements for in vivo expression of inducible nitric oxide synthase.Am J Respir Cell Mol Biol. 1995; 12: 649-661Crossref PubMed Scopus (127) Google Scholar, 17Nijkamp F.P. Folkerts G. Nitric oxide and bronchial responsiveness.Arch Int Pharmacodyn Ther. 1995; 329: 81-96PubMed Google ScholarWith the advent of chemoluminescence analyzers to allow rapid, accurate measurement of NO in exhaled air,18Leone A.M. Gustafsson L.E. Francis P.L. et al.Nitric oxide in exhaled breath in humans: direct GC-MS confirmation.Biochem Biophys Res Commun. 1994; 20: 883-887Crossref Scopus (84) Google Scholar the study of NO in expired air has been an active area of research. The major sources of NO in expired air are the nose19Lundberg J. Weitzerg E. Nordwall S.L. et al.Primarily nasal origin of exhaled nitric oxide and absence in Karfagener's syndrome.Eur Respir J. 1994; 8: 1501-1504Crossref Scopus (359) Google Scholar and sinuses,20Lundberg J. Farkas-Szallasin T. Weitzberg E. et al.High nitric oxide production in human paranasal sinuses.Nat Med. 1995; 1: 370-373Crossref PubMed Scopus (540) Google Scholar although measurements after orotracheal intubation and bronchoscopic sampling from the lobar and segmental bronchi have shown conclusively that expired air contains the NO produced in the lung and airways.21Kharitanov S. Chung K.F. Evans D.J. et al.The elevated level of exhaled nitric oxide in asthmatic patients is mainly derived from the lower respiratory tract [abstract].Eur Respir J. 1995; 8: 3775Google Scholar Higher concentrations are recorded during nasal breathing due to contamination with NO produced in the paranasal sinuses and nasopharynx.22Dillon W.C. Hampl V. Shultz P.J. et al.Origins of breath nitric oxide in humans.Chest. 1996; 110: 930-938Abstract Full Text Full Text PDF PubMed Scopus (75) Google Scholar The use of a mouthpiece and noseclip for collection of expired air reduces the contribution of nasopharyngeal air to the expired air, but some contamination by nasopharyngeal air still occurs.23Kimberly B. Nejadnik B. Giraud G. et al.Nasal contribution to exhaled nitric oxide at rest and during breath holding in humans.Am J Respir Crit Care Med. 1996; 153: 829-836Crossref PubMed Scopus (135) Google Scholar NO is also increased on breath-holding and forced expiration.24Persson M.G. Wiklund N.G. Gustafsson L.E. Endogenous nitric oxide in single exhalation and changes during exercise.Am Rev Respir Dis. 1993; 148: 1210-1214Crossref PubMed Scopus (193) Google Scholar Therefore, close attention to the technical details of sampling of the expired air and the equipment is essential to the interpretation of expired NO.Release of NO in the exhaled air per unit of time (VNO) could yield important information on pulmonary vascular endothelial function. Changes in VNO occur under many physiologic stimuli. VNO increases during exercise in normal human subjects,25Trolin S. Anden T. Hendenstierna G. Nitric oxide in expired air at rest and during exercise.Acta Physiol Scand. 1994; 151: 159-163Crossref PubMed Scopus (43) Google Scholar, 26Bauer J.A. Wals J.A. Dorms S. et al.Endogenous nitric oxide in expired air: effects of acute exercise in humans.Life Sci. 1994; 55: 1903-1909Crossref PubMed Scopus (67) Google Scholar, 27Iwamoto J. Pendergast D.R. Suzuki H. et al.Effect of graded exercise on nitric oxide in expired air in humans.Respir Physiol. 