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PubMed2000

Skeletal muscle endurance is reduced in chronically energy deficient adults.

Fifty eight adult males (well nourished; WN = 25, underweight; UW = 13, chronically energy deficient; CED = 20), aged 18 to 30 yr underwent an assessment of skeletal muscle function using a load cell based handgrip dynamometer coupled to a polygraph. WN subjects had higher handgrip strengths than either the UW or CED subjects (P < 0.05), though not when corrected for forearm muscle area or forearm volume. CED subjects fatigued faster than WN subjects during sustained maximal isometric contraction (P < 0.05) as well as during prolonged isotonic exercise (P < 0.05). During the latter, the onset of fatigue in the CED subjects was also faster than that in their anthropometrically similar UW controls. These data are consonant with reports of decreased productivity in undernourished adults during real life tasks.

Adolescent↗
PubMed1981

Effect of heparin Na on the action of various bronchoconstrictors in guinea pig tracheal strips.

The effect of heparin Na on the actions of various bronchoconstrictors was examined. Guinea pig tracheal strips were suspended in bioassay glass chambers and superfused with Krebs-Henseleit solution, pH 7.4, at 37 degrees C saturated with oxygen and carbon dioxide gas (95:5, v/v). Contraction of the tissue was detected by an isotonic transducer and displayed on a polyrecorder. Heparin Na attenuated histamine-, prostaglandin F2 alpha-, acetylcholine-, serotonin-induced contractile responses dose-dependently, and shifted the dose-response curves of histamine, prostaglandin F2 alpha, acetylcholine, serotonin and bradykinin downward.

Acetylcholine↗
PubMed1969

The steps between depolarization and the increase in the respiration of frog skeletal muscle.

1. For many years it has been known that when muscles are depolarized by raising [K(+)](out) there is an increase in respiration, even at levels of depolarization below the threshold for a detectable contracture.2. K(+)-stimulated respiration occurs in muscles in which protein synthesis is blocked with puromycin. Stimulation does not depend upon activation of phosphorylase kinase. In muscle poisoned with IIA and kept in N(2), depolarizations below the threshold for contracture cause a fall in creatine phosphate. Apparently an ATPase is activated by depolarization; the resulting ADP is probably the trigger for the increase in oxygen uptake.3. When the T-tubules are destroyed by the glycerol-osmotic shock method depolarization does not produce an increase in respiration.4. Caffeine is known to stimulate respiration at concentrations below the threshold for producing a contracture. Muscles that have been made refractory to stimulation by potassium are still stimulated by caffeine: the action of caffeine is not antagonized by an increase in extracellular Mg(2+). Caffeine must act on a later step in excitation-contraction coupling.5. K(+)-stimulated respiration ultimately depends on the presence of Ca(2+) in the Ringer. However, the Ca(2+) can be replaced by Ni(2+). It is known that Ni(2+) does not activate actomyosin. Ni(2+) is not sequestered by isolated fragments of the sarcoplasmic reticulum. It seems that the Ni(2+) or Ca(2+) in the extracellular solution is required for a superficial step in excitation-contraction coupling.6. Respiration is also often stimulated when muscles are placed in an isotonic sucrose solution, even though the fibres are hyperpolarized. A trace amount of Ca(2+) in the sucrose solution is probably necessary for the response.7. An interaction between Ca(2+) and a superficial membrane receptor appears to be an essential, early step in excitation-contraction coupling.

Adenosine Triphosphatases↗
PubMed2004

Effects of acidosis on ventricular myocyte shortening and intracellular Ca2+ in streptozotocin-induced diabetic rats.

