Mechanical restitution in isolated mammalian myocardium: Species differences and underlying mechanisms

Cooper, Ian; Fry, Christopher

doi:10.1016/0022-2828(90)91479-q

Cited by 48 publications

(27 citation statements)

References 32 publications

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“…This sensitivity, together with the calcium compartment models described in a simplified form above, have been used by a number of investigators to gain insights into myocardial calcium handling in a number of different situations (23,36,37,43,44). We similarly have used the force-interval relationship as an indirect measure of myocardial calcium handling in our experiments.…”

Section: Discussionmentioning

confidence: 99%

Myocardial protection after whole body heat stress in the rabbit is dependent on metabolic substrate and is related to the amount of the inducible 70-kD heat stress protein.

Marber¹,

Walker²,

Latchman³

et al. 1994

J. Clin. Invest.

117

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The aims of this study were to examine the effects of whole body heat stress and subsequent stress protein induction on glycolytic metabolism, mitochondrial metabolism, and calcium handling within the heart. The effect of heat stress on glycolytic and mitochondrial pathways was examined by measuring contractile performance in the presence of glucose and pyruvate, respectively. Calcium handling was assessed using force-interval relationships. Right ventricular papillary muscles taken from heat-stressed and control rabbit hearts were superfused with Kreb's solution containing either glucose or pyruvate and rendered hypoxic for 30 min. After reoxygenation, the greatest recovery of contractile function occurred in the heat-stressed muscles with pyruvate as substrate; there was, however, no difference in the force-interval relationship between the groups. The degree of contractile recovery was related to the content of the inducible 70-kD but not the 65-kD, heat stress protein. This study suggests that heat stress enhances the ability of rabbit papillary muscle to use pyruvate, but not glucose, after reoxygenation, and that the differences seen in contractility may be secondary to induction of the 72-kD stress protein.(J. Clin. Invest. 1994. 93:1087-1094

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Section: Discussionmentioning

confidence: 99%

Myocardial protection after whole body heat stress in the rabbit is dependent on metabolic substrate and is related to the amount of the inducible 70-kD heat stress protein.

Marber¹,

Walker²,

Latchman³

et al. 1994

J. Clin. Invest.

117

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“…Isoprenaline has been reported to accelerate deactivation of i K in rabbit sinoatrial node cells and guinea-pig ventricular cells, 26,27 and in human ventricular muscle, adrenaline accelerates the mechanical restitution curve. 28 This suggests that adrenaline accelerates the recovery of the Ca 2ϩ transient, and, in turn, this is expected to accelerate recovery of inward i NaCa . Alternatively, the increase in the steepness of APD restitution by isoprenaline and adrenaline could be the result of their well-known increase of i Ca,L .…”

Section: Underlying Mechanismsmentioning

confidence: 99%

Effect of Adrenergic Stimulation on Action Potential Duration Restitution in Humans

et al. 2003

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Background-Enhanced sympathetic activity facilitates complex ventricular arrhythmias and fibrillation. The restitution properties of action potential duration (APD) are important determinants of electrical stability in the myocardium. Steepening of the slope of APD restitution has been shown to promote wave break and ventricular fibrillation. The effect of adrenergic stimulation on APD restitution in humans is unknown. Methods and Results-Monophasic action potentials were recorded from the right ventricular septum in 18 patients.Standard APD restitution curves were constructed at 3 basic drive cycle lengths (CLs) of 600, 500, and 400 ms under resting conditions and during infusion of isoprenaline (15 patients) or adrenaline (3 patients). The maximum slope of the restitution curves was measured by piecewise linear regression segments of sequential 40-ms ranges of diastolic intervals in steps of 10 ms. Under control conditions, the maximum slope was steeper at longer basic CLs; eg, mean values for the maximum slope were 1.053Ϯ0.092 at CL 600 ms and 0.711Ϯ0.049 at CL 400 ms (ϮSEM). Isoprenaline increased the steepness of the maximum slope of APD restitution, eg, from a maximum slope of 0.923Ϯ0.058 to a maximum slope of 1.202Ϯ0.121 at CL 500 ms. The effect of isoprenaline was greater at the shorter basic CLs. A similar overall effect was observed with adrenaline. Conclusions-The

