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PubMed2004

The effect of myofibroblast on contracture of hypertrophic scar.

Wound contraction in humans has both positive and negative effects. It is beneficial to wound healing by narrowing the wound margins, but the formation of undesirable scar contracture brings cosmetic and even functional problems. The entire mechanism of wound healing and scar contracture is not clear yet, but it is at least considered that both the fibroblasts and the myofibroblasts are responsible for contraction in healing wounds. The myofibroblast is a cell that possesses all the morphologic and biochemical characteristics of both a fibroblast and a smooth muscle cell. Normally, the myofibroblasts appear in the initial wound healing processes and generate contractile forces to pull both edges of an open wound until it disappears by apoptosis. But as an altered regulation of myofibroblast disappearance, they remain in the dermis and continuously contract the scar, eventually causing scar contracture. In this research, to compare and directly evaluate the influence on scar contracture of the myofibroblast versus the fibroblast, dermal tissues were taken from 10 patients who had highly contracted hypertrophic scars. The myofibroblasts were isolated and concentrated from the fibroblasts using the magnetic activating cell-sorting column to obtain the myofibroblast group, which contained about 28 to 41 percent of the myofibroblasts, and the fibroblast group, which contained less than 0.9 percent of the myofibroblasts. Each group was cultured in the fibroblast-populated collagen lattice for 13 days, and the contraction of the collagen gel was measured every other day. In addition, they were selectively treated with tranilast [N-(3',4'-dimethoxycinnamoyl) anthranilic acid] to evaluate the influence on the contraction of the collagen gel lattice. During the culture, the myofibroblast group, compared with the fibroblast group, showed statistically significant contraction of the collagen gel lattice day by day, except on the first day, and only the myofibroblast group was affected by tranilast treatment, showing significant inhibition of gel contraction. By utilizing an in vitro model, the authors have demonstrated that myofibroblasts play a more important role in the contracture of the hypertrophic scar.

Actins↗

PubMed1985

Chromosomal abnormalities associated with congenital contractures (arthrogryposis).

In a study of 350 patients with multiple congenital contractures (arthrogryposis), 80 (23%) patients had mental retardation or were developmentally delayed. Out of that group of 80 patients, 13 (16%) were found to have abnormal karyotypes. Two of the thirteen had a family history of chromosomal abnormalities without congenital contractures, therefore, 11 patients had chromosomal anomalies which appeared to be associated with the congenital contractures. Five of the eleven (45%) had chromosome mosaicism, three of those had tissue mosaicism. Two had abnormal skin fibroblast cell lines and normal peripheral leukocyte chromosome studies and one had a normal bone marrow karyotype with abnormal peripheral leukocyte chromosome studies. Chromosome studies were done in these patients with congenital contractures because of developmental delay and multisystem involvement, or recognition of clinical features typical of a chromosomal syndrome. We recommend first lymphocyte; and if those are normal, then fibroblast studies be done on all patients with multiple joint contractures and developmental delay, particularly if unusual facial features or multisystem abnormalities are present.

Abnormalities, Multiple↗

PubMed1983

Contracture of guinea-pig ileum on withdrawal of methionine5-enkephalin is mediated by substance P.

The effects of methionine5-enkephalin (Met-enkephalin, ME) 5 X 10(-8)-5 X 10(-6) moll-1) were investigated on the resting guinea-pig ileum. While in contact with the ileum, ME reduced the natural tone and movements, but following washout a contracture occurred which increased with increasing duration of the contact period from 0.5 to 32 min and with increasing concentration of the ME present during the contact period. The washout contractures after 2 min contact with ME, 10(-6) moll-1, were abolished by naloxone, 10(-6)moll-1, added prior to the addition of ME, atropine, 5 X 10(-6)moll-1 and the substance P (SP) antagonist, (D-Pro2, D-Phe7, D-Trp9)-SP, 10(-5)moll-1 and were reduced by 5-hydroxytryptamine (5-HT)-autodesensitization. Washout contractures following 32 min contact with ME, 10(-6)moll-1, were significantly inhibited by the SP antagonist and naloxone and were abolished by a combination of atropine and the SP antagonist, but were not significantly reduced by atropine alone or by 5-HT-desensitization. Contractures of ileum occurred on addition of naloxone to ileal segments exposed to ME for 2 or 32 min. These contractures were also inhibited by the SP antagonist but a combination of atropine and SP-desensitization was required to abolish them. It was concluded that gut dependence occurs following very brief exposure to an opioid and that SP plays a central role in the withdrawal response precipitated either by washout or addition of naloxone.