We have investigated the effects of acute acidosis on ventricular myocyte shortening and intracellular Ca2+ in streptozotocin (STZ)-induced diabetic rat. Shortening and intracellular Ca2+ were measured in electrically stimulated myocytes superfused with either normal Tyrode solution pH adjusted to either 7.4 (control solution) or 6.4 (acid solution). Experiments were performed at 35-36 degrees C. At 8-12 weeks after treatment, the rats that received STZ had lower body and heart weights compared to controls, and blood glucose was characteristically increased. Contractile defects in myocytes from diabetic rat were characterized by prolonged time to peak shortening. Superfusion of myocytes from control and diabetic rats with acid solution caused a significant reduction in the amplitude of shortening; however, the magnitude of the response was not altered by STZ treatment. Acid solution also caused significant and quantitatively similar reductions in the amplitude of Ca2+ transients in myocytes from control and diabetic rats. Effects of acute acidosis on amplitude of myocyte contraction and Ca2+ transient were not significantly altered by STZ treatment. Altered myofilament sensitivity to Ca2+ and altered mechanisms of sarcoplasmic reticulum Ca2+ transport might partly underlie the acidosis-evoked reduction in amplitude of shortening in myocytes from control and STZ-induced diabetic rat.

Animals↗
PubMed2004

Assist-control mechanical ventilation attenuates ventilator-induced diaphragmatic dysfunction.

Controlled mechanical ventilation induced a profound diaphragm muscle dysfunction and atrophy. The effects of diaphragmatic contractions with assisted mechanical ventilation on diaphragmatic isometric, isotonic contractile properties, or the expression of muscle atrophy factor-box (MAF-box), the gene responsible for muscle atrophy, are unknown. We hypothesize that assisted mechanical ventilation will preserve diaphragmatic force and prevent overexpression of MAF-box. Studying sedated rabbits randomized equally into control animals, those with 3 days of assisted ventilation, and those with controlled ventilation, we assessed in vitro diaphragmatic isometric and isotonic contractile function. The concentrations of contractile proteins, myosin heavy chain isoform, and MAF-box mRNA were measured. Tetanic force decreased by 14% with assisted ventilation and 48% with controlled ventilation. Maximum shortening velocity tended to increase with controlled compared with assisted ventilation and control. Peak power output decreased 20% with assisted ventilation and 41% with controlled ventilation. Contractile proteins were unchanged with either modes of ventilation; myosin heavy chain 2X mRNA tended to increase and that of 2A to decrease with controlled ventilation. MAF-box gene was overexpressed with controlled ventilation. We conclude that preserving diaphragmatic contractions during mechanical ventilation attenuates the force loss induced by complete inactivity and maintains MAF-box gene expression in control.

Actins↗
PubMed1995

Contraction, relaxation, and economy of force generation in isolated human diaphragm muscle.

Contraction, relaxation, and energetics of normal human diaphragm strips (n = 10) were investigated over the whole load continuum in both twitch and tetanus modes. For a given level of isotonic total force and over a large part of the contraction phase, instantaneous velocity was shown to be a unique function of instantaneous length, regardless of time and initial length. In afterloaded tetanic contractions and over a wide range of loads, the peak lengthening velocity (VL) linearly decreased when maximum extent of muscle shortening (delta L) decreased. Stimulation mode modulated the VL versus delta L relationship, the slope of this linear regression being greater in tetanus than in twitch. Conversely, over a wide range of load, an increase in load linearly accelerated the peak rate of force decay, regardless of the stimulation mode. The energetics of human diaphragm muscle was evaluated in terms of both mechanical activity and economy of force generation. Maximum mechanical work (Wmax) differed significantly according to the stimulation mode, and the relative force at which Wmax occurred was higher in tetanus than in twitch (p < 0.05). The G curvature of the P-V hyperbola and maximum mechanical efficiency were significantly higher in tetanus than in twitch. This strongly suggests that the economy of force generation is higher in tetanus contractions than in twitch.

Adult↗
PubMed1998

Vasoactive effects of cimicifugic acids C and D, and fukinolic acid in cimicifuga rhizome.