1994; 97: 333-345Crossref PubMed Scopus (83) Google Scholar and positive correlation exists between diffusing capacity of carbon monoxide and exhaled NO.28Crenrona G. Higgenbottom T. Borland C. et al.Mixed expired nitric oxide in primary pulmonary hypertension in relation to lung diffusion capacity.QJM. 1994; 87: 547-551Google Scholar A rise in VNO has also been observed in women during the middle of the menstrual cycle.29Kharitanov S.A. Logan-Sinclair R.B. Busset C.M. et al.Peak expiratory nitric oxide differences in men and women: relation to menstrual cycle.Br Heart J. 1994; 72: 243-245Crossref Scopus (140) Google Scholar These changes are generally attributed to the activation of Nos3 in endothelial cells in response to increased capillary blood volume.An increase in the fractional concentration of NO is seen in such disease conditions as sinusitis, and vasomotor and allergic rhinitis due to the release of NO by the inflammatory cells.30Kharitanov S.A. Yates D. Barnes P.J. Increased nitric oxide in exhaled air of normal human subjects with upper respiratory tract infections.Eur Respir J. 1995; 8: 295-297Crossref Scopus (347) Google Scholar VNO increases during an asthma attack,31Kharitanov S.A. Yates D. Robbins R.A. et al.Increased nitric oxide in exhaled air of asthmatic patients.Lancet. 1994; 343: 133-135Abstract Scopus (1311) Google Scholar late asthmatic reactions,32Kharitanov S.A. O’Connor B.J. Evans D.J. et al.Allergen induced late asthmatic reactions are associated with elevation of exhaled nitric oxide.Am J Crit Care Med. 1995; 151: 1894-1899Crossref Scopus (293) Google Scholar and antigen-induced bronchospasm, and decreases after treatment with steroids.33Massaro A.F. Gaston B. Kita-Fanta C. et al.Expired nitric oxide levels during treatment for acute asthma.Am J Respir Crit Care Med. 1995; 152: 800-803Crossref PubMed Scopus (324) Google Scholar However, no rise in VNO is observed during early asthmatic response or bronchospasm after histamine challenge.34Kharitanov S.A. Evans D.J. Barnes P.J. et al.Bronchial provocation challenge with histamine or adenosine 5 monophosphate does not alter exhaled nitric oxide in asthma [abstract].Am J Respir Crit Care Med. 1995; 151: A125Google Scholar The increased NO in the expired air in these instances and in ARDS is attributed to activation of Nos2 in the inflammatory cells, although nonadrenergic, noncholinergic nerves also could be a source of NO in asthma.A decrease in VNO is noted in conditions with poor endothelial cell function. VNO is decreased in many subjects with coronary artery disease.35el Tamimi H. Mansour M. Wargovich T.J. et al.Usefulness of endogenous and exogenous nitric oxide to identify degrees of endothelial dysfunction in patients with stable angina pectoris.Am J Cardiol. 1994; 74: 600-603Abstract Full Text PDF Scopus (5) Google Scholar Reduced endothelial Nos in the lungs of patients with pulmonary hypertension has been reported.36Giaid A. Saleh D. Reduced expression of endothelial nitric oxide synthase in the lungs of patients with pulmonary hypertension.N Engl J Med. 1995; 333: 214-221Crossref PubMed Scopus (1215) Google Scholar Similarly, decreased VNO is noted in patients with pulmonary fibrosis37Cailes J.B. Kharitanov S. Yates D. et al.Decreased endogenous nitric oxide in the exhaled air of systemic sclerosis patients [abstract].Thorax. 1995; 50: 4528Google Scholar and in smokers.38Kharitanov S.A. Robbins R.A. Yates D. et al.Acute and chronic effects of cigarette smoking on exhaled nitric oxide.Am Rev Respir Crit Care Med. 1995; 152: 609-612Crossref Scopus (406) Google ScholarIn this issue of CHEST (see page 44), Riley and colleagues report their findings on VNO in exhaled air in patients with primary pulmonary hypertension (PPH) and pulmonary fibrosis (PF). They noted a lower VNO at rest in PF subjects compared with normal subjects. In subjects with PPH, although the VNO at rest was the same as in normals, it failed to rise with exercise. Destruction of vascular endothelial cells in PF and deficiency of endothelial Nos3 or reduced capillary blood volume in PPH appear to be the most likely explanations for these findings, as postulated by the authors. Although they used an NO analyzer with a slower response time, which led to a delay between sampling and measurement, their results are compatible with known actions