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Titolo:
THE ROLE OF THE RATE OF VASCULAR COLLAPSE IN ISCHEMIA-INDUCED ACUTE CONTRACTILE FAILURE AND DECREASED DIASTOLIC STIFFNESS
Autore:
GALINANES M; HEARSE DJ; SHATTOCK MJ;
Indirizzi:
ST THOMAS HOSP,RAYNE INST LONDON SE1 7EH ENGLAND
Titolo Testata:
Journal of Molecular and Cellular Cardiology
fascicolo: 3, volume: 28, anno: 1996,
pagine: 519 - 529
SICI:
0022-2828(1996)28:3<519:TROTRO>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENERGY-METABOLISM; HEART; HYPOXIA; REPERFUSION; TRANSIENTS; MECHANISM; PRESSURE; RABBIT; FLOW;
Keywords:
VASCULAR COLLAPSE; ISCHEMIA; EARLY CONTRACTILE FAILURE; DIASTOLIC STIFFNESS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
16
Recensione:
Indirizzi per estratti:
Citazione:
M. Galinanes et al., "THE ROLE OF THE RATE OF VASCULAR COLLAPSE IN ISCHEMIA-INDUCED ACUTE CONTRACTILE FAILURE AND DECREASED DIASTOLIC STIFFNESS", Journal of Molecular and Cellular Cardiology, 28(3), 1996, pp. 519-529

Abstract

We investigated the contribution of the rate of vascular collapse to the early contractile failure and decreased diastolic stiffness induced by ischemia. Isolated rat hearts (n = 8/group), perfused at 37 degrees C with blood through a roller pump and paced at 320 beats/min, weresubjected to global ischemia either by switching off the roller pump (slow vascular collapse-group 1) or by reversing the direction of the roller pump for 5 s prior to switch-off (rapid vascular collapse-group2). In group 1, residual coronary pressure declined progressively over the first 20 s of ischemia whereas in group 2 the pressure had fallen to zero within 2 s. The profile of ischemia-induced contractile failure was, however, similar in both groups. Thus, after 2 s of ischemia,when residual perfusion pressure had declined by only 10% in group 1 (60.0 +/- 0.0 to 54.9 +/- 0.8 mmHg) but was virtually non-existent in group 2 (60.0 +/- 0.0 to 0.4 +/- 12.7 mmHg), left ventricular developed pressure had fallen to a similar extent in both groups (86 +/- 2% and 84 +/- 3%, respectively). Curve-fitting analysis for individual hearts showed that the profile of contractile failure was described by a double exponential process that was not significantly affected by the rapid vascular collapse, Left ventricular end-diastolic pressure in group 1 hearts progressively declined over the first 20 s of ischemia, the profile paralleling that of the dissipation of perfusion pressure. In contrast, in group 2 hearts, left ventricular end-diastolic pressurerose rapidly and peaked at 5 s, a period that coincided with the reversed direction of the perfusion pump. Similarly, in a separate study, the analysis of ventricular diastolic stiffness (n = 6/group) showed arapid decline during the first 20 s of ischemia; this decline could be inhibited by the use of rapid vascular collapse. In additional experiments, hearts (n = 8/group) were paced at 220, 320 or 420 beats/min and ischemia was induced by reversing (5 s) and then stopping the perfusion pump. Myocardial oxygen consumption increased in parallel with heart rate and was matched by commensurate increases in the rate of contractile failure. Curve-fitting analysis showed that slow stimulation rates (220 beats/min) significantly delayed contractile failure during the first 60 s of ischemia (first time constant = 14.5 +/- 4.1 s compared with 8.1 +/- 1.1 s at 320 beats/min and 6.3 +/- 1.1 s at 420 beats/min; P<0.05 in both instances). In conclusion, vascular collapse associated with ischemia may contribute to the initial decrease in ventricular diastolic stiffness; however, it does not play a major role in determining the rate of acute contractile failure. Metabolic processes, as reflected by oxygen consumption, do, however, appear to be important. (C) 1996 Academic Press Limited

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 07:01:49