SEARCH · PubMed Health

Results for “Muscle Contraction”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 415 records · Page 23Linked to original sources

PubMed1985

[Dynamics of the efferent regulation of muscle contraction. Analysis of transition processes: frequency of efferent stimulation--muscle length].

Transition processes of the length changes were studied in the ankle extensors of anesthetized cats. The processes were evoked under isotonical conditions by step changes in frequency of distribution stimulation of the efferents supplying these muscles. The system dynamics was essentially nonlinear because the time constants of the processes were dependent on amplitudes and sign of the input signal. The time constants abruptly decreased when the sign of the length changes alternated from minus to plus and continuously decreased when amplitude of the transition process rose in the absolute value. The time constants for the transition processes were 1.15 +/- 0.09 s for soleus shortening and 0.40 +/- 0.07 s for its lengthening. The same parameters in fast muscles were 0.51 +/- 0.085 for shortening and 0.21 +/- 0.04 s for lengthening. These time constants are very close to the parameters of the transition processes: external load-muscles length. The observed properties of the muscles are discussed for their functional significance.

Animals↗

PubMed1999

Adrenergic influence of uterine muscle contractions stimulated by a glycoside from the root of Dalbergia saxatilis.

The mechanism of uterine muscle contraction stimulated by a triterpenoid glycoside (dalsaxin) isolated from the root of D. saxatilis was investigated by in vitro methods in the rat. Dalsaxin caused a dose-related increase in uterine muscle contraction. The contraction was single and transient and was abolished by moderate doses of isoprenaline (1.80 nmol-0.40 mumol) and salbutamol (0.13-25 mumol). Adrenaline (9.10 nmol) also caused a reversible decrease (92.6%; P < 0.01) in myometrial contraction stimulated by this glycoside (0.24 mg/ml). Uterine muscle responses to dalsaxin (0.24 mg/ml) were enhanced by the beta-adrenergic receptor antagonist, propranolol, in a dose related manner. Atipamezole (1.50 ng/ml) but not prazosin (7.72 nmol-15.60 nmol) substantially reduced (80%; P < 0.01) myometrial contractions induced by this uterine spasmogen. The results suggest that dalsaxin enhances uterine muscle contraction by stimulating post junctional alpha 2-adrenergic receptors, presumably by inhibiting plasma membrane adenylate cyclase system and its associated increase in intracellular cAMP content.

Adrenergic alpha-Agonists↗

PubMed1997

Inhibitory effect of sex steroids on guinea-pig airway smooth muscle contractions.

We assessed the possible inhibition of airway smooth muscle contraction by progesterone and pregnanolones (5 alpha and 5 beta-reduced). Progesterone and 5 beta-pregnanolone prevented histamine- or carbachol-induced contraction in isolated guinea-pig trachea and potency was related to their respective chemical structure; progesterone was the most potent inhibitor in a concentration-dependent manner. The steroids also exhibited calcium antagonist activities in this tissue as assessed by their action on calcium entry in depolarized preparations; this event involved the immediate blockade of the extracellular calcium influx in the muscle cell membrane, indicating a nongenomic action. Classical GABAA antagonists did not block the progesterone response, implying no involvement of the GABAA-receptor complex. Our results suggest a bronchodilating effect induced by sex steroids, and probably by other related compounds, before the genomic mechanisms take place. This nongenomic action of steroids could have potential therapeutic usefulness in the treatment of asthma.

Animals↗

PubMed1985

Desensitization of alpha-1 adrenergic receptor-mediated vascular smooth muscle contraction.

Desensitization of alpha-1 receptor-mediated smooth muscle contraction was studied in rabbit aorta. Incubation of rabbit aorta ring segments with epinephrine (10(-6) M) for 7 hr resulted in a 10-fold loss in sensitivity of the tissue to alpha-1 adrenergic receptor-mediated contraction with no change in maximal force of contraction. This loss in sensitivity was specific for alpha-1 receptor-mediated contraction because responses to histamine and serotonin were unchanged in these aortas. Conversely, prolonged exposure of vessels to histamine (10(-5) M) led to desensitization of histamine-mediated contraction without altering responses to alpha-1 receptor stimulation. Using [125I] BE2254, a potent alpha-1 receptor antagonist, the loss in sensitivity to catecholamines was found not to be mediated by down-regulation of alpha-1 receptors nor by a loss in their affinity for epinephrine. However, desensitization was associated with a blunting of alpha-1 receptor stimulation of phosphatidylinositol turnover. These results suggest that desensitization of alpha-1 receptor-mediated contraction in rabbit aorta does not appear to be mediated by changes in receptor number or affinity but may involve alterations in receptor coupling.