Animals↗

PubMed1986

The dependence of the strength of sodium-depletion contractures of isolated frog atrial trabeculae on the membrane potential.

When the Na bathing isolated frog atrial trabeculae voltage clamped at -80 mV is reduced, a strong contracture develops. Upon return to normal extracellular Na concentration [( Na]o) this contracture rapidly relaxes. Hyperpolarization of the membrane by a voltage-clamp pulse during the low-Na contracture produces a rapid relaxation and the extent of this relaxation is dependent upon the size of the hyperpolarizing pulse. The membrane potential at which tension is relaxed to a constant level during low-Na perfusion, is exponentially related to the change in the Na gradient. This relationship shows that changes in the Na gradient, across the cell membrane, have nearly three times more effect on the generation of tension than changes in membrane potential. This would be consistent with the notion that contracture tension is determined by an electrogenic Na/Ca exchange across the cell membrane with a coupling ratio approaching 3 Na+/Ca2+. Exposure of the muscle to strophanthidin reduces the size of the hyperpolarizing pulse required to relax completely the low-Na contracture. As a consequence the apparent coupling ratio is increased to just above 3 Na+/Ca2+. Upon repolarization to -80 mV in low-Na Ringer solution, the redeveloped tension may be larger than that recorded immediately before the hyperpolarizing pulse. This after-effect suggests that hyperpolarization of the membrane may reduce the fall in intracellular [Na] that normally occurs when the bathing [Na] is reduced.

Animals↗

PubMed1989

Role of chloride in hypertonicity-induced contractures of rat soleus muscle.

The role of chloride in contractures induced in rat soleus muscle by mannitol-, sucrose- or urea-containing hypertonic solutions was investigated. Replacement of chloride with nitrate, sulphate or perchlorate reduced the amplitude of mannitol- and sucrose-induced contractures, and the first phase of contractures induced by urea. Addition of 9-anthracene carboxylic acid had similar effects. The presence of diazepam increased the amplitude of 'hypertonic' contractures. The results show that chloride is important in the development of hypertonic contractures.

Animals↗

PubMed1974

A study of the contractures induced in frog atrial trabeculae by a reduction of the bathing sodium concentration.

1. The relationship between the [Ca](o), the [Na](o) and the strength of the contracture evoked when the [Na](o) is reduced has been investigated in isolated frog atrial trabeculae.2. The strength of the contracture varies by the [Ca](o) (2) and by 4 radical([Na](o)) over the lower tension range.3. The contracture induced by reduction of [Na](o) is not sustained, but relaxes spontaneously. The rate of this relaxation is only dependent on the [Na](o) is the presence of strophanthidin.4. After the spontaneous relaxation of an Na-free contracture, the ability of the trabecula to develop tension upon a second challenge with Na-free solution returns in about 3 min if the muscle is perfused with Na-containing fluid. This recovery process is slowed if the [Na](o) is low during the recovery period, but the recovery is hastened by electrical stimulation of the preparation or by perfusion with K-free or strophanthidin containing sodium-Ringer.5. It is suggested that the influx of Ca(2+) which induces the Na-free contracture depends on the presence of Na(+) inside the cells. When the intracellular Na concentration falls, the Ca influx falls, and the muscle relaxes as a result of the activity of an intracellular relaxing structure.

Animals↗

PubMed1975

Graded activation of myofibrils and the effect of diameter on tension development during contractures in isolated skeletal muscle fibres.