Vasoactive effects of cimicifugic acids A-E, fukinolic acid and fukiic acid isolated from Cimicifuga plants were investigated using rat aortic strips. Cimicifugic acid D and fukinolic acid at 3x10(-4) M caused a sustained, slowly developing relaxation of aortic strips precontracted with norepinephrine (NE) in preparations with or without endothelium. Cimicifugic acid C inversely caused a weak contraction. Cimicifugic acids A, B and E and fukiic acid showed no vasoactivity at 3x10(-4) M. Cimicifugic acids A-E and fukinolic acid are esters between cinnamic acids and the hydroxyl group of benzyltartaric acids. For the manifestation of vasoactivity in the rat aorta, it is concluded that in the cinnamic acid moiety, a caffeoyl group might be necessary for the relaxation activity, and the p-coumaroyl group causes contraction. Concentration response curves for the Ca2+-induced contracture of depolarized aortic strips with isotonic high K+ were not affected by cimicifugic acid D or fukinolic acid. The Ca2+-induced contraction of aortic strips, preincubated with 10(-6) M NE in the presence of 10(-6) M nicardipine and 0.01 mM EGTA in Ca2+-free solution, were inhibited by cimicifugic acid D and fukinolic acid. These results indicated that the inhibition by cimicifugic acid D and fukinolic acid of the NE-induced contraction of rat aorta are attributable to the suppression of Ca2+ influx from the extracellular space enhanced by NE.

Animals↗
PubMed1976

Creep after loading in the relaxed and contracted smooth muscle (taenia coli of the guinea pig) under various osmotic conditions.

1. Experiments to investigate the creep phenomena of the taenia coli were performed in hypotonic (207 mosm) and hypertonic (447 or 463 mosm) media, in the relaxed (Ca2+-depletion + verapamil) as well as in the contracted (K2SO4-depolarized) state. They were compared with earlier results in isotonic media. The samples were standardized with respect to their volume (weight) before the beginning of the experiment. 2. Neither in the relaxed, nor in the contracted state was there a statistically significant difference in mean total length observed within each test series after loading with 9928 dyn for 2000 s (about 33 min) in the different osmotic media. We define total length as unloaded initial length lo + initial pure leastic extension lE + creep N. 3. In the contracted state the mean total lengths attained by elastic extension and creep are significantly greater than in the relaxed state in both hypotonic and isotonic media. The greater variance in the data for hypertonic solutions makes any statistical decision of this kind impossible. 4. The typical time course of creep (N) and particularly the hyperbolic dependance of N and dN/dt stated in an earlier paper could also be observed here under varied osmotic conditions. 5. The results suggest that the viscosity of the cell plasma is not significant for the time course and extent of creep in smooth muscles of vertebrates. Creep probably takes place in the solid structures of the cells: most particularly the contractile proteins may be involved.

Animals↗
PubMed1978

The relationship between speed and amplitude of the fastest voluntary contractions of human arm muscles.

The relationship between the speed of the fastest possible voluntary contractions and their amplitude was examined for several hand- and forearm muscles under isometric and isotonic conditions. The consistent finding was the amplitude dependence of the speed of the fastest voluntary efforts: the larger the amplitude, the faster the contraction. The increase of the rate of rise of isometric tension or of the velocity of isotonic movements with rising amplitude was linear. The slope of this relationship was the same for three different hand- and forearm muscles examined. The duration of the contractions measured from onset to peak was approximately constant for all amplitudes. The duration of the EMG-burst recorded from the contracting muscle was similar as the time from onset to peak of the contraction. These results show that the skeleto-motor speed control system operates by adjusting the velocity of a contraction to its amplitude in such a way that the contraction time remains approximately constant. It is suggested that this type of speed control is a necessary requirement for the synchrony of synergistic muscle contractions.

Adult↗
PubMed1992

Pharmacological assessment of Ca2+ dependence of endothelin-1-induced response in rat aorta.

In rat aorta, endothelin-1 (ET-1) induced a slowly developing and sustained contraction in Ca(2+)-containing normal Krebs, nominally Ca(2+)-free Krebs, and Ca(2+)-free Krebs containing EGTA with a decreasing level of contraction. When ET-1-precontracted tissues were washed with Ca(2+)-free Krebs +50 microM EGTA, the tissues spontaneously and slowly relaxed. Readministration of Ca2+ during the early spontaneous relaxation phase caused a rapidly developing tonic contraction. When added during the late spontaneous relaxation phase, Ca2+ evoked slowly developing or, sometimes, biphasic contractions. In the presence of sarcoplasmic reticulum Ca(2+)-pump inhibitor, cyclopiazonic acid, the above biphasic contraction brought about by readministration of Ca2+ converted to a rapidly developing monophasic response. Thus, the first component of the biphasic contraction may be due to refilling of ET-1-sensitive Ca2+ store via the internal membrane Ca(2+)-pump. Furthermore, the ability of the phenylephrine-sensitive pool of internal Ca2+ to refill in the presence of 10(-8) M ET-1 suggests that the phenylephrine-sensitive pool differs from ET-1-sensitive pool and cannot be depleted by ET-1.