Adenylyl Cyclases↗

PubMed1991

Does the pressor response to ischemic exercise improve blood flow to contracting muscles in humans?

The purpose of this study was to determine in humans 1) the gain for the reflex pressor response that occurs when perfusion pressure to rhythmically contracting muscles is reduced and 2) whether the pressor response improves blood flow to the contracting muscles. Six normal subjects performed light, moderate, and heavy rhythmic forearm contractions (30/min) with the forearm enclosed in a Plexiglas box. Pressure in the box was increased 10 mmHg each minute up to 50 mmHg to reduce transmural pressure in the arterial system of the forearm. Mean arterial pressure (MAP) was measured continuously. During light exercise no reflex increase in MAP occurred until box pressure was 50 mmHg. During moderate and heavy exercise MAP began to increase with only 10- to 20-mmHg increases in box pressure. The slope of this increase was 3.5-3.9 mmHg per 10 mmHg of box pressure (approximately 60% of that in dogs). In a further study on six subjects a deep vein draining the active forearm muscles was cannulated and deep venous O2 saturation measured to assess how a 50-mmHg increase in box pressure and subsequent reflex increase in MAP altered blood flow to the contracting muscles during heavy rhythmic exercise. The increase in box pressure reduced blood flow to contracting forearm muscles by 20-25% and was followed by a 19-mmHg increase in MAP that did not appear to improve perfusion of the active muscles. This finding was unexpected, because studies in dogs suggest that the pressor response to rhythmic exercise with restricted muscle blood flow can improve perfusion of the active muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1995

Epithelial modulation of leukotriene-C4-induced human tracheal smooth muscle contraction.

We investigated the role of epithelium in smooth muscle contraction induced by leukotriene C4 (LTC4) in isolated human trachea. The contractile response to LTC4 was potentiated by a gamma-glutamyl transpeptidase (gamma-GTP) inhibitor L-serine borate and by removal of the epithelium. Both L-serine borate (4.5 x 10(-2) M) and removal of the epithelium shifted the concentration-response curves to LTC4 to lower concentrations by 1.2 and 1.0 log units, respectively. Incubation of cultured human tracheal epithelial cells with either LTC4 or LTD4 resulted in the formation of LTD4 or LTE4. The isolated epithelial cells and cultured epithelial cells contained gamma-GTP activity. Histochemical study indicated that gamma-GTP-like activity was present in the epithelial, submucosal, and smooth muscle layers. These findings suggest that the epithelium modulates the contractile response to LTC4 in human trachea by LT-degrading enzymes.

Aged↗

PubMed2005

Computational simulation of human upper airway collapse using a pressure-/state-dependent model of genioglossal muscle contraction under laminar flow conditions.

A three-element, pressure- and state (sleep and wake) -dependent contraction model of the genioglossal muscle was developed based on the microstructure of skeletal muscle and the cross-bridge theory. This model establishes a direct connection between the contractile forces generated in muscle fibers and the measured electromyogram signals during various upper airway conditions. This effectively avoids the difficulty of determining muscle shortening velocity during complex pharyngeal conditions when modeling the muscle's contractile behaviors. The activation of the genioglossal muscle under different conditions was then simulated. A sensitivity analysis was performed to determine the effects of varying each modeled parameter on the muscle's contractile behaviors. This muscle contraction model was then incorporated into our anatomically correct, two-dimensional computational model of the pharyngeal airway to perform a finite-element analysis of air flow, tissue deformation, and airway collapse. The model-predicted muscle deformations are consistent with previous observations regarding upper airway behavior in normal subjects.

Airway Obstruction↗

PubMed1987

Muscle contraction headache. Overview and update of a common affliction.

Muscle contraction headache usually can be correctly diagnosed on the basis of a thorough patient history and physical examination, although diagnostic tests may be necessary to exclude structural or inflammatory disease. Often, symptoms are directly related to emotional conflicts. In most cases, the primary care physician can provide treatment, which includes understanding and emotional support. Pharmacologic therapy and biofeedback are effective in controlling symptoms. Depression should be suspected in patients with chronic headache. Referral for neurologic or psychiatric consultation should be considered if the diagnosis is unclear or therapy is unsatisfactory.

