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PubMed2005

Gender-specific differences in electromyographic changes and perceived pain induced by experimental muscle pain during sustained contractions of the upper trapezius muscle.

The aim of the study was to investigate gender-specific differences in the pain-induced alterations of muscle activity during sustained contractions of the upper trapezius muscle. Surface electromyographic (EMG) signals were recorded bilaterally from the upper trapezius muscles of healthy volunteers (10 men and 9 women). The subjects held the arms at 90 degrees abduction for 5 s (short contraction) and 3 min (sustained contraction). These contractions were performed before, during, and after injection of 0.5 ml of hypertonic saline (5.8%) bilaterally in the upper trapezius muscles. Injection of isotonic saline (0.9%) served as control. The root mean square (RMS) and mean power frequency (MPF) were computed from the EMG signals and normalized to the values obtained during maximal voluntary contractions. In the short contractions, injection of hypertonic saline, but not isotonic saline, induced a less pronounced decrease in RMS in women than men, and a significant decrease in MPF in men but not women. In the sustained contractions, RMS slope increased and MPF slope decreased (less negative) with muscle pain in men but not women. It was concluded that the pain-induced changes in motor control strategies during sustained contractions differ in men and women, which may partly explain gender differences in the incidence of musculoskeletal pain.

Adult↗
PubMed1991

Changes in responsiveness of the canine basilar artery to endothelin-1 after subarachnoid hemorrhage.

The effect of endothelin-1 (ET-1) on the basilar arteries from control and subarachnoid hemorrhage (SAH) dogs were examined. The maximal contraction of the basilar artery in response to ET-1 was markedly decreased in the SAH group. Treatment with 10(-8)M phorbol 12-myristate 13-acetate (PMA) reduced the contractile responses to ET-1 in the basilar arteries from control dogs. ET-1-induced contractions of the basilar arteries from control dogs were similar to those in strips from SAH dogs by the treatment with 10(-8) M PMA. Ca(2+)-induced contraction of the basilar arteries which were depolarized with isotonic K+ (64 mM) were significantly attenuated in SAH dogs. Treatment with PMA also reduced the contractile responses to Ca2+ in the basilar arteries from control dogs. These results indicate that decreased contractile responses of the basilar arteries to ET-1 and Ca2+ in the SAH group may be related to changes in the activity of the protein kinase C in vascular smooth muscle.

Animals↗
PubMed2003

Experimental pain by ischaemic contractions compared with pain by intramuscular infusions of adenosine and hypertonic saline.

Deep tissue pain can be related to reduced muscle blood flow, which comprises the metabolic demand under muscle work. The tissues and receptors involved in nociception after ischaemic muscle contractions are not known. The concentration of adenosine is increased after ischaemic contractions and might act as an algesic substance. In 15 subjects, adenosine, hypertonic saline (algesic), and isotonic mannitol (placebo) were infused into the tibialis anterior muscle and compared with the pain caused by ischaemic contractions. The muscle pain intensity (visual analogue scale; VAS), distribution, and quality were assessed. Pressure pain thresholds were recorded to assess the deep tissue sensitivity. Adenosine did not induce more pain than the placebo. The maximal VAS score after hypertonic saline and ischaemic contractions was higher compared with adenosine/placebo infusions. The duration and area of pain were significantly increased after hypertonic saline infusions compared with ischaemic contractions. Higher scores on the McGill pain questionnaire were given to the "stabbing", "burning", "heavy", and "exhausting" word categories after ischaemic contractions, and "cramping" was rated higher during hypertonic saline-induced muscle pain compared with ischaemic contractions. During hypertonic saline infusions, the pressure pain threshold was decreased compared with before and immediately after the pain had vanished. The present study shows that pharmacological levels of adenosine in skeletal muscle did not induce pain. Excitation of muscle nociceptors by hypertonic saline evoked hyperalgesia, larger areas of pain, and a different quality of pain compared with ischaemic contractions, suggesting that the pain after ischaemic contractions is mediated by other populations of nociceptors in muscle and/or other tissues than excited by hypertonic saline.

Adenosine↗
PubMed2006

Low-dose lactulose produces a tonic contraction in the human colon.

