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Titolo:
Lack of direct role for calcium in ischemic diastolic dysfunction in isolated hearts
Autore:
Eberli, FR; Stromer, H; Ferrell, MA; Varma, N; Morgan, JP; Neubauer, S; Apstein, CS;
Indirizzi:
Boston Univ, Sch Med, Cardiac Muscle Res Lab, Boston, MA 02118 USA Boston Univ Boston MA USA 02118 diac Muscle Res Lab, Boston, MA 02118 USA Med Univ Klin, Wurzburg, Germany Med Univ Klin Wurzburg GermanyMed Univ Klin, Wurzburg, Germany Harvard Univ, Sch Med, Boston, MA USA Harvard Univ Boston MA USAHarvard Univ, Sch Med, Boston, MA USA
Titolo Testata:
CIRCULATION
fascicolo: 21, volume: 102, anno: 2000,
pagine: 2643 - 2649
SICI:
0009-7322(20001121)102:21<2643:LODRFC>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTRACELLULAR CALCIUM; METABOLIC INHIBITION; RAT-HEART; RELAXATION RATE; RABBIT HEARTS; CONTRACTURE; CELLS; REPERFUSION; MYOCARDIUM; TRANSIENTS;
Keywords:
ischemia; calcium; diastole;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
27
Recensione:
Indirizzi per estratti:
Indirizzo: Eberli, FR Univ Hosp Bern, Swiss Cardiovasc Ctr Bern, CH-3010 Bern, Switzerland Univ Hosp Bern Bern Switzerland CH-3010 010 Bern, Switzerland
Citazione:
F.R. Eberli et al., "Lack of direct role for calcium in ischemic diastolic dysfunction in isolated hearts", CIRCULATION, 102(21), 2000, pp. 2643-2649

Abstract

Background-Ischemia is characterized by an increase in intracellular calcium and occurrence of diastolic dysfunction. We investigated whether the myocyte calcium level is an important direct determinant of ischemic diastolicdysfunction. Methods and Results-We exposed isolated, perfused isovolumic (balloon in left ventricle) rat and rabbit hearts to low-flow ischemia and increased extracellular calcium (from 1.5 to 16 mmol/L) for brief periods. Intracellularcalcium was measured by aequorin. Low-flow ischemia resulted in a 270% increase (P<0.05) in diastolic intracellular calcium, a 50% (P<0.05) calcium transient amplitude decrease, and a 52% (P<0.05) slowing of calcium transient decline. Diastolic pressure increased by 6+/-2 mm Hg (P<0.05), and rate of systolic pressure decay decreased by 65% (P<0.05). Experimentally increasing extracellular calcium doubled both intracellular diastolic calcium and calcium transient amplitude, concomitant with a developed pressure increase; however, there was no increase in ischemic diastolic pressure, slowing ofthe calcium transient decay, or further slowing of systolic pressure decay. Similarly, after 45 minutes of low-flow ischemia, after diastolic pressure had increased from 8.5+/-0.6 to 19.7+/-3.5 mm Hg (P<0.001), intracoronaryhigh-molar calcium chloride infusion increased systolic pressure from 36+/-4 to 63+/-11 mmHg (P<0.001), indicating an increase in intracellular calcium, but it decreased diastolic pressure from 19.7+/-3.5 to 17.5+/-3.7 mmHg (P<0.01). Conversely, EGTA infusion decreased systolic pressure, indicatinga decrease in intracellular calcium, but did not decrease diastolic pressure. Conclusions-When calcium availability was experimentally altered during ischemia, there was no alteration in left ventricular diastolic pressure, suggesting that ischemic diastolic dysfunction is not directly mediated by a calcium activated tension.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/09/20 alle ore 00:23:10