scholarly journals Myocardial ischemic contracture. Metabolites affect rigor tension development and stiffness.

1994 ◽  
Vol 74 (5) ◽  
pp. 920-929 ◽  
Author(s):  
R Ventura-Clapier ◽  
V Veksler
Keyword(s):  
Tension Development ◽  
Ischemic Contracture ◽  
Rigor Tension

Red and White Muscle of Fish in Relation to Rigor Mortis

1963 ◽  
Vol 20 (1) ◽  
pp. 45-58 ◽  
Author(s):  
Hans Buttkus
Keyword(s):  
Mechanical Properties ◽  
Electron Micrographs ◽  
White Muscle ◽  
Glycogen Content ◽  
Post Mortem ◽  
Rigor Mortis ◽  
Tension Development ◽  
Ophiodon Elongatus ◽  
Red Muscle ◽  
Rigor Tension

The superficial red muscle of lingcod (Ophiodon elongatus) was shown to exhibit unique properties of post-mortem contraction and tension development. In comparison with white muscle, rigor contraction and isometric rigor tension in red muscle were about three times as great. The rate of contraction of the red muscle was dependent on temperature and also on the oxygen concentration in the surrounding atmosphere. The elastic modulus of the red muscle of trout and lingcod increased with increasing post-mortem time. Following the onset of rigor mortis a gradual increase in elasticity was observed. The maximum effects of contraction, tension and elasticity coincided with the onset of rigor mortis and each could therefore be used as a measure of this phenomenon. It was concluded from these experiments that stiffening of a fish with the onset of rigor mortis is not due to contraction or tension development of the muscles, but rather to their changing mechanical properties. A convenient measure of the changing mechanical properties in the muscle was the elastic modulus.Morphological differences between the very active, myoglobin rich, red muscle and the white muscle of lingcod were demonstrated by means of electron micrographs. The high glycogen content in the area of sarcoplasm of the red muscle, as indicated in electron micrographs, was confirmed by chemical analysis. Red muscle in rested fish was shown to contain from 1 to 3 times more glycogen than white muscle.

Reversible MM-creatine kinase binding to cardiac myofibrils

1987 ◽  
Vol 253 (3) ◽  
pp. C444-C455 ◽  
Author(s):  
R. Ventura-Clapier ◽  
V. A. Saks ◽  
G. Vassort ◽  
C. Lauer ◽  
G. V. Elizarova
Keyword(s):  
Creatine Kinase ◽  
Energy Supply ◽  
Adenine Nucleotides ◽  
Cardiac Contraction ◽  
Tension Development ◽  
Tension Recovery ◽  
Maximal Tension ◽  
Km Value ◽  
Rigor Tension ◽  
Length Changes

Skinned rat papillary muscles and purified preparations of rat cardiac myofibrils were used to study the nature of the interaction of creatine kinase with cardiac myofibrils. High activity of creatine kinase (2 IU/mg protein in fibers and 0.9 IU/mg in purified myofibrils) was due mostly to reversibly bound enzyme. This activity could be removed and rebound. The process of creatine kinase rebinding was characterized by apparent Km value of 0.14 mg/ml (approximately equal to 2 X 10(6) M). Rebinding of creatine kinase to cardiac myofibrils restored the phenomenon of functional compartmentation of adenine nucleotides in myofibrillar space and restored the ability of phosphocreatine to decrease the rigor tension in the presence of MgADP. The physiological experiments with quick length changes showed that rebinding of creatine kinase to skinned papillary muscle also restored Ca sensitivity, increased maximal tension development, decreased stiffness, and restored the tension recovery after quick length changes in muscle under condition of inhibition of endogenous creatine kinase by 1-fluoro-2,4-dinitrobenzene. It is concluded that creatine kinase reversibly bound to cardiac myofibrils is involved in the energy supply for cardiac contraction.

Decreased Myocyte Tension Development and Calcium Responsiveness in Rat Right Ventricular Pressure Overload

Circulation ◽  
1997 ◽  
Vol 95 (9) ◽  
pp. 2312-2317 ◽  
Author(s):  
Dongsheng Fan ◽  
Thomas Wannenburg ◽  
Pieter P. de Tombe
Keyword(s):  
Right Ventricular ◽  
Pressure Overload ◽  
Ventricular Pressure ◽  
Tension Development

VOLKMANN’S ISCHEMIC CONTRACTURE OF THE UPPER EXTREMITY

Hand Clinics ◽  
1998 ◽  
Vol 14 (3) ◽  
pp. 483-497
Author(s):  
Michael J. Botte ◽  
Mary Ann E. Keenan ◽  
Richard H. Gelberman
Keyword(s):  
Upper Extremity ◽  
Ischemic Contracture

scholarly journals FFAR1 activation attenuates histamine-induced myosin light chain phosphorylation and cortical tension development in human airway smooth muscle cells

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Shengjie Xu ◽  
Anthony Schwab ◽  
Nikhil Karmacharya ◽  
Gaoyuan Cao ◽  
Joanna Woo ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Airway Hyperreactivity ◽  
Human Airway Smooth Muscle ◽  
Tension Development ◽  
Cortical Tension ◽  
Human Airway ◽  
Mlc Phosphorylation

Abstract Background Activation of free fatty acid receptors (FFAR1 and FFAR4) which are G protein-coupled receptors (GPCRs) with established (patho)physiological roles in a variety of obesity-related disorders, induce human airway smooth muscle (HASM) cell proliferation and shortening. We reported amplified agonist-induced cell shortening in HASM cells obtained from obese lung donors. We hypothesized that FFAR1 modulate excitation–contraction (EC) coupling in HASM cells and play a role in obesity-associated airway hyperresponsiveness. Methods In HASM cells pre-treated (30 min) with FFAR1 agonists TAK875 and GW9508, we measured histamine-induced Ca2+ mobilization, myosin light chain (MLC) phosphorylation, and cortical tension development with magnetic twisting cytometry (MTC). Phosphorylation of MLC phosphatase and Akt also were determined in the presence of the FFAR1 agonists or vehicle. In addition, the effects of TAK875 on MLC phosphorylation were measured in HASM cells desensitized to β2AR agonists by overnight salmeterol treatment. The inhibitory effect of TAK875 on MLC phosphorylation was compared between HASM cells from age and sex-matched non-obese and obese human lung donors. The mean measurements were compared using One-Way ANOVA with Dunnett’s test for multiple group comparisons or Student’s t-test two-group comparison. For cortical tension measurements by magnetic twisted cytometry, mixed effect model using SAS V.9.2 was applied. Means were considered significant when p ≤ 0.05. Results Unexpectedly, we found that TAK875, a synthetic FFAR1 agonist, attenuated histamine-induced MLC phosphorylation and cortical tension development in HASM cells. These physiological outcomes were unassociated with changes in histamine-evoked Ca2+ flux, protein kinase B (AKT) activation, or MLC phosphatase inhibition. Of note, TAK875-mediated inhibition of MLC phosphorylation was maintained in β2AR-desensitized HASM cells and across obese and non-obese donor-derived HASM cells. Conclusions Taken together, our findings identified the FFAR1 agonist TAK875 as a novel bronchoprotective agent that warrants further investigation to treat difficult-to-control asthma and/or airway hyperreactivity in obesity.

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