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Titolo:
Effects of endotoxin on neutrophil-mediated ischemia/reperfusion injury inthe rat heart in vivo
Autore:
Lipton, BP; Delcarpio, JB; McDonough, KH;
Indirizzi:
Louisiana State Univ, Med Ctr, Dept Physiol, New Orleans, LA 70112 USA Louisiana State Univ New Orleans LA USA 70112 , New Orleans, LA 70112 USA Louisiana State Univ, Med Ctr, Dept Cell Biol & Anat, New Orleans, LA 70112 USA Louisiana State Univ New Orleans LA USA 70112 , New Orleans, LA 70112 USA
Titolo Testata:
EXPERIMENTAL BIOLOGY AND MEDICINE
fascicolo: 4, volume: 226, anno: 2001,
pagine: 320 - 327
SICI:
1535-3702(200104)226:4<320:EOEONI>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
ISCHEMIA-REPERFUSION INJURY; MONOPHOSPHORYL LIPID-A; MYOCARDIAL INFARCT SIZE; NITRIC-OXIDE; BACTERIAL LIPOPOLYSACCHARIDE; RABBIT CARDIOMYOCYTES; ENDOTHELIAL-CELLS; INDUCED TOLERANCE; ADENOSINE; DOGS;
Keywords:
endotoxin; LPS; L-selectin; myocardium; rat;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: McDonough, KH Louisiana State Univ, Med Ctr, Dept Physiol, 1901 Perdido St, New Orleans,LA 70112 USA Louisiana State Univ 1901 Perdido St New OrleansLA USA 70112
Citazione:
B.P. Lipton et al., "Effects of endotoxin on neutrophil-mediated ischemia/reperfusion injury inthe rat heart in vivo", EXP BIOL ME, 226(4), 2001, pp. 320-327

Abstract

We have previously shown that a nonlethal dose of lipopolysaccharide (LPS)decreases L-selectin expression of neutrophils (PMNs), thereby preventing PMN-mediated reperfusion injury in the isolated heart. In the present studywe determined whether or not that dose of LPS would protect hearts during in vivo ischemia and reperfusion by preventing PMN-induced reperfusion injury. Rats receiving saline vehicle showed marked myocardial injury (necroticarea/area at risk = 82% +/- 2%) and significant depression in left ventricular function as assessed in the isolated isovolumic heart preparation at constant flow rates of 5, 10, 15, and 20 ml/min, The administration of LPS (100 mug/kg body wt) 7 hr prior to ischemia resulted in a reduction in myocardial damage (necrotic area/area at risk = 42% +/- 3%) and preservation of function. Myocardial function was similar to that of sham ischemic saline- and LPS-treated rats. Moreover, PMN infiltration as determined by histologywas quantitatively more severe in hearts of saline-treated rats than in hearts of LPS-treated rats. Isolated hearts from vehicle- and LPS-treated animals undergoing sham ischemia in vivo recovered to the same extent after invitro ischemia/reperfusion, suggesting that LPS did not induce protection by altering intrinsic properties of the heart. Our results indicate that LPS-induced protection of the heart from in vivo PMN-mediated ischemia/reperfusion injury may be due to decreased L-selectin expression of PMNs in LPS-treated animals.

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Documento generato il 21/01/20 alle ore 01:07:00