butanedione/chills

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Survival of metabolically inhibited ventricular myocytes is enhanced by inhibition of rigor and SR Ca2+ cycling.

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During severe ATP depletion, sarcolemmal rupture resulting from rigor- and/or Ca(2+)-induced myofilament force development is considered to be an important cause of irreversible cell injury. Recent experiments in our laboratory demonstrated that during prolonged metabolic inhibition (MI) in adult

Effect of 2,3-butanedione monoxime on myocyte resting force during prolonged metabolic inhibition.

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The chemical phosphatase 2,3-butanedione monoxime (BDM) has been reported to inhibit both Ca(2+)-induced myofilament force development and rigor due to ATP depletion. However, during prolonged hypoxia in cultured ventricular myocytes BDM delays but does not prevent a marked increase in resting

Mechanism of action of 2,3-butanedione monoxime on contracture during metabolic inhibition.

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The effect of 2,3-butanedione monoxime (BDM) was investigated during metabolic inhibition (MI) in papillary muscles. MI caused a rapid decrease in developed force and an increase in resting force, along with a decrease in ATP and creatine phosphate (CrP). Addition of BDM before MI decreased maximal

Different Myosin Head Conformations in Bony Fish Muscles Put into Rigor at Different Sarcomere Lengths.

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At a resting sarcomere length of approximately 2.2 µm bony fish muscles put into rigor in the presence of BDM (2,3-butanedione monoxime) to reduce rigor tension generation show the normal arrangement of myosin head interactions with actin filaments as monitored by low-angle X-ray diffraction.

Strain softening behaviour in nonviable rat right-ventricular trabeculae, in the presence and the absence of butanedione monoxime.

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Strain softening is commonly reported during mechanical testing of passive whole hearts. It is typically manifested as a stiffer force-extension relationship in the first deformation cycle relative to subsequent cycles and is distinguished from viscoelasticity by a lack of recovery of stiffness,

Effects of 2,3-butanedione monoxime on the contractile activation properties of fast- and slow-twitch rat muscle fibres.

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1. The effects of 2,3-butanedione monoxime (BDM, 0.2-10 mmol/l) have been examined at different temperatures on calcium transients (measured with aequorin) and isometric force in intact bundles of fibres from soleus (slow-twitch) and extensor digitorum longus (EDL; fast-twitch) muscles of the rat

Effects of vanadate, phosphate and 2,3-butanedione monoxime (BDM) on skinned molluscan catch muscle.

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The effects of orthovanadate (V(i)), inorganic phosphate (P(i)) and 2,3-butanedione monoxime (BDM) on tension, force transients and the catch state (passive tension maintenance) were investigated in saponin-skinned fibre bundles of the anterior byssus retractor muscle (ABRM) of the bivalve mollusc

Mechanisms underlying ischemic diastolic dysfunction: relation between rigor, calcium homeostasis, and relaxation rate.

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Increased diastolic chamber stiffness (upward arrow DCS) during ischemia may result from increased diastolic calcium, rigor, or reduced velocity of relaxation. We tested these potential mechanisms during severe ischemia in isolated red blood cell-perfused isovolumic rabbit hearts. Ischemia (coronary

Volatilome of Chill-Stored European Seabass (Dicentrarchus labrax) Fillets and Atlantic Salmon (Salmo salar) Slices under Modified Atmosphere Packaging.

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Fish spoilage occurs due to production of metabolites during storage, from bacterial action and chemical reactions, which leads to sensory rejection. Investigating the volatilome profile can reveal the potential spoilage markers. The evolution of volatile organic molecules during storage of European

Effect of extracellular ions and modulators of calcium transport on survival of tert-butyl hydroperoxide exposed cardiac myocytes.

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OBJECTIVE The aim was to investigate the effects of extracellular ions and agents that modify calcium translocating pathways on oxidative stress induced cell injury. METHODS Survival of cardiac myocytes exposed to tert-butyl hydroperoxide (t-BHP, 0.2 to 2 mM) was estimated by their ability to

Cross-bridge kinetics in the presence of MgADP investigated by photolysis of caged ATP in rabbit psoas muscle fibres.

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1. The interaction between MgADP and rigor cross-bridges in glycerol-extracted single fibres from rabbit psoas muscle has been investigated using laser pulse photolysis of caged ATP (P3-1(2-nitrophenyl)ethyladenosine 5'-triphosphate) in the presence of MgADP and following small length changes

BDM drives protein dephosphorylation and inhibits adenine nucleotide exchange in cardiomyocytes.

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Contractile dysfunction plays a key role in injury sustained by ischemic myocardium at reperfusion, whereas interventions that impede hypercontracture enhance recovery. In permeabilized adult rat cardiomyocytes, the negative inotrope 2,3-butanedione monoxime (BDM; 10-50 mM) inhibited rigor at low

Characterization of secophalloidin-induced force loss in cardiac myofibrils.

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Secophalloidin (SPH) is known to cause in cardiac myofibrils force without Ca(2+) (half-maximal effect approximately 2 mM) followed by irreversible loss of Ca(2+)-activated force. At maximal Ca(2+) activation, SPH increases force (half-maximal effect < 0.1 mM). We found that SPH at low concentration

Effects of troponin-I extraction with vanadate and of the calcium sensitizer EMD 53998 on the rate of force generation in skinned cardiac muscle.

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The rate of tension development following release of ATP from caged-ATP in the presence of calcium was studied in skinned cardiac fibres from swine. A low-force rigor state was obtained by using butanedione monoxime (BDM) during the induction of rigor. BDM was washed out and following release of ATP

Time-resolved equatorial X-ray diffraction studies of skinned muscle fibres during stretch and release.

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Equatorial X-ray diffraction patterns were recorded from small bundles of one to three chemically skinned frog sartorius muscle fibres (time resolution 250 microseconds) during rapid stretch and subsequent release. In the relaxed state, the dynamic A-band lattice spacing change as a result of a 2 %

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