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“…The third phase of force decline reflects loss of Ca2+ from the cell (Wendt-Gallitelli 1986;Schouten 1990). In rat heart muscle it is very slow and occurs only after intervals lasting several minutes, whereas in guinea-pig or human ventricular myocardium it may be observed already after a few seconds of rest (Schouten 1990;Cooper & Fry 1990). The contribution of these three phases to mechanical restitution, the degree of potentiation and its decay are typical for heart muscle from various regions of the heart and for different species (Cooper & Fry 1990).…”

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confidence: 99%

Mechanical Restitution in Atrial Muscle from Human and Rat Hearts: Effects of Agents that Modify Sarcoplasmic Reticulum Function

Ravens¹,

Gath²,

Hussaini³

et al. 1997

Pharmacology & Toxicology

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Abstract; Force of contraction (F,) of isolated human and rat atrial myocardium shows characteristic patterns of mechanical restitution when single test intervals are interposed in regular stimulation. With several pharmacological agents that modify the function of the sarcoplasmic reticulum we have investigated the role of the sarcoplasmic reticulum in mechanical restitution in these two species. Caffeine, thapsigargin and 2,5-di-(terr-butyl)-l ,4-benzohydroquinone (BHQ) were used to reduce Ca'+ uptake, ryanodine to open Ca2+ release channels, and forskolin to stimulate Ca'+ uptake. Under control conditions, F, recovered rapidly with test intervals shorter than steady-state. and was potentiated with longer than steadystate intervals. In human atrial tissue the maximum potentiation factor was 1.2620.03 after a mean test interval of 9.70% 1.55 s (n=43) as compared to 3.07%0.45 after 30 sec. in rat atria (n=48). Caffeine (3 mM) did not significantly affect steady-state F, but abolished post-rest potentiation in human and rat preparations. Forskolin ( I pM) enhanced and accentuated the mechanical restitution curve in particular for short test intervals. In the presence of thapsigargin (10 pM), steady-state F, and mechanical restitution could not be distinguished from time-matched controls exposed to solvent only.indicating that this agent is ineffective in human and rat atrial tissue. In contrast, the putative Ca2+ uptake inhibitor BHQ (100 pM) strongly reduced steady-state F, and decreased potentiation at all intervals in human muscle, but shifted the mechanical restitution curve in parallel to lower values in rat atria. Ryanodine (10 nM) induced post-rest decay in human and depressed both steady-state F, and post-rest potentiation in rat atrial muscle. From these results it is concluded that human and rat atrial muscle differ in the Ca2+ handling by the sarcoplasmic reticulum during mechanical restitution.In heart muscle, Ca2+ entry via L-type Ca2+ channels triggers the release of further Ca2+ from the sarcoplasmic reticulum. The increase in cytosolic C2+concentration activates contractile proteins for force production. During relaxation, Ca*+ is taken up again into the sarcoplasmic reticulum by the ATP-dependent Ca2+ pump and an amount equivalent to the systolic Ca" entry is transported out of the cell mainly via the Na+/Ca'+ exchanger. When regular pacing is disturbed by a single test pulse of variable interval, force of contraction (F,) changes in a characteristic pattern. The relationship between force of an interposed contraction and the preceding test interval is referred to as mechanical restitution. It consists of three phases (Schouten 1990): The initial one is a short and rapid phase of recovery for intervals shorter than steady-state. The second phase during which F, is potentiated with longer than regular intervals is followed by a third phase of force decline (post-rest decay).The adaptive changes in F, during mechanical restitution are considered to represent a physiological correlate of cellular Ca...

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Mechanical restitution in isolated mammalian myocardium: Species differences and underlying mechanisms

Cited by 48 publications

References 32 publications

Myocardial protection after whole body heat stress in the rabbit is dependent on metabolic substrate and is related to the amount of the inducible 70-kD heat stress protein.

Myocardial protection after whole body heat stress in the rabbit is dependent on metabolic substrate and is related to the amount of the inducible 70-kD heat stress protein.

Effect of Adrenergic Stimulation on Action Potential Duration Restitution in Humans

Mechanical Restitution in Atrial Muscle from Human and Rat Hearts: Effects of Agents that Modify Sarcoplasmic Reticulum Function

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