Animals↗
PubMed1999

Attenuation of Ca paradox injury in guinea pig heart by K+ channel blocker, d-sotalol.

D-sotalol was shown to prevent Ca overload and intermyocyte uncoupling. The aim of this study was to investigate the effect of d-sotalol in Ca paradox conditions. Guinea pig hearts were perfused at 37 degrees C and constant pressure with oxygenated Tyrode solution. Ca paradox was induced by 10 min Ca free perfusion followed by 10 min Ca repletion. 10(-6) M d-sotalol was administered either during Ca depletion or during Ca repletion period. Electrical activity and ventricular contraction were simultaneously recorded and subcellular alterations were analysed. The contraction terminated in 5 min of Ca free perfusion and electrical activity disappeared within 5 min of Ca repletion. Nonuniform injury of myocardial tissue was observed. The majority of cardiomyocytes were irreversibly injured and profound dissociation of intercellular junctions was detected. Administration of d-sotalol during Ca free period preserved electrical activity and restored ventricular contraction accompanied by apparent protection of the ultrastructure, including intercellular connections. Uniform patterns of sarcomeres reflected synchronous contraction and protection of junctional couplings. In conclusion, d-sotalol attenuates Ca paradox injury. It seems that the protective effect of d-sotalol is most likely related to inhibition of potassium efflux antagonizing Na loading during Ca depletion period, as well as to attenuation of excess of [Ca2+]i via acceleration of sarcoplasmic Ca exchange during Ca repletion.

Animals↗
PubMed1987

The Mechanics of Injury to Isolated Protoplasts following Osmotic Contraction and Expansion.

Micro-osmotic manipulation was used to determine the influence of osmotic contraction on the expansion potential of individual protoplasts isolated from rye (Secale cereale L. cv Puma) leaves. For protoplasts isolated from leaves of nonacclimated plants (NA protoplasts), osmotic contraction in sufficiently hypertonic solutions (>1.53 osmolal) predisposed the protoplasts to lysis during osmotic expansion when they were returned to isotonic conditions (0.53 osmolal). In contrast, for protoplasts isolated from leaves of cold acclimated plants (ACC protoplasts), osmotic contraction in either 2.6 or 4.0 osmolal solutions was readily reversible. Following osmotic contraction, the resting tension (gamma(r)) of NA protoplasts was similar to that determined for protoplasts in isotonic solutions (i.e. 110 +/- 22 micronewtons per meter). In contrast, gamma(r) of ACC protoplasts decreased from 164 +/- 27 micronewtons per meter in isotonic solutions to values close to zero in hypertonic solutions. Following expansion in hypotonic solutions, gamma(r)'s of both NA and ACC protoplasts were similar for area expansions over the range of 1.3 to 1.6. Following osmotic contraction and reexpansion of NA protoplasts, hysteresis was observed in the relationship between gamma(r) and surface area-with higher values of gamma(r) at a given surface area. In contrast, no hysteresis was observed in this relationship for ACC protoplasts. Direct measurements of plasma membrane tension (gamma) during osmotic expansion of NA protoplasts from hypertonic solutions (1.53 osmolal) revealed that gamma increased rapidly after small increments in surface area, and lysis occurred over a range of 1.2 to 8 millinewtons per meter. During osmotic expansion of ACC protoplasts from hypertonic solutions (2.6 osmolal), there was little increase in gamma until after the isotonic surface area was exceeded. These results are discussed in relation to the differences in the behavior of the plasma membrane of NA and ACC protoplasts during osmotic contraction (i.e. endocytotic vesiculation versus exocytotic extrusion) and provide a mechanistic interpretation to account for the differential sensitivity of NA and ACC protoplasts to osmotic expansion from hypertonic solutions.

Journal Article↗
PubMedDate not supplied

Imidazole action on guinea pig heart.