Diagnosis, Differential↗

PubMed1975

Prostaglandins and cholera: the occurrence of prostagland in-like smooth muscle contracting substances in cholera diarrhoea.

Prostaglandin-like smooth muscle contracting substances were identified in acid lipid extracts of diarrhoeal faeces taken from patients presenting clinical symptoms of cholera. Five out of the eleven cases studied were bacteriologically confirmed as cholera. The PG-like activity in the individual samples ranged from 3-27 mg PGE2 equivalents /ml of diarrhoeal stool. Parallel bioassay and thin-layer chromatographic analysis of the extracts indicated that about 60% of the activity was due to an F-type PG, 15% to an E-type PG and the rest to unidentified lipid substanc(s). It is proposed that increased PG production in cholera (indicated by these findings) may at least contribute to the disease.

Adult↗

PubMed1990

Stimulation of duodenal muscle contraction by porcine or canine motilin in the dog in vivo.

Motilin is a 22 amino acid polypeptide stimulating intestinal muscle contraction. Structure analysis of motilin purified from hog and from dog intestinal mucosa reveals different amino acids in positions 7, 8, 12, 13, and 14. Previous in vitro experiments suggested this species-related structural heterogeneity could generate different bioactive characteristics for these two peptides. This study was designed to compare the stimulatory mechanism of canine and porcine motilins on dog duodenal motility in vivo, testing the hypothesis that canine motilin stimulates a receptor located on the intestinal muscle, while porcine motilin is acting on intrinsic nerves regulating intestinal muscle contraction. Synthetic porcine and canine motilins were administered through a catheter inserted in the caudal pancreatic duodenal artery to stimulate the contraction of a close irrigated duodenal segment. In acute experiments performed on anaesthetized animals, both peptides induced a similar motor stimulation that was inhibited by tetrodotoxin and atropine. In experiments in conscious animals, canine and porcine motilins were equally potent in inducing premature phase III of the migrating motor complex, and the action of both peptides was abolished by atropine or hexamethonium. This study reveals that the structural heterogeneity between porcine and canine motilin does not influence the bioactivity of both peptides in the dog in vivo and suggests that circulating endogenous motilin stimulates intestinal muscle contraction through intrinsic excitatory nerves.

Anesthesia↗

PubMed1998

Dipeptidase inhibitor and epithelial removal potentiate leukotriene D4-induced human tracheal smooth muscle contraction.

We investigated the role of epithelium in smooth muscle contraction induced by leukotriene D4 (LTD4) in isolated human trachea. The contractile response to LTD4 was potentiated by an inhibitor of dipeptidases L-cysteine and by removal of the epithelium. Both L-cysteine (3 x 10(-3) M) and removal of the epithelium shifted the concentration-response curves to LTD4, to lower concentrations by 0.7 and 0.6 log units, respectively. Incubation of cultured or isolated human tracheal epithelial cells with LTD4 resulted in the formation of LTE4, which was completely blocked by pretreatment with L-cysteine (3 x 10(-3) M). The isolated and cultured human tracheal epithelial cells contained microsomal dipeptidase (MDP) activity. Immunohistochemical study indicated MDP protein was present in the epithelium and endothelial cells of submucosal microvessels in the human trachea. These results suggest that the epithelium modulates the contractile response to LTD4 in human trachea by dipeptidases degrading LTD4.

Acetylcholine↗

PubMed2006

Cardiovascular responses and neurotransmitter changes during static muscle contraction following blockade of inducible nitric oxide synthase (iNOS) within the ventrolateral medulla.