If the space constant of the T-system (lambdaT) its not large in comparison with the radius (a) of a muscle fibre, different levels of depolarization should activate different proportions of the cross-section. This possibility was tested in isolated muscle fibres with isotonic and isometric K contractures. 2. During isonic contractures with more than 40 mM-K, wavy myofibrils appeared in the centre of the fibre. The sarcomere spacings (s) of the wavy myofibrils, measured parallel to the long axis of the myofibrils, were 1-9-1-95 mum. However, the superficial myofibrils could shorten to or below s=1-5 mum without becoming wavy. 3. In the same muscle fibre where myofibrils became wavy during K contractures, no waviness appeared during repetitive electric stimulation in normal Ringer (50 shocks/sec, 12 degrees C), although s decreased below 1-5 mum. Wavy myofibrils were interpreted as not activated. 4. With isometric contractures it was found that the amount of depolarization needed to obtain maximal tension was smaller for fibres of shorter radius. The degree of depolarization for producing maximal tension is related to a by 6 mV/10mum. 5. These results strongly suggest that in K contractures lambdaT is not large in comparison with a.

Animals↗

PubMed1981

Effects of external calcium reduction on the kinetics of potassium contractures in frog twitch muscle fibres.

1. The amplitude and time course of K contractures (Cl- constant) of single twitch muscle fibres of the frog have been analysed in three external Ca2+ concentrations. 2. The resting potential, effective resistance, threshold for the Na current and K-induced depolarizations were not modified by replacing 1.8 mM-Ca2+ by 3 mM-Mg2+ in absence (low-Ca saline: 3-6 micro M-Ca2+) or in the presence of 5 mM-EGTA (Ca-free saline: less than or equal to 10(-9) M-Ca2+). 3. The tension development during the initial phase of K contractures was independent of external Ca2+ while the amplitude, the duration and the time constant of spontaneous relaxation decreased progressively as Ca2+ concentration was diminished. 4. When the concentration of Mg2+ was increased to 5 mM in Ca-free saline K contractures were slower and smaller than those in 3 mM-Mg2+. 5. In Ca-free saline the activation curve (peak tension vs. logarithm of external K+ concentration) shifted by 3-5 mV towards more positive potentials while the inactivation curve (peak tension of the test contracture vs. logarithm of external K+ concentration during the conditioning period) shifted by 16-18 mV towards more negative potentials. Both curves became steeper in Ca-free saline. 6. The effects of external Ca2+ reduction were not modified by replacing all chloride for methanesulphonate. 7. Direct effects of external Ca2+ on excitation-contraction coupling during K contractures could involve the inward Ca current and/or specific interactions between external Ca2+ ions and the coupling mechanism.

Animals↗

PubMed1983

Potassium contractures in mouse limb muscles.

The force of contractures produced by 14-400 mM-K+ (as methanesulphonate) was measured in whole mouse soleus (sol.), extensor digitorum longus (e.d.l.), and in bundles from these muscles. Frog semitendinosus muscles were used for comparison. Whole mouse muscles displayed biphasic contracture responses lasting more than 5 min when provoked by 150m M-K+. Contractures of bundles dissected from these muscles were monophasic and had a short duration. The time required for the muscle bundles to contract and relax to 1/2 maximum force (T) was an inverse function of [K+]. T was increased by lowering [K+] from 400 to 50 mM by a factor of 8.3 and 7.0 in proximal and distal portions of sol. and by a factor of 4.2 and 2.8 in proximal and distal portions of e.d.l., respectively. The force-[K+] relation was steeper for sol. than for e.d.l., and the proximal portions were more sensitive to K+ than the distal portions, particularly in e.d.l. The capability of the muscles to produce force in response to 400 mM-K+ after a 10 min exposure to 30 or 50 mM-K+ was high in sol., somewhat lower in proximal parts of e.d.l. and in frog semitendinosus, and lowest in distal parts of e.d.l. It was concluded that K contractures of mouse muscles are basically monophasic, and that biphasic contractures of whole muscles arise because of K+-diffusion delays, slow responses to intermediate [K+], and differences in responsiveness of the fibres contained in a particular muscle.

