The concept of active state in striated muscle.

Julian, F J; Moss, R L

doi:10.1161/01.res.38.2.53

Cited by 38 publications

(24 citation statements)

References 37 publications

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“…On the other hand, it is well recognized that muscle shortening accelerates the decay of mechanical activity. 37 " 39 Thus, as shorter muscle lengths are reached, deactivation is accelerated and may represent the basis for the minimum length vs. maximum isotonic lengthening rate relation observed in this and previous studies. 16 -22 If a muscle were completely unloaded at any time during isometric force decline, it would shorten.…”

supporting

confidence: 64%

Mechanical determinants of maximum isotonic lengthening rate in rat left ventricular myocardium.

Zile¹,

Gaasch²,

Wiegner³

et al. 1987

Circulation Research

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The effects of changing loading conditions and inotropic state on maximum isotonic lengthening rate ( +dL/dt, muscle lengths/sec) were examined in isolated rat myocardium. Physiologically sequenced contractions were studied in 18 left ventricular papillary muscle preparations (stimulation rate, 12/min). To study the effects of changing loading conditions, only one loading variable (preload, total load, or late load) was changed during each contraction, while the others were held constant. To study the effects of isoproterenol (10~6 M) and temperature (28 vs. 33° C) on maximum isotonic lengthening rate, preload and late load were held constant and +dL/dt was examined at a common total load. When preload was increased from 0. ), +dL/dt rose from 1.6 ± 0.1 muscle lengths/sec at 28° C to 2.4 ± 0.2 muscle lengths/sec at 33° C and 2.05 ±0.1 muscle lengths/sec with isoproterenol. Thus, the load against which the muscle shortens (and/or the length to which it shortens), the magnitude of the late load, and the time at which the late load is applied are independent determinants of maximum isotonic lengthening rate. Under any constant set of loading conditions, both isoproterenol and increased temperature increase the maximum isotonic lengthening rate. A bnormalities of left ventricular (LV) early dia-/ \ stolic chamber filling appear to be sensitive X \ -indicators of myocardial disease 1 " 7 ; chamber filling rate has also been found to be useful in following the natural history and the response to therapy of pathological processes.8 " 14 To understand the effects of disease or pharmacologic therapy on chamber filling rate, it is important to define the specific mechanical and hemodynamic factors that influence the speed of relaxation and filling in the normal heart. Once the mechanical determinants of ventricular filling rate are defined, the effects of the disease process or the effects of pharmacologic treatment on filling rate can be interpreted within the context of changes in these mechanical determinants. In the intact heart, it is difficult to create isolated changes in mechanical variables such as loading conditions. This is true because most interventions cause concomitant changes in LV volume, LV pressure, left atrial pressure, and heart rate, each of which may have an effect on filling rate. Using the isolated muscle preparation, where muscle length and load can be independently and precisely controlled, the effects of isolated changes in loading conditions on isotonic lengthening rate can be studied. In addition, data obtained using this method are not affected by neurohumoral and other factors that might influence relaxation in the intact heart. Accordingly, the purpose of the current study is to define the independent determinants of maximum isotonic lengthening rate using physiologically sequenced isolated papillary muscle preparations. We hypothesize that loading conditions, specifically preload, total load, and late load, are primary mechanical determinants of the maximum isotonic lengthening rate. Ther...

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supporting

confidence: 64%

Mechanical determinants of maximum isotonic lengthening rate in rat left ventricular myocardium.

Zile¹,

Gaasch²,

Wiegner³

et al. 1987

Circulation Research

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“…3) follows an expected reduction in rate constants (factor per 100C change t 2.5). (iv) The kinetics of the increase in light scattering and tension are slower at low temperatures, as is the variation of myoplasrnic Ca2+ concentration (7,16).…”

Section: Discussionmentioning

confidence: 99%

Filament interaction in intact muscle fibers monitored by light scattering.

Katz¹,

Mozo²,

Reuben³

1979

Proc. Natl. Acad. Sci. U.S.A.

