The metabolic consequences of an increase in the frequency of stimulation in isolated ferret hearts.

Elliott, A.; Smith, Godfrey L.; Allen, David G.

doi:10.1113/jphysiol.1994.sp020009

Cited by 36 publications

(25 citation statements)

References 35 publications

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“…Changes of cardiac pH i will occur during whole body acid-base disturbances (25) and during changes in the metabolic workload placed on the heart (2,8). A large drop in pH i also occurs during myocardial ischemia, where it accounts for much of the observed inotropic decline (1,9).…”

mentioning

confidence: 99%

Novel method for measuring junctional proton permeation in isolated ventricular myocyte cell pairs

Swietach

Vaughan‐Jones

2004

American Journal of Physiology-Heart and Circulatory Physiology

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mentioning

confidence: 99%

Novel method for measuring junctional proton permeation in isolated ventricular myocyte cell pairs

Swietach

Vaughan‐Jones

2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…The low rate of stimulation was chosen to minimize the consequences of the low O 2 content of the perfusate which lacks haemoglobin [1]. It has been shown that stimulation at 2 Hz compared to 5 Hz leads to improved metabolite levels in the isolated heart [8] and that the ischemic contracture occurs earlier in hearts stimulated at 5 Hz compared to 2 Hz [45]. Isovolumic left ventricular developed pressure (LVDP) was monitored with a balloon in the left ventricle.…”

Section: Methodsmentioning

confidence: 99%

The cardioprotective effects of Na + /H + exchange inhibition and mitochondrial K ATP channel activation are additive in the isolated rat heart

Xiao

Allen

2003

Pfl�gers Archiv European Journal of Physiology

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The mechanisms of recovery of the isolated rat heart were studied after 30 min of global ischemia. Functional recovery was assessed by the percentage recovery of developed pressure after 30 min reperfusion and by the magnitude of the contracture on reperfusion. After a control ischemia, developed pressure recovered to only 12+/-2% of pre-ischemic control and the reperfusion contracture was very large (81+/-6 mmHg). Activation of the mitochondrial KATP channel with 100 microM diazoxide present throughout ischemia and reperfusion improved recovery of developed pressure to 36+/-3% and reduced the reperfusion contracture (53+/-4 mmHg). Inhibition of the sodium/hydrogen exchanger with 10 microM cariporide caused a larger recovery of developed pressure to 72+/-4% and further reduced the reperfusion contracture (11+/-3 mmHg). The combination of both drugs increased recovery of developed pressure to 96+/-4% and the reperfusion contracture remained small (11+/-5 mmHg). The effectiveness of the timing of exposure to these drugs was explored. When both diazoxide and cariporide were applied 2 min before the end of ischaemia and remained present during reperfusion the recovery of developed pressure was 81+/-4% and the reperfusion contracture was small (12+/-3 mmHg); neither was significantly different to the recovery when both drugs were present throughout ischemia and reperfusion. We conclude that mitochondrial damage, blocked by diazoxide, and the coupled exchanger pathway, blocked by cariporide, are two of the principal damage pathways and functional recovery appears to be complete when both are blocked. The combination of these drugs is also highly effective when given 2 min before the end of ischemia.

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“…The low rate of stimulation was chosen to minimise the consequences of the low O 2 content of the perfusate that lacked haemoglobin [1]. Stimulation at 2 Hz compared with 5 Hz leads to improved metabolite levels in the isolated heart [8] and the ischaemic contracture occurs earlier in hearts stimulated at 5 than at 2 Hz [43]. Isovolumic left ventricular developed pressure (LVDP) was monitored with a balloon in the left ventricle.…”

Section: Methodsmentioning

confidence: 99%

The role of endogenous angiotensin II in ischaemia, reperfusion and preconditioning of the isolated rat heart

Xiao

Allen

2003

Pflugers Arch - Eur J Physiol

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We examined the possibility that endogenous angiotensin II (AII) is involved in the regulation of the cardiac Na(+)/H(+) exchanger (NHE1) during ischaemia, reperfusion and preconditioning. Mechanical function and intracellular sodium ([Na(+)](i)) were studied in isolated, perfused rat hearts. To test whether AII production might underlie the increased activity of NHE1 on reperfusion, we applied the AII receptor antagonist losartan during ischaemia and reperfusion. Losartan significantly improved mechanical performance on reperfusion and reduced the peak [Na(+)](i) on reperfusion. It has been proposed that preconditioning inhibits the activity of NHE1 in early reperfusion. To test whether this might be because of impaired action of AII on NHE1 we applied AII throughout ischaemia and reperfusion in preconditioned hearts. AII abolished the improved mechanical recovery caused by preconditioning and the peak [Na(+)](i) on reperfusion was similar to that after ischaemia alone. Addition of the NHE1 antagonist cariporide or losartan simultaneously with AII, reversed the deleterious effects of AII on the preconditioned heart. These studies suggest that AII contributes to the activation of NHE1 in early reperfusion and that part of the beneficial effect of preconditioning may be attributed to the abolition of AII-induced activation of NHE1.

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The metabolic consequences of an increase in the frequency of stimulation in isolated ferret hearts.

Abstract: 1. The metabolic consequences of an increase in the frequency of stimulation were examined in isolated ferret hearts. Intracellular pH (pHj) and the intracellular concentrations of phosphocreatine ([PCr]

Cited by 36 publications

References 35 publications

Novel method for measuring junctional proton permeation in isolated ventricular myocyte cell pairs

Novel method for measuring junctional proton permeation in isolated ventricular myocyte cell pairs

The cardioprotective effects of Na + /H + exchange inhibition and mitochondrial K ATP channel activation are additive in the isolated rat heart

The role of endogenous angiotensin II in ischaemia, reperfusion and preconditioning of the isolated rat heart

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