Imidazole (IM) exerts a positive inotropic effect on the guinea pig heart in a dose-dependent manner. This effect is not controlled by any of histamine receptors. Both, mepyramine - a H1-histamine receptor blocker, and cimetidine - a H2-histamine receptor blocker have no influence on IM responses. A positive inotropic action of IM on the heart has been shown in both, normal Ringer-Locke solution and in solutions with calcium deficit, however, the relative increase in contraction amplitude was higher at lower calcium concentrations than in solutions with normal calcium content. In calcium - free solution IM produces a marked delay of heart arrest, but fails to restore the heart action stopped by absence of calcium in the perfusion medium. The effects of IM and theophylline are additive. It is concluded that the action of IM on the guinea pig heart is not connected with histamine receptors, and a possible role of IM as a regulator of free calcium ions is suggested.

Animals↗
PubMedDate not supplied

Role of sarcoplasmic reticulum in the contractile function of vascular smooth muscle as studied by 2,5-di-(tert-butyl)-1,4-benzohydroquinone.

The effects of 2,5-di-(tert-butyl)-1,4-benzohydroquinone (tBuBHQ), a potent selective inhibitor of hepatocyte endoplasmic reticulum Ca(2+)-ATPase, were functionally examined in rat aorta in order to assess whether tBuBHQ also acts as a Ca2+ pump inhibitor of sarcoplasmic reticulum (SR) in vascular smooth muscle. tBuBHQ elicited a slowly developing and gradually decreasing contraction which was dependent on extracellular Ca2+. We utilize the phenylephrine (PE)-induced transient contractile response in Ca(2+)-free medium as an indirect index on the status of intracellular Ca2+ store. When preparations, depleted of their PE-sensitive Ca2+ store, were allowed to replete their stores in Ca(2+)-containing medium, a sustained contraction in tBuBHQ-treated preparations was observed, whereas in untreated control preparations, readministration of Ca2+ elicited no contraction, or occasionally a weak, transient contraction. In control tissues, subsequent application of PE in Ca(2+)-free medium after Ca2+ loading resulted in full restoration of the transient contraction to PE; but such a transient contraction was not observed in the presence of tBuBHQ. These results indicated that the sequestration of Ca2+ into the PE-sensitive pool was inhibited by tBuBHQ. We also assessed effects of tBuBHQ on phentolamine-induced relaxation in PE-precontracted tissues in Ca(2+)-containing medium. A slower rate of relaxation was observed in preparations treated with tBuBHQ. In conclusion, our findings are consistent with the hypothesis that tBuBHQ acts as a SR Ca2+ pump inhibitor, interfering with effective refilling of PE-sensitive intracellular Ca2+ stores.

Animals↗
PubMed2006

ANG II enhances contractile responses via PI3-kinase p110 delta pathway in aortas from diabetic rats with systemic hyperinsulinemia.

We investigated the involvement of ANG II and phosphatidylinositol 3-kinase (PI3-K) in the enhanced aortic contractile responses induced by hyperinsulinemia in chronic insulin-treated Type 1 diabetic rats. Plasma ANG II levels were elevated in untreated compared with control diabetic rats and further increased in insulin-treated diabetic rats. Aortic contractile responses and systolic blood pressure were significantly enhanced in chronic insulin-treated diabetic rats compared with the other groups. These insulin-induced increases were largely prevented by cotreatment with losartan (an ANG II type 1 receptor antagonist) or enalapril (an angiotensin-converting enzyme inhibitor). LY-294002 (a PI3-K inhibitor) diminished the increases in contractile responses in ANG II-incubated aortas and aortas from chronic insulin-treated diabetic rats. The norepinephrine (NE)-stimulated levels of p110 delta-associated PI3-K activity and p110 delta protein expression were increased in aortas from insulin-treated diabetic compared with control and untreated diabetic rats, and chronic administration of losartan blunted these increases. Contractions were significantly larger in aortas from diabetic rats incubated with a low concentration (inducing approximately 10% of the maximum contraction) of ANG II or with NE or isotonic K+ than in aortas from nonincubated diabetic rats. NE-stimulated p110 PI3-K activity was elevated in aortas from diabetic rats coincubated with a noncontractile dose of ANG II. These results suggest that, in insulin-treated Type 1 diabetic rats with hyperinsulinemia, chronic ANG II type 1 receptor blockade blunts the increases in vascular contractility and blood pressure via a decrease in p110 delta-associated PI3-K activity.

