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Titolo:
THE ROLE OF NITRIC-OXIDE IN REGULATION OF DEFORMABILITY OF RED-BLOOD-CELLS IN ACUTE-PHASE OF ENDOTOXEMIA IN RATS
Autore:
STARZYK D; KORBUT R; GRYGLEWSKI RJ;
Indirizzi:
JAGIELLONIAN UNIV,COLL MED,CHAIR PHARMACOL,16 GRZEGORZECKA 16 PL-31531 KRAKOW POLAND JAGIELLONIAN UNIV,COLL MED,CHAIR PHARMACOL PL-31531 KRAKOW POLAND
Titolo Testata:
Journal of Physiology and Pharmacology
fascicolo: 4, volume: 48, anno: 1997,
pagine: 731 - 735
SICI:
0867-5910(1997)48:4<731:TRONIR>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
DIFFRACTOMETER RHEODYN SSD; ERYTHROCYTE DEFORMABILITY;
Keywords:
RED BLOOD CELL DEFORMABILITY; SEPTIC SHOCK; LIPOPOLYSACCHARIDE (LPS); ERYTHROCYTE FRAGILITY; NITRIC OXIDE; NITRIC OXIDE SYNTHASE INHIBITORS;
Tipo documento:
Article
Natura:
Periodico
Citazioni:
8
Recensione:
Indirizzi per estratti:
Citazione:
D. Starzyk et al., "THE ROLE OF NITRIC-OXIDE IN REGULATION OF DEFORMABILITY OF RED-BLOOD-CELLS IN ACUTE-PHASE OF ENDOTOXEMIA IN RATS", Journal of Physiology and Pharmacology, 48(4), 1997, pp. 731-735

Abstract

Using the shear stress laser diffractometer (Rheodyn) we have studiedthe role of nitric oxide on erythrocyte deformability during the initial 10 min after the i.v. administration of LPS at a dose of 5 mg/kg. At the stress shear force of 30 Pa the control erythrocytes elongationindex (E) of untreated animals was 38% +/- 1.5 (mean +/- SD n = 6) while in LPS treated animals it was decreased to 33% +/- 1.8 (n = 6) indicating significant (p < 0.01) loos of red blood cell deformability. The loss of deformability was accompanied by increased fragility of erythrocyte membranes as measured by enhanced release of free hemoglobin (E-lambda 420 = 0.43 +/- 0.05 in control vs. E-lambda 420 = 0.65 +/- 0.07 in LPS group) from isolated erythrocytes exposed to centrifuging at a speed of 3000 rpm for 10 min. Inhibitor of NO-synthase, N-G-nitro-L arginine methyl ester (L-NAR?E; 10 mg/kg i.v.), significantly decreased deformability (Ei = 33.5 +/- 4.6, n = 6, p < 0.01) but did not influence fragility (E-lambda 420 = 0.36 +/- 0.14, n = 6) of erythrocytes. However, when L-NAME was administered 10 min. prior to LPS it significantly improved the LPS-impaired fragility (E-lambda 420 = 0.38 +/- 0.1, n = 6, p < 0.01) as compared to rats treated with LPS-alone (E-lambda 420 = 0.65 +/- 0.07, n = 6). A similar protective effect of L-NAMEwas observed for LPS-induced impairment of erythrocyte deformability. It is concluded that NO seems to influence deformability and fragility of erythrocytes at the first stage of sepsis. During an acute phase of LPS action, possibly reflected by stimulation of endothelial constitutive (ecNOS) but not inducible NO-synthase (iNOS), the excessive amount of NO leads to a damage of erythrocyte plasticity and then the pretreatment with L-NAME exerts a protective action on LPS-impaired deformability and fragility of erythrocytes. On the other hand, basal release of NO maintains erythrocyte deformability at the physiological range and lowering of the basal level of NO by NOS-inhibitors leads to impairment or erythrocyte deformability.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/07/20 alle ore 01:15:12