of NO in maintaining normal vascular tone and preventing microvascular proliferation. Similar results have been reported by others, but the present work is unique in comparing normal subjects and those with PPH and PF under similar settings.Riley and colleagues have contributed to the growing body of work suggesting a possible clinical role for measurements of NO in expired air. However, this will have to await the availability of accurate and relatively inexpensive analyzers with fast response and recording capabilities. Even when such equipment is available, the technique to avoid nasopharyngeal contamination would need to be standardized. The normal ranges of V˙NO and FNO in expired air and their response to exercise and other physiologic states and illnesses also must be clarified before measurements of NO can be used clinically. Nevertheless, this is an area of intense ongoing research and NO measurement may eventually become a useful pulmonary function test for airway inflammation, delayed type of hypersensitivity, nonadrenergic, noncholinergic nerve and endothelial cell function, and response to treatment. Just 10 years ago, who would have thought that a lethal gas that was “… found in unsavory places as cigarette smoke and smog …” and was a “… destroyer of ozone, suspected carcinogen and precursor of acid rain …”1Culotta E. Koshland Jr, D.E. NO news is good news.Science. 1992; 258: 1862-1865Crossref PubMed Scopus (696) Google Scholar would one day be recognized as playing a crucial role in mammalian physiology? Since 1987 when Palmer et al2Palmer R. Fergie A.C. Moncada S. Nitric oxide release accounts for the biological activity of endothelium derived relaxing factor.Nature. 1987; 327: 524-526Crossref PubMed Scopus (9260) Google Scholar and Ignaro et al3Ignaro L.J. Buga G.M. Wood K.S. et al.Endothelium derived relaxing factor produced and released from artery and vein in nitric oxide.Proc Natl Acad Sci USA. 1987; 84: 9261-9265Crossref Scopus (91) Google Scholar independently identified nitric oxide (NO) as the endothelium-derived relaxing factor, this gas has generated a phenomenal amount of interest.4Koshland Jr, D. Molecule of the year [editorial].Science. 1992; 258: 1861Crossref PubMed Scopus (416) Google Scholar Many excellent reviews of the biochemical, physiologic, and clinical aspects of NO have appeared,5Moncada S. Palmer R.M.J. Higgs E.A. Nitric oxide: physiology, pathophysiology, and pharmacology.Pharmacol Rev. 1991; 43: 109-142PubMed Google Scholar, 6Moncada S. Higgs A. The L-arginine-nitric oxide pathway.N Engl J Med. 1993; 329: 2002-2012Crossref PubMed Scopus (5686) Google Scholar, 7Barnes P.J. Bebisi M.G. Nitric oxide and lung disease.Thorax. 1993; 48: 1034-1043Crossref PubMed Scopus (368) Google Scholar including a review by Mitzutani and Layon8Mizutani T. Layon A.J. Clinical applications of nitric oxide. Review.Chest. 1996; 110: 506-524Abstract Full Text Full Text PDF PubMed Scopus (48) Google Scholar and an editorial by Brett and Evans9Brett S.J. Evans T.W. Endogenous nitric oxide in exhaled human breath: a new means of monitoring airway disease or another NO-NO?.Chest. 1996; 110: 873-874Abstract Full Text Full Text PDF Scopus (4) Google Scholar in recent issues of CHEST. The role of NO in human physiology can be briefly summarized as follows. NO is synthesized by the enzyme, NO synthase (Nos), from the amino acid L-arginine. The two major isoforms of constitutive Nos (cNoS) are present in the vascular endothelial cells (Nos3) and neurons (Nosl). These isoforms release NO in rapid short bursts with potent vasodilator and neurotransmitter actions. NO thus released also possesses antithrombotic properties10Schultz P.J. Roji L. Endogenously synthesized nitric oxide prevents endotoxin induced glomerular thrombosis.J Clin Invest. 