Elevation in cytosolic free calcium concentration early in myocardial ischemia in perfused rat heart.

Steenbergen, Charles; Murphy, Elizabeth; Levy, Louis; London, Robert E.

doi:10.1161/01.res.60.5.700

Cited by 453 publications

(180 citation statements)

References 26 publications

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“…Our results are in agreement with ®ndings of previous studies showing a transcriptional and translational up-regulation of calpain I in the non-infarcted hypertrophied rat myocardium (Sandmann et al, 2001). Additionally, studies on rats demonstrated an increase in diastolic myocardial [Ca 2+ ] i in ventricular myocytes of the failing heart which were associated with cardiac hypertrophy following pressure overload (Gwathmey & Morgan, 1985;Steenbergen et al, 1987b) and MI (Sandmann et al, 1999). This might be related to an increased Ca 2+ -inward movement (Elliott et al, 1989;Sipido et al, 2000) and/or to a reduced Ca 2+ -reuptake by the sarcoplasmatic reticulum (SR) (De la Bastie et al, 1990;O'Rourke et al, 1999;Szymanska et al, 2000).…”

Section: Calpain I In the Non-infarcted Myocardium Post Misupporting

confidence: 93%

Activity profile of calpains I and II in chronically infarcted rat myocardium – influence of the calpain inhibitor CAL 9961

Sandmann

Prenzel

Shaw

et al. 2002

British J Pharmacology

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1 The calpains have been proposed to be activated following cardiac ischaemia and to contribute to myocyte damage after myocardial infarction (MI). In this study, the activity of calpains I and II in the infarcted and non-infarcted rat myocardium and the action of the selective calpain inhibitor, CAL 9961, has been investigated. 2 MI was induced by permanent ligation of the left coronary artery. One, 3, 7 and 14 days post MI, the enzymes calpain I and II were separated from homogenates of the interventricular septum (IS) and left ventricular free wall (LVFW) by chromatography on DEAE-Sepharose. The activity of the calpains was measured in sham-operated and MI animals chronically treated with placebo or CAL 9961 (15 mg kg 71 d 71 s.c.) in a synthetic substrate assay. Treatment was started 3 days before MI induction. 3 Calpain I activity reached highest values in IS 14 days post MI, whereas maximum activity of calpain II was measured in LVFW 3 days post MI. In experiments in vitro, CAL 9961 completely inhibited both calpains. In vivo, chronic treatment of MI animals with CAL 9961 partially prevented the increase in calpain I activity in IS and reduced calpain II activity in LVFW to sham levels. 4 Our ®ndings demonstrate that calpains I and II are activated after MI, however, both enzymes di er in their regional and temporal activation within the infarcted myocardium. Chronic inhibition of these enzymes with CAL 9961 might limit the calpain-induced myocardial damage and preserve cardiac structural integrity post MI.

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Section: Calpain I In the Non-infarcted Myocardium Post Misupporting

confidence: 93%

Activity profile of calpains I and II in chronically infarcted rat myocardium – influence of the calpain inhibitor CAL 9961

Sandmann

Prenzel

Shaw

et al. 2002

British J Pharmacology

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“…Subsequently, several studies*" 7 demonstrated that calcium channel antagonist agents protect against ventricular fibrillation during acute myocardial ischemia and following reperfusion of the acutely ischemic myocardium. In a recent communication, Steenbergen and coworkers 8 showed cytosolic free calcium to be increased within 10 minutes of acute global ischemia in the perfused rat heart. Definitive evidence has been presented that cytosolic calcium is increased within 10 minutes of reperfusion of the acutely ischemic cat heart.…”

mentioning

confidence: 97%

Ryanodine and caffeine prevent ventricular arrhythmias during acute myocardial ischemia and reperfusion in rat heart.

Thandroyen

McCarthy

Burton

et al. 1988

Circulation Research

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“…Steenbergen et al 28 investigated the ionic alterations in perfused hearts of rats undergoing preconditioning. The 2 study groups underwent 30min of global ischemia, and one of the groups was treated with 4 periods of 5-min ischemia with 5-min intervals of reperfusion (preconditioning) at 37 o C between them.…”

Section: Groupmentioning

confidence: 99%

“…Murry et al 8 reported that after 40min of ischemia, the production of lactate in preconditioned hearts was 40% lower than that in nontreated hearts. Steenbergen et al 28 suggest that this reduction in the production of lactate may be due to a lower acidification of the intracellular medium. A lower concentration of hydrogen may reduce intracellular sodium and calcium increase through Na + -H + and Na + -Ca +2 exchangers, respectively.…”

Section: Groupmentioning

confidence: 99%

Influence of ischemic preconditioning in myocardial protection in patients undergoing myocardial revascularization with intermittent crossclamping of the aorta. Analysis of ions and blood gases

Pêgo-Fernandes¹,

Jatene²,

Gentil³

et al. 2001

Arq. Bras. Cardiol.

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Objective -To test the hypothesis that short periods of ischemia may increase the myocardial protection obtained with intermittent crossclamping of the aorta. Methods -In the control group (18 patients)Despite theoretical criticism of the technique of intermittent crossclamping of the aorta with hypothermia at 32ºC, the simplicity of the procedure and its good clinical results have led several surgeons to use it, particularly in myocardial revascularization surgery 1,2 .In Brazil, Jatene et al 3 have been using it since 1969, with good clinical results. A few randomized studies 4,5 comparing the efficacy of intermittent crossclamping of the aorta with the use of cardioplegic solutions exist, but none of them conclude that one method is superior to the others.One question about the technique is that the repetition of ischemic episodes, which are individually reversible, may cause cumulative damage resulting in necrosis. Reimer et al 6 disproved this concept by showing experimentally that intermittent reperfusion avoids cumulative metabolic deficit and myocardial ischemia with cell death and that the first episode of ischemia reduces the consumption of high energy phosphates in subsequent episodes. Other studies 7 have shown that short periods of ischemia do not induce irreversible cellular damage and that they do not result in cumulative metabolic, structural, and functional deficits. It has also been reported that, paradoxically, short periods of ischemia increase the tolerance of the heart instead of making it more vulnerable to subsequent ischemic episodes. This induction of tolerance to ischemia is called ischemic preconditioning 8 .The objective of this study was to assess the influence of ischemic preconditioning on myocardial protection obtained with intermittent crossclamping of the aorta in patients undergoing myocardial revascularization.

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Elevation in cytosolic free calcium concentration early in myocardial ischemia in perfused rat heart.

Cited by 453 publications

References 26 publications

Activity profile of calpains I and II in chronically infarcted rat myocardium – influence of the calpain inhibitor CAL 9961

Activity profile of calpains I and II in chronically infarcted rat myocardium – influence of the calpain inhibitor CAL 9961

Ryanodine and caffeine prevent ventricular arrhythmias during acute myocardial ischemia and reperfusion in rat heart.

Influence of ischemic preconditioning in myocardial protection in patients undergoing myocardial revascularization with intermittent crossclamping of the aorta. Analysis of ions and blood gases

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