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Titolo:
POSTISCHEMIC FUNCTION AND PROTEIN-KINASE-C SIGNAL-TRANSDUCTION
Autore:
ROHS TJ; KILGORE KS; GEORGES AJ; BOLLING SF;
Indirizzi:
UNIV MICHIGAN HOSP,THORAC SURG SECT,TAUBMAN CTR 2120D,1500 E MED CTR DR,BOX 0344 ANN ARBOR MI 48109 UNIV MICHIGAN,MED CTR,THORAC SURG SECT ANN ARBOR MI 48109
Titolo Testata:
The Annals of thoracic surgery
fascicolo: 6, volume: 65, anno: 1998,
pagine: 1680 - 1684
SICI:
0003-4975(1998)65:6<1680:PFAPS>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
CARDIAC TROPONIN-I; ISOLATED RAT-HEART; ADENOSINE RECEPTORS; ACTOMYOSIN MGATPASE; RABBIT HEART; PHOSPHORYLATION; INFARCTION; INHIBITOR;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
22
Recensione:
Indirizzi per estratti:
Citazione:
T.J. Rohs et al., "POSTISCHEMIC FUNCTION AND PROTEIN-KINASE-C SIGNAL-TRANSDUCTION", The Annals of thoracic surgery, 65(6), 1998, pp. 1680-1684

Abstract

Background. The protective effects of myocardial preconditioning may occur by way of multiple mechanisms, with G-protein-mediated protein kinase C (PKC) translocation as a final common pathway. In this study we investigate the pharmacologic induction of preconditioning, by PKC translocation, using PKC agonists/antagonists to reveal its effects on contractile function after myocardial ischemia. Methods. Langendorff-perfused rabbit hearts received: (1) control; (2) dimethyl sulfoxide (vehicle); (3) acetylcholine (0.55 mmol/L; PKC agonist); (4) 1,2-s,n-dioctanoylglycerol (DOG; 22 mmol/L; PKC agonist); (5) chelerythrine (0.8 mmol/L; PKC antagonist); or (6) DOG-chelerythrine followed by a 2-hourischemic period, using modified St. Thomas cardioplegia and a 45-minute reperfusion period. The period of ischemia was chosen so as to allow for improvement by appropriate agonists. To observe metabolic changes, tissue nucleotides and nucleosides were measured. Membrane and cytosolic fractions of PKC were determined by an anti-PKC antibody directed against the PKC delta isozyme. Lactate levels and myocardial pH weremeasured. Results. The PKC agonists DOG and acetylcholine showed the greatest recovery of developed pressure (68% +/- 2%, 60% +/- 9%, respectively). Although pH, lactate, and nucleotide levels were similar between groups at all times, myocyte PKC translocation demonstrated 25% of PKC delta isoforms on cell membrane sites during baseline, which shifted to 67% +/- 17% with unprotected ischemia. DOG mimicked this shiftwith 58% +/- 12% of PKC delta isoforms on membranes, which was also blocked by chelerythrine to 35% +/- 7%. Conclusions. These data demonstrate that PKC translocation results in improved postischemic function,not by alteration of energetics or metabolism, and deserves further investigation. (C) 1998 by The Society of Thoracic Surgeons.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 07/07/20 alle ore 21:00:28