1992; 90: 1718-1725Crossref PubMed Scopus (283) Google Scholar, 11Azyma H. Ishikawa M. Sekizaki S. Endothelium dependent inhibition of platelet aggregation.Br J Pharmacol. 1986; 88: 411-415Crossref Scopus (465) Google Scholar, 12Radoimski M.W. Palmer R.M. Moncada S. Endogenous nitric oxide inhibits human platelet adhesion to vascular endothelium.Lancet. 1987; : 1057-1058Abstract Scopus (1220) Google Scholar and inhibits the proliferative response of the intima to vascular injury.13Garg V.C. Haasid A. Nitric oxide generating vasodilators and 8-bronco cyclic guanosine monophosphate inhibits mitogenesis and proliferation of cultured rat smooth vacular muscle cells.J Clin Invest. 1989; 83: 1774-1777Crossref PubMed Scopus (1987) Google Scholar A second category of Nos, known as inducible (iNos), is formed de novo under the influence of cytokines released in immunologic or inflammatory reactions.5Moncada S. Palmer R.M.J. Higgs E.A. Nitric oxide: physiology, pathophysiology, and pharmacology.Pharmacol Rev. 1991; 43: 109-142PubMed Google Scholar, 6Moncada S. Higgs A. The L-arginine-nitric oxide pathway.N Engl J Med. 1993; 329: 2002-2012Crossref PubMed Scopus (5686) Google Scholar, 7Barnes P.J. Bebisi M.G. Nitric oxide and lung disease.Thorax. 1993; 48: 1034-1043Crossref PubMed Scopus (368) Google Scholar Release of NO by iNos occurs for prolonged periods and has antimicrobial, immunologic, and inflammatory activities. The lung contains all three isoforms of Nos. Nos3 is present in vascular endothelium and plays a key role in the maintenance of vascular tone through the release of NO in response to increase in intracellular calcium.14Griffith T.M. Edwards D.H. Davies R.L. et al.EDRF coordinates the behavior of vascular resistance vessels.Nature. 1987; 329: 442-445Crossref PubMed Scopus (255) Google Scholar Exercise or volume overload or biochemical mediators like thrombin, bradykinin, or adenosine diphosphate activate Nos3. NO is released and rapidly diffuses to the smooth muscles, producing relaxation. Nosl, the primary neurotransmitter, is in nonadrenergic, noncholinergic nerves,15Belvisi M.G. Ward J.K. Mitchell J.A. et al.Nitric oxide as a neurotransmitter in human airways.Arch Int Pharmacodyn Ther. 1995; 329: 97-100PubMed Google Scholar whose stimulation also leads to increased NO production. Finally, iNos (Nos2) is present in alveolar macrophages, airway cells, Clara cells, neutrophils, bronchial epithelium, and alveolar pneumocytes, and is activated in immunologic, inflammatory, or irritant reactions.16Warner R.L. Paine R III Christensen P.J. et al.Lung sources and cytokine requirements for in vivo expression of inducible nitric oxide synthase.Am J Respir Cell Mol Biol. 1995; 12: 649-661Crossref PubMed Scopus (127) Google Scholar, 17Nijkamp F.P. Folkerts G. Nitric oxide and bronchial responsiveness.Arch Int Pharmacodyn Ther. 1995; 329: 81-96PubMed Google Scholar With the advent of chemoluminescence analyzers to allow rapid, accurate measurement of NO in exhaled air,18Leone A.M. Gustafsson L.E. Francis P.L. et al.Nitric oxide in exhaled breath in humans: direct GC-MS confirmation.Biochem Biophys Res Commun. 1994; 20: 883-887Crossref Scopus (84) Google Scholar the study of NO in expired air has been an active area of research. The major sources of NO in expired air are the nose19Lundberg J. Weitzerg E. Nordwall S.L. et al.Primarily nasal origin of exhaled nitric oxide and absence in Karfagener's syndrome.Eur Respir J. 1994; 8: 1501-1504Crossref Scopus (359) Google Scholar and sinuses,20Lundberg J. Farkas-Szallasin T. Weitzberg E. et al.High nitric oxide production in human paranasal sinuses.Nat Med. 1995; 1: 370-373Crossref PubMed Scopus (540) Google Scholar although measurements after orotracheal intubation and bronchoscopic sampling from the lobar and segmental bronchi have shown conclusively that expired air contains the NO produced in the lung and airways.21Kharitanov S. Chung K.F. Evans D.J. et al.The elevated level of exhaled nitric oxide in asthmatic patients is mainly derived from the lower respiratory tract [abstract].Eur Respir J. 1995; 8: 3775Google Scholar Higher concentrations are recorded during nasal breathing due to contamination with NO produced in the paranasal sinuses and nasopharynx.22Dillon W.C. Hampl V. Shultz P.J. et al.Origins of breath nitric oxide in humans.Chest. 