Animals↗

PubMed1990

The role of [Ca2+]i and [Ca2+] sensitization in the caffeine contracture of rat myocytes: measurement of [Ca2+]i and [caffeine]i.

1. Fluorescence measurements have been made in single, isolated rat ventricular myocytes using the Ca2(+)-sensitive indicators Fura-2 and Indo-1. In Fura-2-loaded cells, the application of caffeine (2-20 mM) produced a change of fluorescence indicating an increase of [Ca2+]i which then spontaneously decayed to control levels. These changes of [Ca2+]i were accompanied by a contracture. 2. In contrast, in Indo-1-loaded cells, in addition to the changes of fluorescence expected for the transient increase of [Ca2+]i produced by caffeine, there was a maintained decrease of fluorescence. 3. Measurements in vitro showed that caffeine quenches the fluorescence of Indo-1 (but not of Fura-2) in a [Ca2+]-and wavelength-independent manner. Caffeine therefore had no effect on the ratio of Indo-1 fluorescence measured at two wavelengths. This inhibition by caffeine could be described by an apparent Ki of 4 mM. In the cell the Ki was considerably larger (18 mM). 4. We have separated the Indo-1 fluorescence changes into caffeine- and [Ca2+]i-dependent components. The time course of change of intracellular caffeine was calculated. When [caffeine]o was rapidly increased, [caffeine]i changed with a rate constant of 8 s-1 giving an apparent permeability to caffeine of 2 x 10(-3) cm s-1. 5. This method was used to measure [caffeine]i and [Ca2+]i simultaneously during caffeine-induced contractures. The shape of the caffeine contracture was found to depend on both the speed of application of caffeine and the concentration applied. If caffeine was applied quickly then the contracture developed within 1 s to a maximum level and then relaxed to a lower maintained level. With slower application, there was a more complete relaxation of the initial contraction followed by a slower redevelopment of contraction. 6. Despite the difference in contraction time course, irrespective of the flow rate, [Ca2+]i decayed monotonically. The slow secondary development of contraction has the same time course as the increase of [caffeine]i. The caffeine contracture can be reproduced by a model in which both [Ca2+]i and [caffeine]i affect contraction. 7. The increase of [Ca2+]i is not greatly affected by altering the caffeine concentration from 2.5 to 50 mM. In contrast the maintained level of contraction increases over this range showing that the Ca2(+)-independent effects of caffeine on the myofilaments have a low affinity for caffeine.

Animals↗

PubMed1984

Blockade of Ca2+ channels inhibits K+ contractures but not twitches in skeletal muscle.

The effects of the voltage-sensitive, calcium channel blocking agents, D-600 and verapamil, on twitches and K+-induced contractures were studied using frog's toe muscles. K+-contracture tension was reduced by concentrations as low as 10(-8) M and the contractures were blocked by 10(-6) M. There was no significant difference in the effects of the two drugs. Twitches were potentiated by 5 X 10(-5) M D-600 and blocked only at 3 X 10(-4) M. The latter concentration also produced contractures in the toe muscles. As shown by other workers, the higher concentration also blocks action potential production and this is probably the way in which it blocks the twitch. Raising the bathing solution Ca2+ concentration from 1.08 to 10 or 20 mM, produced only a small, inconsistent, noncompetitive antagonism of the D-600 block of K+ contractures.

Animals↗

PubMed1988

The effect of diazepam on potassium contractures, contraction threshold, and resting tension in rat skeletal muscles.

The effects of diazepam on potassium contractures, contraction threshold, and resting tension have been examined in rat soleus muscle fibres. Two actions of the drug were defined that could not be attributed to changes in the resting membrane potential or depolarization in high potassium solutions. The major effect was an increase in the amplitude of submaximal tension during either twitches or potassium contractures and an increase in resting tension. At 400 microM diazepam, there was (a) a fourfold increase in 40 mM potassium contracture tension, (b) a negative shift of 8 mV in the membrane potential for half maximum tension estimated from the best fit of a Boltzmann-type equation to average potassium contracture data, (c) a negative shift of 8 mV in the threshold for contraction measured under voltage clamp conditions, and (d) a contracture of variable amplitude to a level that was occasionally equivalent to maximum tetanic tension. These potentiating actions of diazepam depended on drug concentration within the range of 100-800 microM. In contrast, the second effect of diazepam, depression of maximum tension by 10-15%, was independent of drug concentration between 100 and 400 microM. The results support the idea that diazepam produces an increase in resting myoplasmic calcium concentrations.