The enzyme nitric oxide synthase (NOS) which is necessary for the production of nitric oxide from L-arginine exists in three isoforms: neuronal NOS (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS). Our previous studies have demonstrated the roles of nNOS and eNOS within the rostral (RVLM) and caudal ventrolateral medulla (CVLM) in modulating cardiovascular responses during static skeletal muscle contraction via altering localized glutamate and GABA levels (Brain Res. 977 (2003) 80-89; Neuroscience Res. 52 (2005) 21-30). In this study, we investigated the role of iNOS within the RVLM and CVLM on cardiovascular responses and glutamatergic/GABAergic neurotransmission during the exercise pressor reflex. Bilateral microdialysis of a selective iNOS antagonist, aminoguanidine (AGN; 1.0 microM), for 60 min into the RVLM attenuated increases in mean arterial pressure (MAP), heart rate (HR), and extracellular glutamate levels during a static muscle contraction. Levels of GABA within the RVLM were increased. After 120 min of discontinuation of the drug, MAP and HR responses and glutamate/GABA concentrations recovered to baseline values during a subsequent muscle contraction. In contrast, bilateral application of AGN (1.0 microM) into CVLM potentiated cardiovascular responses and glutamate concentration while attenuating levels of GABA during a static muscle contraction. All values recovered after 120 min of discontinuation of the drug. These results demonstrate that iNOS within the ventrolateral medulla plays an important role in modulating cardiovascular responses and glutamatergic/GABAergic neurotransmission that regulates the exercise pressor reflex.

Animals↗

PubMed2006

Cavernosus muscle contraction during erection: is it voluntary or reflex, given the striated nature of the muscles?

The bulbo- and ischio-cavernosus muscles (BCM, ICM) contract in the rigid erection phase, leading to a suprasystolic cavernosal pressure. We investigated the hypothesis that the contraction of cavernosal muscles is reflexogenic despite their striated nature. The intracavernosal pressure (ICP) and the cavernosus muscles' electromyography (EMG) were recorded in 18 healthy volunteers in the flaccid and erectile phases. The test was repeated after separate anesthetization of the cavernosus muscles and the corpora cavernosa while the penis was in the rigid erection phase. The ICM and BCM showed no EMG activity with tumescence and full erection. When the ICP reached a mean of 148.6 +/- 9.4 cm H2O, both the ICM and BCM showed increased EMG activity. The suprasystolic pressure was intermittent and corresponded to the intermittent BCM and ICM contraction. Voluntary cavernosus muscle contraction did not increase the ICP at the different stages of erection. Anesthetization of the penis in the rigid erection phase led to disappearance of the cavernosus muscles' EMG activity, while bland gel application did not. Anesthetization of the 2 contracting cavernosus muscles, while the penis was in the rigid phase, produced an ICP drop to 69.5 +/- 7.6 cm H2O; repetition with saline did not affect the ICP. Cavernosus muscle contraction on corporal pressure elevation seems to be reflex and mediated through the corporo-cavernosal reflex (CCR). Changes in the evoked response amplitude would indicate a defect in the reflex pathway.

Adult↗

PubMed2005

[Is electrical stimulation with voluntary muscle contraction of physiologic interest in aging women?].

OBJECTIVE: To analyze the physiological effects of electrical stimulation with voluntary muscle contraction exercise in postmenopausal women. MATERIALS AND METHODS: Thirty-two females aged 62 to 75 years were randomly assigned to three groups to perform four activity sessions for six weeks: group ME (N =11) climbed up and down stairs, group ES (N =11) practised electrostimulation, and group ME + ES (N = 10) undertook both activities. Physiological adaptations of body composition (lean and fat masses and bone mineral density), muscular strength (isometric and dynamic), vertical jump and posturokinetic activities (balance and gait) were analysed. RESULTS: For the three groups, the isometric strength at angle 100 degrees (average increase right and left legs, ME: 19 N.m; ES: 4.5 N.m; ME + ES: 11.5 N.m), the dynamic strength at speed 60 degrees.s(-1) (average increase right and left leg, ME: 15 N.m; ES: 14 N.m; ME+ES: 18.5 N.m) and the vertical jump (ME: 23 mm; ES: 16 mm; ME + ES: 34 mm) increased contrary in the body composition and posturokinetic activities. Nevertheless, the group ME + ES adapted differently on some parameters of bone mineral density (P < 0.05) and dynamic strength (P < 0.01) in relation to the groups ES and ME. CONCLUSION: Electrostimulation with voluntary muscle contraction exercise could induce different physiologic adaptations compared with electrostimulation or voluntary muscle contraction exercise alone.

Adaptation, Physiological↗

PubMed1994

Recombinant stem cell factor-induced mast cell activation and smooth muscle contraction in human bronchi.