Lactulose (10-20 g day(-1)) is used to treat constipation. At this therapeutic dose, its effects on colonic motility remain unknown. Twenty-two healthy subjects swallowed a probe with an infusion catheter, six perfused catheters and a balloon connected to a barostat. Colonic phasic and tonic motor activity was recorded in fasting state. In group 1, four volunteers ingested 15 g lactulose and motility was recorded for 5 h after entry of lactulose into the caecum; in group 2, motility was recorded during (3 h) and 2 h after intracolonic infusion of isoosmotic and isovolumetric solutions containing sodium chloride alone (n = 9) or with 15 g lactulose (n = 9). In a last group of volunteers, isotopic colonic transit after ingestion of lactulose (10 g,n = 9) was assessed and compared with a control group (n = 17). Ingestion or intracolonic infusion of 15 g lactulose significantly decreased barostat bag volume (maximal decrease: 45 +/- 12% and 35 +/- 9% of basal value respectively). Phasic contractions remained unchanged. Tonic and phasic motility was unchanged by the isotonic and isovolumetric infusion of saline. Ingestion of lactulose significantly accelerated isotopic colonic transit time compared with the control group. We conclude that in healthy humans, 10-15 g ingestion or intracaecal infusion of lactulose produces a prolonged tonic contraction that may be involved in the laxative effect of lactulose.

Administration, Oral↗
PubMed2000

Increased intra-abdominal pressure alters the contractile properties of rabbit bladder.

OBJECTIVE: To evaluate the effects of increased intra-abdominal pressure (IAP) on the contractility of the rabbit bladder, as the dynamics of the bladder may be impaired in conditions associated with a high IAP, e.g. constipation and pregnancy. Material and methods The study comprised 22 adult male New Zealand rabbits; six served as the control group, eight had an IAP of 7 cmH2O imposed for 10 days by instilling air into the abdominal cavity and this IAP was maintained for 60 days in a further eight rabbits. After treatment, the rabbits were killed, and the bladders removed and cut into 3 x 12 mm strips. The contractile activity of the muscle strips was then recorded isometrically. Electrical field stimulation (EFS) was applied using a pair of platinum ring electrodes in trains of 3 s duration every 100 s (1 ms, 100 V, 2-100 Hz). Contractile responses to carbachol and isotonic KCl were also evaluated. RESULTS: EFS induced a frequency-dependent increase in contractile activity in all bladder strips. Ten days of high IAP resulted in an increased responsiveness to EFS, but high IAP for 60 days reduced the EFS-induced responses to the control levels. Carbachol (10-9-10-3 mol/L) elicited concentration-dependent contractions in all groups. From the concentration-response curves of carbachol, the log EC50 values (the concentration producing half the maximum effect) of the control and 60-day treated animals were comparable, at -6.24 (0.05) and -6.25 (0.04), respectively. However, the log EC50 of the 10 day-treated group was -4.97 (0.08) and significantly (P < 0.01) lower than that of both groups. Isotonic KCl produced contractions in all preparations; these contractions in the control and 60-day treated animals were similar, while the 10 day-treated group had significantly (P < 0.05) higher contraction amplitudes. CONCLUSION: Increased IAP alters the contractile properties of the bladder and its responsiveness to carbachol and KCl. As the intravesical pressure closely reflects the IAP, both should be increased in the present experimental design.

Abdomen↗
PubMed1984

Centrally programmed patterns of muscle activity in voluntary motor behavior of humans.

Rapid voluntary limb movements are accompanied by a triphasic electromyogram (EMG): the agonist muscle discharges briefly to generate the initial limb displacement and then, in sequence, an antagonist and second agonist burst occur. The origins of these bursts of EMG have been attributed to both peripheral and central sources. We attempted to determine in human subjects whether somesthetic afferent inputs related to passive muscle stretch or joint rotation were necessary for the appearance of the three bursts. EMGs were recorded while subjects performed rapid isotonic movements before and after forearm afferent function was blocked by ischemia. EMG patterns were also studied during phasic and sustained isometric contractions of forearm muscles. When the forearm was ischemically deafferented the triphasic EMG pattern persisted though the amplitudes of the three bursts were modified. In separate experiments, a similar three burst pattern was also observed while phasic isometric contractions were performed but not when rapid-onset sustained isometric contractions were executed. These data support the view that somesthetic afferent information related to muscle length or joint rotation is not necessary for the occurrence of the three burst pattern during rapid motor behaviors. Since bursts of EMG activity were observed when torque rose and fell quickly during fast isotonic movements and phasic isometric contractions, the triphasic pattern appears to be a fundamental property of the central program underlying such rapid motor behaviors.