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Measurement of changes in optical properties of intact muscle fibers during contraction has proven to be difficult or, in some cases, impossible due to movement of the muscle relative to the incident beam. In this paper we describe a technique for immobilizing single fibers in clear gelatin, which permits measurement of light scattering signals undistorted by movement artifacts. We also describe the phase and amplitude relationship between changes in intensity of light scattering (at 900 to incident beam) and tensions induced by electrically activating single fibers. With tensions that range up to 50% P0 (P0 = maximal tension measured by exposure of fibers to 200 mM K+), the maximal increase in light scattering is about 25% of that for resting fibers. The scattering increase precedes tension, and at low temperatures the interval between the two peaks can be 50-100 msec. We interpret these data on intact fibers, as we did our earlier data from studies on skinned fibers, as indicating that increases in light scattering power of muscle are primarily due to attachment of myosin cross-bridges to actin filaments.In a recent study on chemically skinned rabbit psoas fibers (1), we found a large increase in the light scattering power of the fibers (900 to incident beam) upon induction of rigor and Ca2+ activation. The rigor-induced increase in scattering is maximal when thick-thin filament overlap is maximal and is nearly abolished by stretching fibers to lengths where overlap is minimal. This observation, as well as other data, led us to propose that the increase in light scattering accompanying rigor and contraction results from the attachment of myosin crossbridges to actin filaments.In the course of extending the study to include contracting intact fibers we found, as did others (2,3), that movement of the fibers during development of tension distorts the optical signal. We have, in large measure, eliminated movement artifacts by embedding fibers in gelatin. This method and its validation are described in the text. In our earlier study on skinned fibers (1) only steady-state signals were measured. With the high reproducibility of these signals and with no apparent effect of fiber movement, immobilization by gelatin was not necessary.The present findings on intact fibers are in accord with our previous data on skinned fibers-i.e., a large increase in light scattering accompanies thick-thin filament interaction. The data further disclose that the increase in scattering precedes tension, and the magnitude of the lead time is temperature dependent. According to current cross-bridge models (4) and biochemical schemes of the ATP hydrolysis cycle (5) states involving cross-bridge attachment lead the force-generating step.Of relevance to the interpretation of our data on intact crayfish fibers are recent studies relating the time course of tension in frog fibers to cross-bridge extension as measured by low angle x-ray scattering (6) and myoplasmic Ca2+ concentration variations measured by aequorin luminescence (7). M...

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“…It has been proposed from studies of isolated cardiac muscle that the maximum velocity of shortening of unloaded muscle (Vma,) on the one hand and the force generated by the cardiac muscle on the other may be dependent upon different mechanisms with different time constants. 18 Indeed, Tyberg et al 19 found, in the isolated papillary muscle contracting isometrically, that the rate of force generated was less sensitive to hypoxia than the actual amount of force generated and proposed that early ischemia might shorten the duration of the active state, while affecting its intensity only slightly. Similarly, in anesthetized animals, hemorrhagic shock depressed cardiac pump performance as reflected by cardiac output and left ventricular diastolic pressure more than it affected V max .…”

Section: Discussionmentioning

confidence: 99%

Initial myocardial adjustments to brief periods of ischemia and reperfusion in the conscious dog.

Pagani¹,

Vatner²,

Baig³

et al. 1978

Circulation Research

118

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SUMMARY The changes in left ventricular (LV) dynamics induced by brief periods of ischemia (100 seconds) and subsequent reperfusion were analyzed in conscious dogs. Global LV ischemia, induced by partially occluding the left main coronary artery, reduced LV flow homogeneously and impaired LV function as reflected by decreases in LV stroke "work" (89 ± 4% M ± SE), systolic shortening (72 ± 4%), velocity of shortening (56 ± 6%), LV systolic pressure (34 ± 5%), and dP/dt (59 ± 6%). Regional LV ischemia, induced by occluding either the left circumflex or anterior descending coronary artery completely, reduced flow to the ischemic segment (82 ± 3%) while decreasing segment work (96 ± 5%), shortening (82 ± 3%), and velocity of shortening (70 ± 5%), with minimal depression of overall LV function. In both groups the extent of shortening was reduced more rapidly and greater (P < 0.01) than shortening velocity. Moreover, with localized ischemia, segment work was reduced more (P < 0.01) than shortening. With reperfusion, a transient overshoot in function above preischemic control levels was observed in both groups (global work increased by 60 ± 12% and regional work by 28 ± 4% above control). This overshoot was not dependent on adrenergic mechanisms, but was prevented by inhibiting reactive hyperemia. Thus myocardial ischemia induces a dissociation between extent and rate of myocardial shortening. A further dissociation between shortening and work is apparent with regional ischemia. After reperfusion there is a transient overshoot in function which appears to be dependent upon the associated reactive hyperemia.INTEREST in the effects of coronary artery occlusion on the action of the heart was evident as early as 1698, 1 and by the beginning of this century it was recognized that coronary occlusion was associated with a fall in arterial pressure 2 and severe arrhythmias. 3 However, it was not until 1935 that Tennant and Wiggers 4 described in a quantitative manner the sequential changes in myocardial contraction which occur when brief periods of acute myocardial ischemia are induced in the experimental animal. Since these initial studies, it has become well recognized, largely as a result of investigations on openchest anesthetized animals, that acute myocardial ischemia exerts a negative inotropic influence, characterized by reductions in the extent and velocity of myocardial fiber shortening and in the external work performed by the ischemic myocardium. However, general anesthesia, per se, not only interferes with the response of the circulation to a variety of perturbations, 5 but it depresses myocardial contractility directly 6 '' and might complicate the interpretation of the effects of acute ischemia. In the last few years, a number of studies on myocardial function in the presence of regional 8 " 10 as well as global" ischemia have been performed in the conscious dog. It has been observed that prompt reductions in myocardial performance occur and that function recovers completely upon reperfusion following brief epis...

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The concept of active state in striated muscle.

Cited by 38 publications

References 37 publications

Mechanical determinants of maximum isotonic lengthening rate in rat left ventricular myocardium.

Mechanical determinants of maximum isotonic lengthening rate in rat left ventricular myocardium.

Filament interaction in intact muscle fibers monitored by light scattering.

Initial myocardial adjustments to brief periods of ischemia and reperfusion in the conscious dog.

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