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Titolo:
INHIBITION OF MYOCARDIAL CROSSBRIDGE CYCLING BY HYPOXIC ENDOTHELIAL-CELLS - A POTENTIAL MECHANISM FOR MATCHING OXYGEN-SUPPLY AND DEMAND
Autore:
SHAH AM; MEBAZAA A; YANG ZK; CUDA G; LANKFORD EB; PEPPER CB; SOLLOTT SJ; SELLERS JR; ROBOTHAM JL; LAKATTA EG;
Indirizzi:
UNIV WALES COLL MED,DEPT CARDIOL,HEATH PK CARDIFF CF4 4XN S GLAM WALES NIA,CARDIOVASC SCI LAB,GERONTOL RES CTR,NATL INST HLTH BALTIMORE MD 21224 JOHNS HOPKINS MED INST,PULM ANESTHESIA LAB BALTIMORE MD 21205 NHLBI,MOL CARDIOL LAB,NATL INST HLTH BETHESDA MD 20892 UNIV PENN,SCH MED,SCH MED,CARDIOVASC SECT PHILADELPHIA PA 19104 LARIBOISIERE HOSP,DEPT ANESTHESIOL PARIS FRANCE
Titolo Testata:
Circulation research
fascicolo: 5, volume: 80, anno: 1997,
pagine: 688 - 698
SICI:
0009-7330(1997)80:5<688:IOMCCB>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT-HEART MYOCYTES; PROTEIN KINASE-C; CARDIAC MYOCYTES; NITRIC-OXIDE; CONTRACTILE FAILURE; BLOOD-FLOW; HYPERTROPHIC CARDIOMYOPATHY; CORONARY VASODILATATION; MUSCLE-CONTRACTION; BETA-MYOSIN;
Keywords:
CARDIAC CONTRACTION; HYPOXIA; ENDOTHELIAL CELL; HIBERNATION; MYOFILAMENT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
62
Recensione:
Indirizzi per estratti:
Citazione:
A.M. Shah et al., "INHIBITION OF MYOCARDIAL CROSSBRIDGE CYCLING BY HYPOXIC ENDOTHELIAL-CELLS - A POTENTIAL MECHANISM FOR MATCHING OXYGEN-SUPPLY AND DEMAND", Circulation research, 80(5), 1997, pp. 688-698

Abstract

Previous studies have shown that cardiac endothelial cells release substances that influence myocardial contraction. Since PO2 is an important stimulus that modulates endothelial function, we investigated the effects of acute moderate hypoxia and reoxygenation on the release of cardioactive factors by endothelial cells. Endothelial cells cultured from several vascular beds were superfused with normoxic (equilibratedwith room air; PO2, approximate to 160 mm Hg) or hypoxic (PO2, 40 to 50 mm Hg) physiological buffer solution, and the superfusates were reequilibrated to a PO2 of approximate to 160 mm Hg and then tested for their effects on various myocardial assays. Endothelial cell viability and buffer ionic composition were unaltered after the superfusion procedures. The superfusates of hypoxic endothelial cells induced rapid, potent, reversible inhibition of isolated cardiac myocyte contraction without reducing cytosolic Ca2+ transients. This activity was not lost after heating (95 degrees C) and was present in low molecular weight (M-r, <500) superfusate fractions. Hypoxic endothelial superfusate reduced unloaded shortening velocity of human skinned soleus muscle fibers. It markedly depressed in vitro actin motility over cardiac myosin and reduced the rate of actin-activated cardiac myosin ATPase activity but had no effect on corresponding smooth muscle myosin assays. Reoxygenation of hypoxic endothelial cells resulted in loss of this inhibitory activity. These data indicate that cultured endothelial cells respond to acute moderate hypoxia by releasing an unidentified substance(s) that inhibits myocardial crossbridge cycling, independent of Ca2+ or other second messenger signaling pathways. Such a mechanism could have important implications for the regulation of oxygen supply-demand balance in the heart and be relevant to conditions such as myocardial hibernation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 20:09:23