Adult↗
PubMed1990

The effects of tetracaine on charge movement in fast twitch rat skeletal muscle fibres.

1. The effects of tetracaine, a local anaesthetic that inhibits muscle contraction, on membrane potential and intramembrane charge movements were investigated in fast twitch rat muscle fibres (extensor digitorum longus). 2. The resting membrane potentials of surface fibres from muscles bathed in isotonic Ringer solution containing 2 mM-tetracaine were well maintained, but higher concentrations of tetracaine caused a time-dependent fall of potential. Muscle fibres bathed in hypertonic solutions containing 2 mM-tetracaine were rapidly depolarized. In both isotonic and hypertonic solutions, the depolarizing effect of tetracaine could not be reversed. 3. Charge movement measurements were made using the middle-of-the-fibre voltage clamp technique. The voltage dependence of charge movements measured in cold isotonic solutions was well fitted by a Boltzmann distribution (Q(V) = Qmax/(1 + exp(-(V-V)/k] where Qmax = 37.3 +/- 2.8 nC muF-1, V = -17.9 +/- 1.2 mV and k = 12.6 +/- 0.8 mV (n = 6, 2 degrees C; means +/- S.E. of means). Similar values were obtained when 2 mM-tetracaine was added to the isotonic bathing fluid (Qmax = 40.6 +/- 2.3 nC microF-1, V = -14.1 +/- 1.3 mV, k = 15.3 +/- 0.8 mV; n = 8, 2 degrees C). 4. Charge movements measured around mechanical threshold in muscle fibres bathed in hypertonic solutions were reduced when 2 mM-tetracaine was added to the bathing fluid. The tetracaine-sensitive component of charge was well fitted with an unconstrained Boltzmann distribution which gave: Qmax = 7.5 nC microF-1, V = -46.5 mV, k = 5.5 mV. The e-fold rise of the foot of the curve was 9.3 mV.

Action Potentials↗
PubMed1981

Myocardial and ventricular function. Part I: Isolated muscle.

The force of isometric contraction of cardiac muscle is dependent on the initial muscle length and the contractility. The resting length-tension curve is characterized by a relatively high stiffness of cardiac muscle which can be correlated with the inability to stretch the cardiac sarcomere beyond a length of about 2.2 microns, the length at which the degree of overlap between actin and myosin filaments is optimal for contraction (Lmax). The length-active tension curve shows that an increase in the initial fiber length is associated with an increase in the maximal tension in isometric contractions and an increase in the maximal shortening during unloaded contractions. Increments in resting muscle length are accompanied by proportionate increases in sarcomere length. With active shortening of the sarcomeres tension developed at one muscle length is actually generated at a shorter sarcomere length. Peak isometric force is obtained only with obligatory sarcomere shortening, at the expense of series compliance, during contraction. Developed tension critically depends on sarcomere length at the peak of contractile activity; the final sarcomere length during contraction is primarily determined by the load rather than initial length or mode of shortening. In tetanic contractions, there is no intrinsic difference between isometric and isotonic end-systolic length tension relation. The force velocity relationship helps distinguish two major ways in which cardiac performance may be altered, i.e., changing initial muscle length (the Frank-Starling phenomenon) and changing the contractile state, only the latter of which can affect an increase in the maximal velocity. For a given contractile state, the force-velocity-length relationship is unique; preload is pertinent only insofar as it sets the limit of the length range over which shortening can occur. In cardiac muscle the relationship between muscle length and active tension development is not clearly understood in terms of relating sarcomere length and degree of myofilament overlap to force production. With respect to the mechanics of relaxation, the early filling phase of cardiac diastole is primarily determined by the rate of isovolumetric pressure decline, the latter phase is dominated by the resting or diastolic compliance of the ventricular chamber.

Biomechanical Phenomena↗
PubMed1982

Inulin uptake and washout in contracting and quiescent rat papillary muscle.

