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Titolo:
Role of NO and endothelin in hemoglobin-induced pulmonary vasoconstriction
Autore:
Heller, A; Ragaller, M; Schmeck, J; Fluth, H; Muller, M; Albrecht, DM; Koch, T;
Indirizzi:
Univesden,Carl Gustav Carus, Dept Anesthesiol & Intens Care Med, D-01307 Dr Univ Hosp Carl Gustav Carus Dresden Germany D-01307 Care Med, D-01307 Dr Univmanyp, Dept Anesthesiol & Operat Intens Care Med, D-68167 Mannheim, Ger Univ Hosp Mannheim Germany D-68167 ntens Care Med, D-68167 Mannheim, Ger
Titolo Testata:
SHOCK
fascicolo: 6, volume: 10, anno: 1998,
pagine: 401 - 406
SICI:
1073-2322(199812)10:6<401:RONAEI>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
CROSS-LINKED HEMOGLOBIN; NITRIC-OXIDE; CEREBRAL VASOSPASM; BASILAR ARTERIES; RABBIT; BLOOD; INHIBITION; RELEASE; CELLS; RAT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Heller, A UnivrHosp Carl Gustav Carus, Dept Anesthesiol & Intens Care Med,Fetscherst Univ Hosp Carl Gustav Carus Fetscherstr 74 Dresden Germany D-01307
Citazione:
A. Heller et al., "Role of NO and endothelin in hemoglobin-induced pulmonary vasoconstriction", SHOCK, 10(6), 1998, pp. 401-406

Abstract

The underlying mechanisms of hemoglobin (Hb)-induced vasoconstriction are not yet well understood. The aim of this study was to elucidate the influence of nitric oxide (NO) and endothelin (ET) on Hb-induced pulmonary vasoconstriction. Therefore, an autologous Hb preparation was administered into isolated rabbit lungs, in which pulmonary artery pressure (PAP) and weight gain was monitored. Either glyceroltrinitrate (GTN; 10(-5) M; n = 6), L-arginine (10(-2) M; n = 6), L-NAME (10(-4)M; n = 6), ETA- or ETB-receptor antagonists (BQ(123), 10(-6)M, n = 6) or (BQ(788), 10(-6) M, n = 6) were added tothe perfusion fluid and NOx and thromboxane A, levels were measured. Results: in the control group the Hb-stimulation resulted in a pressure responseup to 25.1 +/- 2.1 mmHg (p < .05), which was 136 +/- 6% of the reference value. The PAP increase was significantly (p < .05) blunted after GTN (71 +/- 5%), L-arginine (93 +/- 6%) and BQ(788) (88 +/- 7%). Pretreatment with L-NAME (139 +/- 13%) or BQ(123) (115 +/- 9%) did not show significant changesin PAP. Conclusion: The reduction of the Hb-induced pulmonary hypertensionby NO-donors points toward the inactivation of NO by free hemoglobin. Likewise, ETB-receptor mediated vasoconstrictive effects without changes in NOxconcentrations seem to play a pathogenetic role in the Hb-induced pulmonary vasoconstriction.

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Documento generato il 03/08/20 alle ore 12:51:24