Angiotensin II↗
PubMed1989

Contractile function of isolated feline cardiocytes in response to viscous loading.

The classical force-velocity relationship is a standard measure of the contractile function of isolated linear cardiac muscle, but no such simple index of contractile function exists for the isolated mammalian cardiocyte. Therefore, this study established an analogous viscosity-velocity relationship for the characterization of cardiocyte contractile function. For this purpose, force was imposed on unfettered adult feline cardiocytes as a series of defined viscous loads, which provided resistance to cardiocyte shape changes during contraction. This was done by increasing the viscosity of the Krebs superfusate (37 degrees C, pH 7.4) in graded, reproducible steps from 1 to 500 centipoise by the addition of methylcellulose. Sarcomere motion within each contracting cardiocyte was measured as movement of the diffraction pattern cast onto a photodiode array by a laser beam passing through the cell. Both the rate and extent of sarcomere shortening varied inversely with increasing viscosity, whereas neither resting sarcomere length nor osmolarity was altered. Further, increased inotropism effected by paired-pulse stimulation of cardiocytes caused an upward shift of the entire viscosity-velocity relationship. Thus the cardiocyte viscosity-velocity relationship is analogous in form to the force-velocity relationship of isolated linear cardiac muscle and provides a simple reproducible method for characterizing the contractile performance of relatively large numbers of cardiocytes isolated from a single specimen of myocardium.

Animals↗
PubMed1983

Hypertonicity and force development in frog skeletal muscle fibres.

Mechanical experiments were performed on isolated fibre bundles of frog semitendinosus muscle, using solutions made hypertonic by the addition of sucrose or NaC1. Muscle stiffness was measured with 1-ms step changes of length, from the plateau of an isometric tetanus. Within 20 min in hypertonic Ringer, isometric tetanus tension fell by 50% or more. The rate of tension redevelopment following stepwise shortening was reduced in hypertonic solution. Point voltage clamp studies showed that even when isometric tension had fallen to this extent, the stimulus strength--duration relation for mechanical activation was identical to that for controls. Point voltage clamp was used to intermittently repolarize fibres depolarized in solutions of high ionic strength, reactivating the excitation contraction coupling mechanism. Subsequent depolarization of the fibres allowed a visual test to be made of the fibres' ability to contract. The period during which contraction could be seen grew shorter as the ionic strength of the bathing medium was raised. The results of these different types of mechanical experiments suggested that the increased intracellular ionic strength caused by osmotic shrinkage in hypertonic Ringer's solution slows the rate at which individual cross bridges can form and develop tension, as well as reducing the maximum amount of tension they can generate. Muscle stiffness did not remain at control level in hypertonic solution; nor did it fall as much as did developed tension. The most obvious, although not the only, interpretation of this observation was that cross bridges are less stretched when isometric force is reduced and the length-tension relation of the elastic element is nonlinear.

Action Potentials↗
PubMed1990

Effects of strophanthidin on the force-frequency relationship in dog ventricular working and conducting tissues.

Effects of strophanthidin on force-frequency relationship were studied in dog working ventricular myocardium (VM) and Purkinje fibers (PF). In VM, both strophanthidin (0.3-1 x 10(-6) M) and driving rate increase within physiological range of 1 to 2 Hz potentiated the force of contraction. In PF, the following different responses were observed. 1. The contractile force decreased as the driving rate increased within the same range (negative staircase). 2. The positive inotropic effect of strophanthidin first increased and then declined. During the rising phase of strophanthidin inotropy, the staircase was still negative. The staircase became positive as strophanthidin inotropy declined. 3. Strophanthidin also potentiated the contractile force of extrasystolic and post-extrasystolic beats as revealed by the Johnson's two-state experiments. 4. The inotropic effects of strophanthidin were mimicked by high [Ca2+] (8.1-12.1 mM) and reversed by Ca channel blockers. Effects of Ca2+ overloading are discussed and a quantitative difference in regulation of cytosolic Ca2+ between VM and PF is suggested.

Amiodarone↗