Diastolic stress-strain relation of nonexcised blood-perfused canine papillary muscle

Kitabatake, A.; Suga, Hiroyuki

doi:10.1152/ajpheart.1978.234.4.h416

Cited by 18 publications

(8 citation statements)

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“…The passive tension-sarcomere length relationship of single frog atrial cells appears to be described adequately by an exponential function over the sarcomere length range of about 2.2 fixn to about 3.5 /xm used in the present investigation. The exponential index (a), obtained from the Lagrangian stress-sarcomere length relationships, is on the order of 5.3, which is similar to a value of 6-7, which can be calculated from data on semitendinosus muscle (Moss and Halpern, 1977), but it is considerably less than the values of 18-37 that have been reported for intact mammalian cardiac muscle (Kitabatake and Suga, 1978).…”

Section: Tension-length Relation Of Single Heart Cells/tarr Et Alsupporting

confidence: 59%

“…Fung (1967) suggested that the relationships between passive tension and length could be described by an exponential relationship of the form T = T* exp (a) (A-X*), where T is the tension or stress, A is the extension ratio (length divided by nonstressed length), (a) is an exponential index, and T* is the tension (or stress) at a specific extension ratio X*. Such an exponential function has been used to describe the passive tension-length relationships of skeletal muscle (Moss and Halpern, 1977) and cardiac muscle (Kitabatake and Suga, 1978). The passive tension-sarcomere length relationship of single frog atrial cells appears to be described adequately by an exponential function over the sarcomere length range of about 2.2 fixn to about 3.5 /xm used in the present investigation.…”

Section: Tension-length Relation Of Single Heart Cells/tarr Et Almentioning

confidence: 99%

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Sarcomere length-resting tension relation in single frog atrial cardiac cells.

Tarr¹,

Trank²,

Leiffer³

et al. 1979

Circulation Research

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IT IS well established that the resting tension (stress)-sarcomere length relationships of a variety of intact preparations of cardiac muscle are different from those of skeletal muscle preparations. In contrast to skeletal muscle in which resting tension is negligible at sarcomere lengths below about 2.3 jim (Gordon et al., 1966;Lannergren and Noth, 1973; Moss and Halpem, 1977), mammalian cardiac preparations have relatively high resting tensions at these sarcomere lengths (Spiro and Sonnenblick, 1964), and the resting tension increases markedly at sarcomere lengths beyond 2.3 /im. In nonmammalian cardiac preparations, variable results have been obtained. Starling (1918) found in intact tortoise ventricle that the resting tension remained relatively small over a wide range (approximately 6-fold) of diastolic volumes, which included the rising phase and the relatively broad range (approximately 2-fold) of the active tension-diastolic volume relationship. In contrast, both Winegrad (1974) and Matsubara and Maruyama (1977) found that the resting tension increased significantly over the sarcomere length range of 2.0-2.6 /xm in small bundles of frog atrial tissue. Nassar et al. (1974) found

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Section: Tension-length Relation Of Single Heart Cells/tarr Et Alsupporting

confidence: 59%

Section: Tension-length Relation Of Single Heart Cells/tarr Et Almentioning

confidence: 99%

Sarcomere length-resting tension relation in single frog atrial cardiac cells.

Tarr¹,

Trank²,

Leiffer³

et al. 1979

Circulation Research

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“…We assessed passive stiffness from the stress-strain relationship calculating the elastic constants a and ,8 as described by Glantz and Kernoff (11). Because the stress-strain relationship of cardiac muscle is monoexponential over the physiologic range of stress (11,12), the elastic constants can be derived from: a = a (e#' -1) where a = force/instantaneous cross sectional area and e (Lagrangian strain) = 1 -10/10, 1 being unstressed muscle length. We also calculated the tangent modulus or elastic stiffness (da/ de) from do/de = ,a + #a (11).…”

Section: Methodsmentioning

confidence: 99%

Hydroxyproline and passive stiffness of pressure-induced hypertrophied kitten myocardium.

Williams¹,

Potter²,

Hern³

et al. 1982

J. Clin. Invest.

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A B S T R A C T Passive stiffness and hydroxyproline content of myocardium hypertrophied by pressureloading were determined in kittens 2, 8-16, and 24-52 wk after pulmonary artery banding, which initially elevated right ventricular systolic pressure by 10-15 mm Hg. Right ventricular mass increased by -75%, three-quarters of which occurred during the first 2 wk after banding. Passive stiffness was assessed from resting length-tension relations of isometrically contracting isolated right ventricular papillary muscles. Stiffness constants, a and B were determined from the relationship a = a(ee -1) where a = stress and e = Lagrangian strain. Elastic stiffness (dl/dE) was derived from: da/de = f#a + ,3a. Right ventricular hydroxyproline increased in proportion to muscle mass so that hydroxyproline concentration remained unchanged after banding. Both a, f, and elastic stiffnessstress relations were similar to values in nonbanded controls. Thus, we did not observe an increase in passive stiffness or hydroxyproline concentration of pressure-induced hypertrophied myocardium in contrast to most previous studies.

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“…Direct evidence for this relationship has been demonstrated in cardiac papillary muscle, which becomes stiffer with increased perfusion (Kitabatake & Suga, 1978). Indirect evidence for an effect of vascular perfusion on upper airway wall stiffness comes from both animal and human experiments.…”

Section: The Effect Of Rem Sleep On the Upper Airwaymentioning

confidence: 99%

The effect of rapid eye movement (REM) sleep on upper airway mechanics in normal human subjects

Rowley

Zahn

Babcock

et al. 1998

The Journal of Physiology

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It has been proposed that the upper airway is more compliant during rapid eye movement (REM) sleep than during non‐rapid eye movement (NREM) sleep. The purpose of this study was to test this hypothesis in a group of subjects without sleep‐disordered breathing. On the first night, the effect of sleep stage on the relationship of retropalatal cross‐sectional area (CSA; visualized with a fibre‐optic scope) to pharyngeal pressure (PPH) measured at the soft palate during eupnoeic breathing was studied. Breaths during REM sleep were divided into phasic (associated with eye movements) and tonic (not associated with eye movements). There was a significant decrease in pharyngeal CSA during NREM sleep compared with wakefulness. There was no further decrease observed during either tonic or phasic REM sleep. Pharyngeal compliance, defined as the slope of the regression CSA versus PPH, was significantly increased during NREM sleep compared with wakefulness and REM sleep, with the compliance during both tonic and phasic REM sleep being similar to that observed in wakefulness. On the second night, the effect of sleep stage on pressure‐flow relationships of the upper airway was investigated. There was a trend towards the upper airway resistance being highest in NREM sleep compared with wakefulness and REM sleep. We conclude that the upper airway is stiffer and less compliant during REM sleep than during NREM sleep. We postulate that this difference is secondary to differences in upper airway vascular perfusion between REM and NREM sleep.

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Diastolic stress-strain relation of nonexcised blood-perfused canine papillary muscle

Cited by 18 publications

References 0 publications

Sarcomere length-resting tension relation in single frog atrial cardiac cells.

Sarcomere length-resting tension relation in single frog atrial cardiac cells.

Hydroxyproline and passive stiffness of pressure-induced hypertrophied kitten myocardium.

The effect of rapid eye movement (REM) sleep on upper airway mechanics in normal human subjects

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