Unstimulated force during hypoxia of rat cardiac muscle: stiffness and calcium dependence

Leijendekker, W. J.; Gao, Wei Dong; Keurs, H. E. D. J. Ter

doi:10.1152/ajpheart.1990.258.3.h861

Cited by 7 publications

(18 citation statements)

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“…In this study, we also determined k m by use of sinusoidal muscle length perturbations at frequencies of 1 and 100 Hz. In an active muscle, k m , when measured at 100 Hz of length perturbations, increases as more cross bridges are attached, whereas k m at 1 Hz remains nearly the same compared with a nonactivated muscle (19,36). We have also shown previously that measurement of the k m ratio (100 over 1 Hz) is a sensitive method to establish whether active cross-bridge cycling is present.…”

Section: Force-[ca 2ϩmentioning

confidence: 54%

Increased cross-bridge cycling rate in stunned myocardium

Gao¹,

Dai²,

Nyhan³

2006

American Journal of Physiology-Heart and Circulatory Physiology

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Decreased Ca2+ responsiveness of the myofilaments underlies myocardial stunning. Given that cross-bridge cycling is a major determinant of myofilament behavior, we quantified cross-bridge cycling rate in stunned myocardium. After stabilization, rat hearts were subjected to 20 min of no-flow global ischemia and 30 min of reperfusion at 37 degrees C. Control hearts were perfused continuously at 37 degrees C for 60 min. Trabeculae were dissected and chemically skinned with 1% Triton X-100. The muscles were then activated with solutions of varied Ca2+ concentration ([Ca2+]). Force-[Ca2+] relations, rate of force redevelopment after release (k(tr)), muscle stiffness (k(m)), and myofilament ATP consumption were determined. Maximal Ca2+-activated force (Fmax) was depressed in stunned myocardium (49 +/- 5 vs. 82 +/- 5 mN/mm2, P < 0.01). Western immunoblotting showed degradation of troponin I in stunned myocardium. The k(tr) at Fmax was significantly increased in stunned muscles (19.82 +/- 2.74 vs. 13.19 +/- 0.96 s(-1), 22 degrees C, P < 0.01; 7.49 +/- 0.52 vs. 5.81 +/- 0.54 s(-1), 10 degrees C, P < 0.05). The ratio of k(m) measured at 100 Hz over that at 1 Hz, during Fmax, is lower in stunned muscles (8.22 +/- 1.56 vs. 12.94 +/- 0.71, P < 0.05). In comparison with k(m) at rigor, k(m) at Fmax is significantly lower in the stunned group (78.82 +/- 6.11 vs. 93.27 +/- 3.03%, P < 0.05). Myofilament ATP consumption at Fmax did not change in stunned muscles (5,901 +/- 952 vs. 5,596 +/- 972 pmol x microl(-1) x min(-1), P = 0.49). These results show that cross-bridge cycling is increased in stunned myocardium. Such increases are likely the result of increased transition rate from force-generating states to non-force-generating states. Thus stunned myocardium still maintains ATP consumption in spite of lower force development, rationalizing the long-standing paradox of decreased force but unchanged oxygen consumption in the postischemic heart.

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Section: Force-[ca 2ϩmentioning

confidence: 54%

Increased cross-bridge cycling rate in stunned myocardium

Gao¹,

Dai²,

Nyhan³

2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…To interrogate our data more completely, we utilized the index of cross-bridge cycling (index XB, Eq. 2) devised by Leijendekker et al (25) (Fig. 4).…”

Section: Resultsmentioning

confidence: 96%

“…Because of the well-documented small increase in the amplitude of stiffness with frequency of passive muscle tissue (19,34), index XB will always be Ͼ1. As the name implies, index XB increases with increasing crossbridge activity (25).…”

Section: Discussionmentioning

confidence: 98%

“…2), the ratio of high-frequency (in this instance, the average of 57-, 69-, 85-, and 100-Hz values) to low-frequency (in this instance, the average of 0.78-, 0.95-, 1.2-, and 1.4-Hz values) stiffness amplitude, has previously been used as an index of cross-bridge cycling (25). These indexes of cross-bridge cycling were calculated for the three interventions (groups) in the presence and absence of BDM.…”

Section: Discussionmentioning

confidence: 99%

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Effects of BDM, [Ca²⁺]_o, and temperature on the dynamic stiffness of quiescent cardiac trabeculae from rat