1996; 110: 930-938Abstract Full Text Full Text PDF PubMed Scopus (75) Google Scholar The use of a mouthpiece and noseclip for collection of expired air reduces the contribution of nasopharyngeal air to the expired air, but some contamination by nasopharyngeal air still occurs.23Kimberly B. Nejadnik B. Giraud G. et al.Nasal contribution to exhaled nitric oxide at rest and during breath holding in humans.Am J Respir Crit Care Med. 1996; 153: 829-836Crossref PubMed Scopus (135) Google Scholar NO is also increased on breath-holding and forced expiration.24Persson M.G. Wiklund N.G. Gustafsson L.E. Endogenous nitric oxide in single exhalation and changes during exercise.Am Rev Respir Dis. 1993; 148: 1210-1214Crossref PubMed Scopus (193) Google Scholar Therefore, close attention to the technical details of sampling of the expired air and the equipment is essential to the interpretation of expired NO. Release of NO in the exhaled air per unit of time (VNO) could yield important information on pulmonary vascular endothelial function. Changes in VNO occur under many physiologic stimuli. VNO increases during exercise in normal human subjects,25Trolin S. Anden T. Hendenstierna G. Nitric oxide in expired air at rest and during exercise.Acta Physiol Scand. 1994; 151: 159-163Crossref PubMed Scopus (43) Google Scholar, 26Bauer J.A. Wals J.A. Dorms S. et al.Endogenous nitric oxide in expired air: effects of acute exercise in humans.Life Sci. 1994; 55: 1903-1909Crossref PubMed Scopus (67) Google Scholar, 27Iwamoto J. Pendergast D.R. Suzuki H. et al.Effect of graded exercise on nitric oxide in expired air in humans.Respir Physiol. 1994; 97: 333-345Crossref PubMed Scopus (83) Google Scholar and positive correlation exists between diffusing capacity of carbon monoxide and exhaled NO.28Crenrona G. Higgenbottom T. Borland C. et al.Mixed expired nitric oxide in primary pulmonary hypertension in relation to lung diffusion capacity.QJM. 1994; 87: 547-551Google Scholar A rise in VNO has also been observed in women during the middle of the menstrual cycle.29Kharitanov S.A. Logan-Sinclair R.B. Busset C.M. et al.Peak expiratory nitric oxide differences in men and women: relation to menstrual cycle.Br Heart J. 1994; 72: 243-245Crossref Scopus (140) Google Scholar These changes are generally attributed to the activation of Nos3 in endothelial cells in response to increased capillary blood volume. An increase in the fractional concentration of NO is seen in such disease conditions as sinusitis, and vasomotor and allergic rhinitis due to the release of NO by the inflammatory cells.30Kharitanov S.A. Yates D. Barnes P.J. Increased nitric oxide in exhaled air of normal human subjects with upper respiratory tract infections.Eur Respir J. 1995; 8: 295-297Crossref Scopus (347) Google Scholar VNO increases during an asthma attack,31Kharitanov S.A. Yates D. Robbins R.A. et al.Increased nitric oxide in exhaled air of asthmatic patients.Lancet. 