title: Persistence of the altered polymorphonuclear leukocyte rheological and metabolic variables after 12 months in juvenile myocardial infarction.
abstract: Acute myocardial infarction (AMI) is associated with an elevated polymorphonuclear leukocyte (PMN) count and a PMN rheological impairment. In this study we evaluated two major rheological aspects (membrane fluidity and cytosolic Ca2+ concentration) in a group of young adults with AMI. We enrolled 41 AMI patients (39 men and 2 women; mean age 41.0 +/- 4.0 years), who were examined 5-10 days after AMI (T1) and 12 months later (T2). The membrane fluidity was obtained labelling granulocytes with the fluorescent probe 1-[4-(trimethylamino)phenyl]-6-phenyl-1,3,5-hexatriene (TMA-DPH) and considering the degree of fluorescence polarization, inversely correlated to the membrane lipid fluidity. The cytosolic Ca2+ content was obtained marking PMN cells with the fluorescent probe Fura-2AM and considering the ratio between the Fura 2-Ca2+ complex and the unchelated Fura 2 fluorescence intensity. Both parameters were evaluated at baseline and after in vitro activation with 4-phorbol 12-myristate 13-acetate (PMA) at the concentration of 4.5 muM, prolonged for 5 and 15 minutes. At T1 the PMN membrane fluidity and cytosolic Ca2+ content in AMI patients were respectively decreased and increased in comparison with control group. At T2 the membrane fluidity was not any more different from control subjects, but there was also a further increase in cytosolic Ca2+ content. In vitro, PMN activation caused no significant variation of these parameters in the control group, while in AMI patients membrane fluidity significantly decreased and cytosolic Ca2+ content increased not only during the initial stage, but also after 12 months. The long-term functional alteration of PMN cells observed in young adults with AMI confirms the role of these cells in the inflammatory response following AMI. In the light of these data, the use of molecules able to modulate granulocyte activity, such as calcium channel blockers or pentoxifylline, should be reconsidered in myocardial infarction, together with the usual pharmacological treatment.
authors.affiliation: Dipartimento di Medicina Interna, Malattie Cardiovascolari e Nefrourologiche, Università degli Studi di Palermo, Italy.
authors.forename: Rosalia
authors.initials: R
authors.lastname: Lo Presti
authors.forename: Maria Giuliana
authors.initials: MG
authors.lastname: Tozzi Ciancarelli
authors.forename: Enrico
authors.initials: E
authors.lastname: Hoffmann
authors.forename: Egle
authors.initials: E
authors.lastname: Incalcaterra
authors.forename: Baldassare
authors.initials: B
authors.lastname: Canino
authors.forename: Maria
authors.initials: M
authors.lastname: Montana
authors.forename: Teresa
authors.initials: T
authors.lastname: D'Amico
authors.forename: Anna
authors.initials: A
authors.lastname: Catania
authors.forename: Gregorio
authors.initials: G
authors.lastname: Caimi
mesh_terms: D000328:Adult; D017668:Age of Onset; D000704:Analysis of Variance; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D002118:Calcium / Q000032:analysis*; D002462:Cell Membrane / Q000502:physiology*; D003600:Cytosol / Q000737:chemistry; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology; D008297:Male; D008560:Membrane Fluidity; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*; D009504:Neutrophils / Q000737:chemistry / Q000378:metabolism* / Q000473:pathology; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D010975:Platelet Aggregation Inhibitors; D002118:Calcium