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Titolo:
IMPAIRED POSTHYPOXIC RELAXATION IN SINGLE CARDIAC MYOCYTES - ROLE OF INTRACELLULAR PH AND INORGANIC-PHOSPHATE
Autore:
BERTONI AG; ADRIAN S; MANKAD S; SILVERMAN HS;
Indirizzi:
JOHNS HOPKINS UNIV HOSP,DIV CARDIOL,600 N WOLFE ST BALTIMORE MD 21287 JOHNS HOPKINS UNIV HOSP,DIV CARDIOL,600 N WOLFE ST BALTIMORE MD 21287 UNIV PITTSBURGH,SCH MED PITTSBURGH PA 15261
Titolo Testata:
Cardiovascular Research
fascicolo: 11, volume: 27, anno: 1993,
pagine: 1983 - 1990
SICI:
0008-6363(1993)27:11<1983:IPRISC>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
CONTRACTILE FAILURE; METABOLIC INHIBITION; MYOCARDIAL HYPOXIA; FERRET HEART; RAT; MUSCLE; MECHANISM; CALCIUM; CELLS; REOXYGENATION;
Keywords:
HYPOXIA; REOXYGENATION; MYOCYTE; RELAXATION; PH; PHOSPHATE; MYOFILAMENTS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
36
Recensione:
Indirizzi per estratti:
Citazione:
A.G. Bertoni et al., "IMPAIRED POSTHYPOXIC RELAXATION IN SINGLE CARDIAC MYOCYTES - ROLE OF INTRACELLULAR PH AND INORGANIC-PHOSPHATE", Cardiovascular Research, 27(11), 1993, pp. 1983-1990

Abstract

Objective: The aim was to examine the effects of alterations in intracellular pH and inorganic phosphate concentration (known to influence myofilament kinetics and to change rapidly during hypoxia) on cell contraction relaxation, and the Ca'' transient in normoxic and hypoxic myocytes. Methods: Single adult rat ventricular myocytes were electrically stimulated (0.2 Hz) and cell length (photodiode array), intracellular Ca2+ (indo-I fluorescence), or intracellular pH (SNARF-I fluorescence) measured. Hypoxia was induced in a special open chamber in which alaminar layer of argon prevented the back diffusion of atmospheric oxygen. Results: Electrically stimulated contraction was preserved during exposure to hypoxia. At reoxygenation 10 minutes later the time fromthe stimulus to the peak of contraction (TPK) increased by 30(SEM 9)%and the time from the peak of contraction to 50% recovery of cell length (RT50) increased by 59(13)% relative to prehypoxic values (n = 8). These changes were not accompanied by a change in the kinetics of theCa2+ transient. pH(i) fell from a baseline of 7.33(0.04) to 7.25(0.03) during hypoxia and then overshot to 7.44(0.03) at reoxygenation (n =5). Since an intracellular alkalosis can slow myofilament relaxation,proton extrusion routes were blocked to examine posthypoxic relaxation in the absence of an alkalosis. Despite inhibition of the pH(i) overshoot, posthypoxic relaxation remained impaired. Intracellular inorganic phosphate levels were manipulated in two protocols (2-deoxyglucose to ''trap'' phosphate and Tris(hydroxymethyl)-aminomethane to buffer phosphate) and both TPK and RT50 increased in normoxic cells. Having established that these two interventions, which would be expected to decrease intracellular inorganic phosphate, result in a slowing of relaxation, myocytes were first phosphate loaded (exposed to 5.0 mM phosphate) and then made hypoxic and reoxygenated after 10 min to blunt the expected fall in phosphate accompanying reoxygenation. This led to a reduction in the slowing of contraction and relaxation following reoxygenation [TPK increased by 7(5)% and RT50 by 17(9)%, n = 8; p < 0.05 v cells studied in control buffer]. Conclusions: Impaired posthypoxic relaxation is not the result of changes in pH(i) but is attenuated by phosphate loading of cells and may be due to a rapid decrease in intracellular phosphate accompanying the resynthesis of high energy phosphates at reoxygenation.

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Documento generato il 28/11/20 alle ore 23:44:05