1994; 343: 133-135Abstract Scopus (1311) Google Scholar late asthmatic reactions,32Kharitanov S.A. O’Connor B.J. Evans D.J. et al.Allergen induced late asthmatic reactions are associated with elevation of exhaled nitric oxide.Am J Crit Care Med. 1995; 151: 1894-1899Crossref Scopus (293) Google Scholar and antigen-induced bronchospasm, and decreases after treatment with steroids.33Massaro A.F. Gaston B. Kita-Fanta C. et al.Expired nitric oxide levels during treatment for acute asthma.Am J Respir Crit Care Med. 1995; 152: 800-803Crossref PubMed Scopus (324) Google Scholar However, no rise in VNO is observed during early asthmatic response or bronchospasm after histamine challenge.34Kharitanov S.A. Evans D.J. Barnes P.J. et al.Bronchial provocation challenge with histamine or adenosine 5 monophosphate does not alter exhaled nitric oxide in asthma [abstract].Am J Respir Crit Care Med. 1995; 151: A125Google Scholar The increased NO in the expired air in these instances and in ARDS is attributed to activation of Nos2 in the inflammatory cells, although nonadrenergic, noncholinergic nerves also could be a source of NO in asthma. A decrease in VNO is noted in conditions with poor endothelial cell function. VNO is decreased in many subjects with coronary artery disease.35el Tamimi H. Mansour M. Wargovich T.J. et al.Usefulness of endogenous and exogenous nitric oxide to identify degrees of endothelial dysfunction in patients with stable angina pectoris.Am J Cardiol. 1994; 74: 600-603Abstract Full Text PDF Scopus (5) Google Scholar Reduced endothelial Nos in the lungs of patients with pulmonary hypertension has been reported.36Giaid A. Saleh D. Reduced expression of endothelial nitric oxide synthase in the lungs of patients with pulmonary hypertension.N Engl J Med. 1995; 333: 214-221Crossref PubMed Scopus (1215) Google Scholar Similarly, decreased VNO is noted in patients with pulmonary fibrosis37Cailes J.B. Kharitanov S. Yates D. et al.Decreased endogenous nitric oxide in the exhaled air of systemic sclerosis patients [abstract].Thorax. 1995; 50: 4528Google Scholar and in smokers.38Kharitanov S.A. Robbins R.A. Yates D. et al.Acute and chronic effects of cigarette smoking on exhaled nitric oxide.Am Rev Respir Crit Care Med. 1995; 152: 609-612Crossref Scopus (406) Google Scholar In this issue of CHEST (see page 44), Riley and colleagues report their findings on VNO in exhaled air in patients with primary pulmonary hypertension (PPH) and pulmonary fibrosis (PF). They noted a lower VNO at rest in PF subjects compared with normal subjects. In subjects with PPH, although the VNO at rest was the same as in normals, it failed to rise with exercise. Destruction of vascular endothelial cells in PF and deficiency of endothelial Nos3 or reduced capillary blood volume in PPH appear to be the most likely explanations for these findings, as postulated by the authors. Although they used an NO analyzer with a slower response time, which led to a delay between sampling and measurement, their results are compatible with known actions of NO in maintaining normal vascular tone and preventing microvascular proliferation. Similar results have been reported by others, but the present work is unique in comparing normal subjects and those with PPH and PF under similar settings. Riley and colleagues have contributed to the growing body of work suggesting a possible clinical role for measurements of NO in expired air. However, this will have to await the availability of accurate and relatively inexpensive analyzers with fast response and recording capabilities. Even when such equipment is available, the technique to avoid nasopharyngeal contamination would need to be standardized. The normal ranges of V˙NO and FNO in expired air and their response to exercise and other physiologic states and illnesses also must be clarified before measurements of NO can be used clinically. Nevertheless, this is an area of intense ongoing research and NO measurement may eventually become a useful pulmonary function test for airway inflammation, delayed type of hypersensitivity, nonadrenergic, noncholinergic nerve and endothelial cell function, and response to treatment." @default.
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• W2091940904 title "Just Say NO" @default.
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