Equilibration and washout curves of inulin were determined in isolated rat papillary muscles. Inulin uptake did not reach a steady-state value even after a long equilibration time. The effects of contractile activity were investigated. Isometric contractions increased the rate of inulin uptake and washout. In isotonic conditions, a smaller increase in the uptake and washout was observed. These changes could be attributed to an actual increase of inulin distribution space and/or to an accelerated diffusion kinetics.

Animals↗
PubMedDate not supplied

Effects of hyperkalemia on neonatal endothelium and smooth muscle.

BACKGROUND: Contradictory results have been reported regarding the effect of hyperkalemic cardioplegic or organ preservation solutions on endothelial and smooth muscle cells. The present study was designed to determine the effects of potassium concentrations and exposure times to hyperkalemia on endothelium-derived relaxing factor (nitric oxide) biosynthesis and release, and smooth muscle function in neonatal vessels. METHODS: Aortic rings taken from neonatal rabbits were studied in organ baths at physiologic pressure. The effect of Krebs' solution containing 5, 25, 50, or 100 mmol/L potassium incubated for 45 minutes (group 1), St. Thomas' Hospital cardioplegic solution containing 16, 25, 50, or 100 mmol/L potassium for 45 minutes (group 2), and Krebs' solution containing 5 and 50 mmol/L potassium or St. Thomas' Hospital cardioplegic solution containing 16 and 50 mmol/L potassium for 135 minutes (group 3) or 270 minutes (groups 4 and 5) was examined. The rings were then washed and contracted with U46619 (30 nmol/L). The ability to release endothelium-derived relaxing factor (nitric oxide) in response to acetylcholine was tested. RESULTS: The maximal relaxation induced by acetylcholine did not decrease in any group. Evidence of slight alteration of smooth muscle contraction was seen only in the rings incubated in Krebs' solution with 50 mmol/L potassium for 270 minutes (group 4) with unchanged maximal contraction and sensitivity to potassium (group 5). CONCLUSIONS: We conclude that after exposure for a limited time (4 1/2 hours), hyperkalemia per se does not significantly alter the function of endothelium to release endothelium-derived relaxing factor (nitric oxide) in response to acetylcholine and only slightly alters the contraction speed of smooth muscle in the neonatal rabbit aorta.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1989

Mechanical and electrical properties of cardiomyopathic hearts of Syrian hamsters.

To determine whether the cardiomyopathy that develops in the Syrian hamster before the occurrence of congestive heart failure is associated with mechanical and electrical alterations consistent with myocardial dysfunction, left ventricular posterior papillary muscles of control and cardiomyopathic animals at 120 days of age were studied in vitro. Moreover, the electrocardiographic response to ouabain was investigated in vivo to analyze the arrhythmogenic potential of the cardiomyopathic heart to glycoside exposure. Results showed a decreased tension-generating ability of the myocardium in the diseased animals, which was accompanied by a prolongation of the timing parameters of contraction and an increase in the duration of the repolarization phase of the transmembrane action potential. Furthermore, the velocity of isotonic muscle shortening and relengthening was depressed at all physiological loads. Glycoside infusion elicited premature ventricular contractions, ventricular tachycardia, and ventricular fibrillation in diseased hamsters much earlier in time than in healthy controls. The impairment in mechanical performance in association with the abnormality in membrane electrical activity may be responsible for the progression of the disease process and the occurrence of lethal arrhythmias in this animal model.

Action Potentials↗
PubMed1991

Inhibition by ouabain and veratridine of acetylcholine-evoked phasic contraction in the guinea-pig taenia coli.