The effect of human recombinant stem cell factor (SCF) on inflammatory mediator release and smooth muscle contraction was evaluated in human isolated intralobar bronchi. Bronchi from 21 of 26 donors contracted in response to SCF. The threshold concentration was approximately 0.01 micrograms/ml. At 1 micrograms/ml, the tissues contracted to about 60% of the carbamylcholine-induced maximum contraction. The responses to SCF mimicked those obtained with anti-IgE. Thus, the contractions to SCF and anti-IgE were inhibited to a similar extent by a combination of a cysteinyl-leukotriene receptor antagonist and a histamine H1 receptor antagonist. SCF also mimicked the effect of anti-IgE in releasing histamine, i-LTD4, and PGD2 from the bronchi. At a threshold concentration for contraction (0.01 micrograms/ml), SCF had no effect on subsequent responses to anti-IgE in the bronchi. The data suggest that human recombinant SCF contracts airway smooth muscle by stimulating the release of contractile mediators from bronchial mast cells. The data fail to support the hypothesis that SCF primes bronchial mast cells to subsequent immunologic stimuli.

Antibodies, Anti-Idiotypic↗

PubMed2001

Inhibition of dynamic thigh muscle contraction by electrical stimulation of the posterior cruciate ligament in humans.

We investigated the influence of electrical stimulation of the posterior cruciate ligament (PCL) on the motoneuron pool of the thigh muscle during voluntary static and dynamic muscle contraction. The study group comprised nine young men with no history of injury to the knee joints. Multistranded Teflon-insulated stainless-steel wires were inserted into the PCL guided by ultrasound. In three subjects wires were also inserted into the fat pad of the knee. The PCL was electrically stimulated during static, concentric, or eccentric muscle contraction with a constant load of 20% of the maximal voluntary contraction of either the quadriceps or the hamstrings. Electromyographic signals were recorded with bipolar surface electrodes placed over the vastus medialis, rectus femoris, vastus lateralis, biceps femoris caput longum, and semitendinosus muscles. The stimuli consisted of four pulses delivered at 200 HZ; the stimulus amplitude was two to three times the sensory threshold. The electrical stimulation of the PCL inhibited the ongoing muscle activity in both the quadriceps and hamstrings with latencies of 114-150 ms and 99-130 ms, respectively. Stimulation of the fat pad of the knee did not influence the muscle activity. The study suggests that the mechanoreceptors in the PCL are involved in controlling muscle activity during both static and active muscle contractions. The relative long latency of the reflex makes it unlikely that it can serve as a directly protective reflex for the cruciate ligaments.

Adult↗

PubMed1999

Phosphorylation events associated with cyclic nucleotide-dependent inhibition of smooth muscle contraction.

Activation of cyclic nucleotide-dependent signaling pathways leads to relaxation of bovine carotid artery smooth muscle contractions and is associated with increased phosphorylation of the small heat shock-related protein (HSP20). Previous reports have shown that human umbilical artery smooth muscle is uniquely resistant to cyclic nucleotide-dependent relaxation, and HSP20 is not phosphorylated. In this investigation, we determined the phosphorylation events associated with cyclic nucleotide-dependent inhibition of smooth muscle contraction. In carotid artery, activation of cyclic nucleotide-dependent signaling pathways inhibited contractile responses to serotonin but did not inhibit myosin light chain phosphorylation or oxygen consumption. The inhibition of contraction was associated with increases in HSP20 phosphorylation. In umbilical artery, activation of cyclic nucleotide-dependent signaling pathways did not inhibit serotonin-induced contraction or myosin light chain phosphorylation. The lack of contractile inhibition in umbilical artery was not associated with significant increases in HSP20 phosphorylation. In conclusion, cyclic nucleotide-dependent contractile inhibition is independent of the inhibition of myosin light chain phosphorylation or oxygen consumption but does correlate with increased HSP20 phosphorylation.

Animals↗

PubMed1988

Comparison of mucus flow rate, radiolabelled glycoprotein output and smooth muscle contraction in the ferret trachea in vitro.

1. The concentration-response curves for rate of mucus output, labelled-glycoprotein output and smooth muscle contraction in response to methacholine, phenylephrine and salbutamol were determined in the ferret trachea in vitro. 2. The potencies of methacholine and phenylephrine are both in order: smooth muscle contraction, glycoprotein output, rate of mucus output. 3. At lower concentrations methacholine is more potent than is phenylephrine on smooth muscle contraction, glycoprotein output and rate of mucus output. 4. Concentration-response curves for salbutamol show very little change in rate of mucus output but a large increase in glycoprotein output. 5. It is concluded that the glycoprotein output induced by salbutamol may come from a source different from those induced by methacholine and phenylephrine.

Albuterol↗