Kirton¹,

Taberner²,

Nielsen³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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([Ca 2ϩ ]o). More recently, the negative inotropic agent 2,3-butanedione monoxime (BDM) has been used. However, there remains a lack of data regarding the influence of temperature, Ca 2ϩ , and BDM on the passive mechanical properties of cardiac tissue. We have used the dynamic stiffness technique, a sensitive measurement of cross-bridge activity, in which minute (ϳ0.2% of muscle length) sinusoidal perturbations are applied at various frequencies (0.2-100 Hz) to quiescent, viable right ventricular rat trabeculae at two temperatures (20°C and 26°C) and at two [Ca 2ϩ ]o (0.5 and 1.25 mM) in the presence and absence of BDM (20 mM). The stiffness spectra (amplitude and phase) were sensitive to temperature and [Ca 2ϩ ]o in the absence of BDM but insensitive in the presence of BDM. From the index of cross-bridge cycling (the ratio of high-to low-frequency stiffness amplitude), we infer that BDM inhibits a small degree of spontaneous sarcomere activity, thereby allowing the true passive properties of trabeculae to be determined. In the absence of BDM, the extent of spontaneous sarcomere activity decreases with increasing temperature. We caution that the measured mechanical properties of passive cardiac tissue are critically dependent on the experimental conditions under which they are measured. Experiments must be performed at sufficiently high temperatures (Ͼ25°C) to ensure a low resting concentration of intracellular Ca 2ϩ or in the presence of an inhibitor of cross-bridge cycling. cardiac muscle; sinusoidal length perturbation; passive mechanics; 2,3-butanedione monoxime; extracellular calcium concentration THE MECHANICAL PROPERTIES of passive cardiac tissue are important, inasmuch as they help determine the stroke volume of the heart (3) and, hence, play a major role in diastolic dysfunction observed clinically. Mechanical tests are commonly performed on isolated hearts or samples of cardiac tissue and are conducted at various temperatures and extracellular Ca 2ϩ concentrations ([Ca 2ϩ ] o ). Recent studies (10, 11) have exploited the negative inotropic action (37) and cardioprotective properties (30) of the chemical agent 2,3-butanedione monoxime (BDM), whereas earlier studies utilized other forms of arrest.It ] o (9, 32), although Pinto and Patitucci (32) stated that temperature had little effect on the rate of creep of passive cardiac tissue. BDM has been reported to offer protection from cutting injury (30) and the Ca 2ϩ paradox (5), as well as from hypoxia and reperfusion injury (31). It also inhibits, but does not prevent, contracture (17).To ensure that cardiac muscle preparations are truly "passive," experiments have traditionally been conducted at low [Ca 2ϩ ] o and, for convenience, at room temperature. More recently, the use of BDM has further ensured passivity (10, 11); yet its effects on the mechanical properties of quiescent cardiac tissue at room temperature (20 -22°C) and low [Ca 2ϩ ] o have not been explored. At 26°C and 0.5 mM [Ca 2ϩ ] o , BDM was found to have no effect on the...

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“…(1) formation of rigor bridges, (2) stimulation of cross bridge cycling and (3) alterations of the elastic properties of the titin filament system. In several ischemia models, it has been shown that the first two conditions, i.e., formation of rigor bridges and stimulation of cross bridge cycling, interact with each other and that both mechanisms contribute to a different degree to resting tension dependent on the degree of ischemia [24].…”

Section: Cardiac Function Of Ab/hspb2-/-micementioning

confidence: 99%

Ischemia-induced increase of stiffness of αB-crystallin/HSPB2-deficient myocardium

Golenhofen

Redel

Wawrousek

et al. 2005

Pflugers Arch - Eur J Physiol

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The two small heat shock proteins (sHSPs), alphaB-crystallin and HSPB2, have been shown to translocate within a few minutes of cardiac ischemia from the cytosol to myofibrils; and it has been suggested that their chaperone-like properties might protect myofibrillar proteins from unfolding or aggregation during stress conditions. Further evidence of an important role for HSPs in muscle function is provided by the fact that mutations of the alphaB-crystallin gene cause myopathy and cardiomyopathy. In the present study, we subjected isolated papillary muscles of alphaB-crystallin/HSPB2-deficient mice to simulated ischemia and reperfusion. During ischemia in alphaB-crystallin/HSPB2-deficient muscles, the development of contracture started earlier and reached a higher value compared to the wildtype mice. The recovery of contracture of alphaB-crystallin/HSPB2-deficient muscles was also attenuated during the simulated reperfusion period. However, twitch force was not significantly altered at any time of the experiment. This suggests that during ischemic insults, alphaB-crystallin/HSPB2 may not be important for the contraction process itself, but rather serve to maintain muscular elasticity.

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Unstimulated force during hypoxia of rat cardiac muscle: stiffness and calcium dependence

Cited by 7 publications

References 0 publications

Increased cross-bridge cycling rate in stunned myocardium

Increased cross-bridge cycling rate in stunned myocardium

Effects of BDM, [Ca²⁺]_o, and temperature on the dynamic stiffness of quiescent cardiac trabeculae from rat

Ischemia-induced increase of stiffness of αB-crystallin/HSPB2-deficient myocardium

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Unstimulated force during hypoxia of rat cardiac muscle: stiffness and calcium dependence

Cited by 7 publications

References 0 publications

Increased cross-bridge cycling rate in stunned myocardium

Increased cross-bridge cycling rate in stunned myocardium

Effects of BDM, [Ca2+]o, and temperature on the dynamic stiffness of quiescent cardiac trabeculae from rat

Ischemia-induced increase of stiffness of αB-crystallin/HSPB2-deficient myocardium

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Effects of BDM, [Ca²⁺]_o, and temperature on the dynamic stiffness of quiescent cardiac trabeculae from rat