Inhibitory action of ouabain and veratridine on acetylcholine (ACh)-evoked phasic contraction was examined in the guinea-pig taenia coli. ACh (5 x 10(-4)M) produced a biphasic (phasic and tonic) contraction. As the phasic contraction, but not the tonic contraction, was resistant to gallopamil (D600, 2 x 10(-7)M), a blocker of voltage-dependent Ca2+ channels, all experiments were carried out in the presence of gallopamil at this concentration. Addition of high Ca2+ (30 mM) to the solution containing ACh induced a sustained contraction, which increased in the presence of ouabain (10(-5)M), an inhibitor of the Na(+)-K+ exchange system. On the other hand, the ACh-evoked phasic contraction was suppressed by ouabain (10(-7)-10(-5) M) in a time- and dose-dependent manner. The suppression by ouabain (10(-6)M) of the phasic contraction was transiently potentiated by the addition of veratridine (10(-6)M), an activator of Na+ channel. In contrast, the greater suppression by ouabain (10(-5)M) of the contraction was antagonized by amiloride (10(-4)M), a blocker of Na+ channel. This antagonism by amiloride was transiently inhibited in the presence of veratridine. In the absence of ouabain, the amplitude of the phasic contraction was transiently reduced by adding veratridine but was increased by amiloride. In addition, the phasic contraction by ACh increased 80 min after exposure to Na(+)-free isotonic high-K+ solution (K+, 143 mM), which elicited greater depolarization of the cell membrane. In a fluorescence study with Fura-2, an intracellular free-Ca2+ indicator, ACh increased the fluorescence intensity from the tissue by excitative light at 340 nm, which coupled with the phasic contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed2004

Mechanism of activation of the tonic component of contraction in myocytes of guinea pig heart.

AIM: Contractions of myocytes of guinea pig heart consist of a phasic component relaxing independently on the voltage and a tonic component relaxing upon repolarization. We found previously that Ca(2+) activating the tonic component is released from the sarcoplasmic reticulum. In this study, we analysed the mechanism of activation and maintenance of this release. METHODS: Experiments were performed at 37 degrees C in ventricular myocytes of guinea pig heart. Voltage-clamped myocytes were stimulated by the pulses of the duration of 300 ms to 15-45 s from the holding potential of -40 to +5 mV. [Ca(2+)](i) was monitored as fluorescence of Indo-1 and contractions were recorded with the TV edge-tracking system. RESULTS: Myocytes responded to the short and long pulses with phasic contraction or Ca(2+) transient followed by the sustained contraction or increase in [Ca(2+)](i). Repolarization brought about relaxation. 10 mmol L(-1) Ni(2+) blocking Na(+)/Ca(2+) exchange superfused during the tonic component increased its amplitude. Superfusion of Ca(2+)-free solution during sustained contraction brought about relaxation both in normal cells and in cells superfused with Ni(2+) despite preserved sarcoplasmic reticulum Ca(2+) content assessed with caffeine spritz. Relaxing effect of Ca(2+)-free solution was not affected by carboxyeosin, a blocker of sarcolemmal Ca(2+)-ATPase. Tonic component of contraction and of Ca(2+) transient was inhibited by 200 micromol L(-1) ryanodine, a blocker of Ca(2+) release channels of the sarcoplasmic reticulum and by 20 micromol L(-1) nifedipine, a blocker of L-type I(Ca). CONCLUSION: Tonic component of contraction results from Ca(2+) release via the sarcoplasmic reticulum Ca(2+) channels activated by sustained, nifedipine-sensitive and Ni(2+)-insensitive Ca(2+) influx. Alternatively, the SR Ca(2+) release is activated by voltage, the dihydropyridine receptors acting like voltage sensors.

Animals↗
PubMed1993

Inhibition by alpha 2-adrenoceptor agonists of contractions of rabbit isolated colon elicited by pelvic nerve stimulation.

1. Segments of rabbit distal colon were set up for isotonic recording and the extrinsic pelvic parasympathetic nerves were stimulated for 30 s periods at 2 Hz. 2. Atropine (100 nM) abolished acetylcholine-induced contractions, but only partly reduced responses to nerve stimulation. 3. Clonidine and related compounds, UK14819, UK14304, UK15121, UK11957 and UK42620, inhibited nerve stimulation-evoked contractions at concentrations which had no effect on the response to exogenous acetylcholine, suggesting that the compounds inhibited transmitter release. 4. The imidazolidine compounds UK14819, UK14304 and UK15121 had three to five times the potency of clonidine. Another imidazolidine, UK11957, was about three times less potent than clonidine and appeared to have lower intrinsic activity. The morpholinocatechol UK42620 was about 100 times less potent than clonidine. Phenylephrine was about 10,000 times less potent than clonidine. 5. Idazoxan (1-10 microM) and yohimbine (300 nM-3 microM) reversed the depressant effects of clonidine and the UK compounds, indicating that the effects were exerted on alpha 2-adrenoceptors. This was confirmed by the finding that the slope of Schild plot of idazoxan against UK14304 was close to unity with the pA2 value = 7.14. 6. Atropine-resistant neurogenic contractions were completely abolished by UK14819 (100 nM) and this effect was completely reversed by idazoxan (10 microM). 7. Depending on other (especially centrally mediated) effects, the more potent inhibitors of neurogenic colonic motor activity, with their higher alpha 2-adrenergic agonist activity, may have advantages over clonidine as antidiarrhoeal drugs.