Animals↗

PubMed1992

Effects of reduced external sodium concentration and multivalent cations on caffeine contractures in young ferret atrial trabeculae.

The characteristics of caffeine (1.25-80 mM) transient contractures have been examined in small atrial trabeculae (diameters 50-250 microns) isolated from young (1-1.5 months) ferret hearts. In the control medium, the half-saturation constant and the maximum contracture strength (at infinite caffeine concentration) were 37.8 +/- 10.2 mM and 0.9 +/- 0.2 kN.kg-1 (n = 11), respectively. The contractile response to caffeine was markedly enhanced following reduction of external sodium (70-0 mM). The perfusion of young ferret trabeculae with the sodium-free medium (up to 3 min) decreased the half-saturation constant by a factor of three (12.4 +/- 1.6 mM, n = 8) with an increase in maximum contracture strength (1.09 +/- 0.3 kN.kg-1, n = 8). The effects of various divalent and trivalent cations have been tested on the 10 mM caffeine contracture in trabeculae perfused with Na-containing (140 mM) solution. The order of cation effectiveness is Gd3+ (half effect 0.04-0.07 mM) greater than Cd2+ (0.15-0.25 mM) greater than Ni2+ (2-2.5 mM) greater than Co2+ (7-7.5 mM) much greater than Mn2+. In conclusion, the present work has shown that in atrial trabeculae isolated from young ferret hearts, the strength of the caffeine contracture was markedly affected by the activity of the sarcolemmal Na-Ca exchange.

Animals↗

PubMed1997

BAY K 8644 and ClO4- potentiate caffeine contracture without Ca2+ release channel activation.

Effects of perchlorate (ClO4-) and BAY K 8644 on caffeine contracture and Ca2+ release channel current were studied in frog skeletal muscle. Single fibers produced a small transient contracture on addition of 2.2 mM caffeine. ClO4 at 10 mM enhanced caffeine contracture 3.7-fold. This effect was inhibited by 10 microM nifedipine pretreatment. An increase in caffeine contracture was also obtained after exposure to 0.1 microM BAY K 8644 for 1 h. At 20 mM, external K+ potentiated caffeine contracture 2.2-fold. ClO4- (< 10 mM) and BAY K 8644 (0.1-1 microM) did not affect open probability (Po), unitary conductance, and open and closed time constants of the Ca2+ release channel current. BAY K 8644 at 0.1 microM did not further enhance the channel that had been activated by 2 mM caffeine. However, 20-30 mM ClO4 increased Po significantly and led the channel to a long open state by increasing the slow open time constant and decreasing the fast closed time constant. These results suggest that binding of ClO4 and BAY K 8644 to dihydropyridine receptors elicits a further increase in Ca2+ release from the sarcoplasmic reticulum.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1981

Excitation-contraction coupling in mammalian cardiac muscle during Ba2+-induced contracture.

The membrane potential and tension were recorded during contracture of mammalian ventricular muscles bathed in Tyrode solution with Ba2+ in the place of Ca2+. Strength of contracture increased with increasing Ba2+ concentration from 0.1 to 4 mM and reached a plateau above 4 mM. The membrane potential was depolarized to about -35 mV with 0.1 mM Ba2+ and to -20 mV with 5 mM Ba2+. When 0.5 mM Mn2+ was added to Ba2+-Tyrode solution, in which the muscle had been in a state of steady contracture, the muscle immediately started to relax to the resting level. In contrast, addition of 2 micrograms/ml epinephrine to Ba2+-Tyrode solution increased the strength of the contracture. Neither epinephrine nor Mn2+ caused any noticeable changes of the depolarized membrane potential. The results suggest that Ba2+ not only activates the contractile system but also depolarizes the membrane potential independently of activating the contractile system. These two remarkable actions of Ba2+ seem to be responsible for the long-lasting contracture.

