This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sánchez de Miguel, L. Articles by López-Farré, A. Search for Related Content PubMed PubMed Citation Articles by Sánchez de Miguel, L. Articles by López-Farré, A.

CLINICAL STUDY: ACUTE CORONARY SYNDROMES

Nitric oxide production by neutrophils obtained from patients during acute coronary syndromes: expression of the nitric oxide synthase isoforms

Lourdes Sánchez de Miguel, PhD, M. a Mar Arriero, PhD^*, Jerónimo Farré, MD, PhD, Petra Jiménez, PhD, Antonio García-Méndez, PhD, Trinidad de Frutos, PhD, Ana Jiménez, PhD, Rosa García, PhD, Fernando Cabestrero, MD, Juan Gómez, MD, Raimundo de Andrés, MD, Mercedes Montón, PhD^*, Edita Martín, RN, Luz M. De la Calle-Lombana, RN, Luis Rico, MD, José Romero, MD and Antonio López-Farré, PhD^*,*

^* Cardiovascular Research and Hypertension Laboratory, Fundación Jiménez Díaz, Madrid, Spain
Cardiology Department, Fundación Jiménez Díaz, Madrid, Spain
Cardiovascular Research Hypertension Laboratory, Emergency Department, Fundación Jiménez Díaz, Madrid, Spain
Cardiovascular Research Hypertension Laboratory, Internal Medicine Department, Fundación Jiménez Díaz, Madrid, Spain

Manuscript received May 18, 2001; revised manuscript received November 20, 2001, accepted December 6, 2001.

^* Reprint requests and correspondence: Dr. Antonio López-Farré, Fundación Jiménez Díaz, Cardiovascular Research and Hypertension Laboratory, Avda. Reyes Católicos, 2, 28040 Madrid, Spain.
alopeza{at}fjd.es

OBJECTIVES: To analyze the differences in the nitric oxide (NO) forming system between neutrophils obtained from patients during unstable angina (UA) and during acute myocardial infarction (AMI).

BACKGROUND: Neutrophils are involved in the regulation of thrombus formation through the release of active substances such as NO. Acute myocardial infarction is the result of an occlusive thrombus; unstable angina is attributed to intermittent thrombus formation.

METHODS: We studied 49 patients admitted to hospital within 24 h after the onset of chest pain: 31 experienced AMI and 18 experienced UA. Acute myocardial infarction was defined as CK greater than two-fold the upper limit of normal value of biochemical laboratory, with CK-MB >10% total CK. Unstable angina was defined as transient ST segment changes without significant increases in CK and CK-MB.

RESULTS: The amount of NO generated by neutrophils from AMI patients was significantly higher than that generated by neutrophils from UA patients. Neutrophils from UA and AMI patients showed low levels of endothelial-like NO synthase protein expression and a marked expression of the inducible NO synthase (iNOS) isoform. Although neutrophils from patients during acute coronary syndromes generated high amounts of NO, they did not demonstrate an increased ability to stimulate cyclic guanosine monophosphate (cGMP) synthesis in platelets. This lack of activity to release NO by neutrophils from patients during AMI was unrelated to a defect in the platelet cGMP-forming system; sodium nitroprusside, an exogenous NO donor, similarly increased cGMP levels in platelets from AMI patients and healthy donors.

CONCLUSIONS: Neutrophils from patients during AMI and UA showed an increased production of NO and a marked expression of the iNOS isoform. However, NO released from these neutrophils showed a deficient functionality. These findings could have clinical implications because they show differences in thrombus growth in patients with UA versus patients with AMI.

Abbreviations and Acronyms   cGMP   AMI   acute myocardial infarction   cGMP   cyclic guanosine monophosphate   eNOS   endothelial nitric oxide synthase   iNOS   inducible nitric oxide synthase   NO   nitric oxide   PRP   platelet-rich plasma   SOD   superoxide dismutase   UA   unstable angina

This article has been cited by other articles:

				L. Nunez, M. Vaquero, R. Gomez, R. Caballero, P. Mateos-Caceres, C. Macaya, I. Iriepa, E. Galvez, A. Lopez-Farre, J. Tamargo, et al. Nitric oxide blocks hKv1.5 channels by S-nitrosylation and by a cyclic GMP-dependent mechanism Cardiovasc Res, October 1, 2006; 72(1): 80 - 89. [Abstract] [Full Text] [PDF]

				K. E. Wyche, S. S. Wang, K. K. Griendling, S. I. Dikalov, H. Austin, S. Rao, B. Fink, D. G. Harrison, and A. M. Zafari C242T CYBA Polymorphism of the NADPH Oxidase Is Associated With Reduced Respiratory Burst in Human Neutrophils Hypertension, June 1, 2004; 43(6): 1246 - 1251. [Abstract] [Full Text] [PDF]

				T. H. Han, E. Qamirani, A. G. Nelson, D. R. Hyduke, G. Chaudhuri, L. Kuo, and J. C. Liao Regulation of nitric oxide consumption by hypoxic red blood cells PNAS, October 14, 2003; 100(21): 12504 - 12509. [Abstract] [Full Text] [PDF]

				G. Cotter, E. Kaluski, O. Milo, A. Blatt, A. Salah, A. Hendler, R. Krakover, A. Golick, and Z. Vered LINCS: L-NAME (a NO synthase inhibitor) In the treatment of refractory Cardiogenic Shock: A prospective randomized study Eur. Heart J., July 2, 2003; 24(14): 1287 - 1295. [Abstract] [Full Text] [PDF]

				E. Courtois, M. Marques, A. Barrientos, S. Casado, and A. Lopez-Farre Lead-Induced Downregulation of Soluble Guanylate Cyclase in Isolated Rat Aortic Segments Mediated by Reactive Oxygen Species and Cyclooxygenase-2 J. Am. Soc. Nephrol., June 1, 2003; 14(6): 1464 - 1470. [Abstract] [Full Text] [PDF]