Acetylcholine↗
PubMed2006

Evidence for positive force feedback during involuntary aftercontractions.

We examined the involuntary isotonic muscle aftercontraction which follows a 1-min voluntary contraction at 60% of maximum voluntary force. Aftercontractions provide a unique paradigm for investigating the automatic postural control of the upper limb in man. Previous work has shown that the strength of these contractions in m. deltoid is linearly dependent on the inclination of the subject's body in the gravitational field. The current experiments were designed to test if this was due to the gravitational loading on the arm as this also changes with body inclination. The subject sat with the head stationary to prevent changes in vestibular orientation. Aftercontractions in m. deltoid were evoked with the normal weight of the arm present and also with arm loadings equal to 0, 25, 50 and 75% of this value. These reductions were produced by a counter lever apparatus. The results showed that the EMG amplitude of this involuntary contraction depended linearly on the loading of the arm. This is interpreted as being the result of positive load feedback. Aftercontraction EMG amplitude at 100% load was 2.7 times greater than at 0% load. The results are discussed in the context of recent work on positive load feedback in man and animals.

Adult↗
PubMed1995

Effect of omega-conotoxin GVIA on tetrodotoxin-insensitive acetylcholine release by nicotine in guinea-pig bladder.

1. Contractile responses and acetylcholine release evoked by nicotine and electrical field stimulation (EFS) were determined by isotonic transducer and radioimmunoassay, respectively. 2. Nicotine-induced contraction was reduced to 30% by nicotinic receptor antagonist, hexamethonium but was insensitive to tetrodotoxin. EFS-induced contraction was abolished by tetrodotoxin but was insensitive to hexamethonium. Replacement of external Na by choline completely abolished the contractile responses evoked by nicotine and EFS. 3. Both contractions evoked by nicotine and EFS were inhibited by omega-conotoxin GVIA, and inhibitory effects of the toxin were greater in low Ca concentrations. 4. In the condition that external Na or Ca is omitted from physiological solution, acetylcholine release evoked by nicotine was not observed. Nicotine-induced acetylcholine release was partially inhibited by omega-conotoxin but was insensitive to tetrodotoxin. 5. In conclusion, nicotine interacts with nicotinic receptors located on nerve terminals and produces transmitter release which depends on external Na through tetrodotoxin-insensitive mechanisms. It is suggested that voltage-dependent omega-conotoxin sensitive Ca channels are partially involved in the nicotine-induced transmitter release.

Acetylcholine↗
PubMed1997

Neurotensin decreases pepsin output and gastrointestinal motility in chickens.

Two experiments were conducted to determine the effect of neurotensin on gastric secretion and gastrointestinal motility in conscious chickens. Chickens were surgically fitted with a cannula to collect secretions from the proventriculus and strain gauge transducers sutured to the gizzard, duodenum, and ileum in order to detect contractions. Peripheral intravenous infusion of physiological levels of neurotensin inhibited pepsin output from the proventriculus, but had no effect on the volume or pH of gastric secretions. Neurotensin also inhibited both the frequency and strength of gastrointestinal contractions when compared to motility patterns following infusion of isotonic 0.9% (wt/vol) saline. The frequency of occurrence of small intestinal refluxes was not affected by neurotensin. These results coupled with our earlier work, which demonstrated that neurotensin is released by the presence of oleic acid in the duodenum, indicate that neurotensin may function as an enterogastrone released by lipids in the gastrointestinal tract of the chicken. This overall inhibitory effect of neurotensin on the avian gut indicates that it is involved in the postprandial regulation of digestion, especially lipid digestion.

Analysis of Variance↗