Action Potentials↗

PubMed1989

Effects of isoflurane and halothane on rapid cooling contractures in myocardial tissue.

The effects of isoflurane and halothane on the availability of Ca2+ stored in and released from the sarcoplasmic reticulum (SR) were studied in isolated rabbit papillary muscles by measuring the effects of the anesthetics on rapid cooling contractures, which are known to be activated by Ca2+ released from the SR. Isoflurane (0.3%) reduced the force of the rapid cooling contracture to 57% of control with a marked slowing of the average rate of contracture development and increased the force of the first contraction after rewarming to 133% of control. In contrast, 1.7% halothane, which reduced the rapid cooling contracture to 51% of control (comparable to the value in the presence of 0.3% isoflurane), had little effect on the rate of contracture development and strongly inhibited the first contraction after rewarming to 5% of control. Halothane, but not isoflurane, strongly inhibited postrest potentiated-state contractions, which are also known to be activated by Ca2+ released from the SR. These results suggest that 1) isoflurane inhibits rapid cooling-induced Ca2+ release from the SR without inhibiting Ca2+ release triggered by rapid depolarization as occurs in the potentiated-state contraction, and 2) halothane inhibits contractile activity dependent on Ca2+ released from the SR regardless of mechanism involved.

Animals↗

PubMed1991

Reperfusion-induced contracture develops with a decreasing [Ca2+]i in single heart cells.

The causal relationship between intracellular Ca2+ overloading and reperfusion-induced contracture was examined from changes in intracellular Ca2+ concentration ([Ca2+]i) at rest, changes in the magnitude and time course of intracellular Ca2+ transients, and the development of contracture. Single myocytes isolated from guinea pig hearts were subjected to the conditions mimicking ischemia and reperfusion. Ischemic condition was produced by superfusing myocytes with hypoxic substrate-free solutions containing elevated concentrations of K+, H+, and lactate as described by Ferrier et al. (Circ. Res. 56: 184-194, 1985). Changes in [Ca2+]i were estimated using fura-2 as the Ca2+ indicator. Under these conditions, twitch contractions were suppressed during simulated ischemia associated with an early and gradual rise of [Ca2+]i. The development of contracture, however, was not observed. Upon "reperfusion" of myocytes that had been subjected to 20 min of the above "ischemic" condition, the elevated [Ca2+]i declined rapidly. With the recovery of twitch contractions, contracture developed despite a substantial decrease in [Ca2+]i. These results indicate that reperfusion-induced contracture is not associated with a concomitant increase in [Ca2+]i in isolated myocytes.

Animals↗

PubMed1995

Preconditioning accelerates contracture and ATP depletion in blood-perfused rat hearts.

We investigated the effect of preconditioning on the ischemia-induced depletion of ATP in the blood-perfused rat heart. Isolated hearts (n = 5/group) were aerobically perfused with whole blood from a support rat and subjected to zero-flow global ischemia (37 degrees C) for periods up to 35 min. Frozen hearts were taken for metabolic analysis. Ischemic contracture was assessed with an isovolumic intraventricular balloon. The study groups were 1) control (C) with unprotected ischemia, 2) preconditioning (PC; 2 cycles of 3-min ischemia/3-min reperfusion), and 3) cardioplegia (CP; St. Thomas') before ischemia. Preconditioning accelerated, whereas cardioplegia delayed, ischemic contracture (time to peak contracture: PC = 8.1 +/- 0.3 and CP = 25.1 +/- 0.2 min vs. C = 15.6 +/- 0.3 min, P < 0.05). The ischemia-induced decline in ATP was delayed by cardioplegia but accelerated by preconditioning (P < 0.05). In a parallel study, preconditioning and cardioplegia protected postischemic contractile function to a similar extent. Thus, in the blood-perfused rat heart, preconditioning accelerated ischemic contracture and depletion of ATP. In contrast, cardioplegia slowed ischemic contracture and ATP depletion.

Adenosine Triphosphate↗