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At least 37 records · Page 2Linked to original sources
PubMed1997

Stretch-shortening contraction in Parkinson patients: evidence of normal muscle contraction execution with low efficiency.

The aim of this study was to compare different muscle contraction types in Parkinson patients and controls. Ten patients with mild to moderate Parkinsonism (7 men, 3 women, mean age 62.3) and 11 controls (7 men, 4 women, mean age 66.0) were investigated. Measurements in eccentric, concentric contraction and stretch-shortening contraction were made using modified Cybex 11 equipment. The torque areas in ankle dorsiflexors at 30 degrees/second, 120 degrees/second and 180 degrees/second were measured. The power (Nm/second) was calculated in a defined range of motion. The power at different angular velocities and contraction types was significantly lower in the patient group than in the control group. In both groups the power in eccentric and stretch-shortening contraction was significantly larger than in concentric contraction. The relative improvement in power in stretch-shortening contraction in patients was equal to the improvement made by the controls. Patients generated significantly more EMG than controls in concentric and eccentric contractions. The EMG in the stretch-shortening cycle was the same in both groups at higher velocities. The patients performed voluntary isolated muscle contraction in the same way as controls, but with a lower efficiency in contraction. The eccentric torque and the supplement of torque generated from the combined eccentric and concentric (stretch-shortening) contraction might be important for achievement of adequate dynamic movements in patients with Parkinson's disease.

Aged↗
PubMed1992

Arginine vasopressin inhibits phasic contractions and stimulates giant contractions in monkey colon.

Abdominal cramps and urgent defecation are common side effects of clinical doses of arginine vasopressin, indicating that the drug may have stimulating effects on colonic motor activity. Four strain-gauge transducers were implanted on the colon in six monkeys. A blood flow probe was fixed on the inferior mesenteric artery. After a 1-hour control recording, vasopressin, 0.13, 1.3, or 13.0 ng.kg-1.min-1, was infused intravenously for 90 minutes. The frequency of basal colonic contractions was reduced with increasing doses of vasopressin, but their mean amplitude and duration were not altered. Giant migrating contractions associated with defecation were initiated by the highest dose of vasopressin. Atropine had no effect on these giant migrating contractions but completely inhibited normal phasic contractions. Hexamethonium completely inhibited both giant migrating contractions and phasic contractions. Parasympathetic denervation of the colon did not inhibit giant migrating contractions initiated by vasopressin. Our findings suggest that the physiological concentrations of serum vasopressin present perioperatively may transiently inhibit spontaneous colon contractions but are unlikely to be the major cause of postoperative ileus. The giant migrating contractions initiated by vasopressin may account for the defecation associated with pharmacological doses of vasopressin. The initiation of giant migrating contractions by vasopressin may be mediated through a neural pathway.

Animals↗
PubMed2003

The shape of the force-elbow angle relationship for maximal voluntary contractions and sub-maximal electrically induced contractions in human elbow flexors.

The force-length relationship is a basic property of skeletal muscle. Knowledge of this relationship is necessary for most analyses of human movement, and in simulation models predicting movement control strategies. Studies on animal muscles have shown that force-length relationships for sub-maximal contractions are not related through a simple scaling procedure to the relationship for maximal contractions. Furthermore, potentiation might produce a shift of sub-maximal relative to maximal force-length relationships. In this study, we tested the hypothesis that human force-elbow angle relationships for sub-maximal unpotentiated contractions are shifted to larger elbow angles (i.e. larger muscle lengths) compared to the relationship for maximal voluntary contractions (MVC), and that this shift is reduced, or even abolished, for sub-maximal potentiated contractions. Force-elbow angle relationships (48-160 degrees) were obtained from healthy subjects (n=13). At each of nine tested elbow angles, the test set consisted of a single twitch (ST(pre)) and a doublet twitch (DT(pre)) stimulation of m. biceps brachii, followed by an MVC, followed by another single twitch (ST(post)) and a doublet twitch (DT(post)) stimulation. The single and doublet twitches induced sub-maximal contractions. The force-elbow angle relationships for the pre-MVC (unpotentiated) twitch contractions were shifted to larger angles compared to those obtained for MVC. The force-elbow angle relationships for the post-MVC (potentiated) twitch contractions were shifted to smaller angles compared to those obtained for the unpotentiated twitch contractions. These results support the idea that the shift to larger muscle lengths for the sub-maximal, unpotentiated force-length relationships relative to the relationship for maximal contractions may be caused by a length-dependent Ca(2+) sensitivity that may be offset, at least in part, by potentiation.

Adaptation, Physiological↗
PubMed1995

Evidence for a functional alpha 1A- (alpha 1C-) adrenoceptor mediating contraction of the rat epididymal vas deferens and an alpha 1B-adrenoceptor mediating contraction of the rat spleen.

1. The alpha 1-adrenoceptor subtype mediating contraction of the rat epididymal vas deferens and rat spleen has been investigated by use of alpha 1-adrenoceptor antagonists that have shown selectivity between the different cloned receptor subtypes. 2. In the rat epididymal vas deferens the potency of noradrenaline and phenylephrine was increased in the presence of neuronal and extra-neuronal uptake blockers, cocaine and beta-oestradiol, but these did not alter that of methoxamine. The order of potency of the agonists in the presence or absence of uptake blockade was noradrenaline > phenylephrine > methoxamine. In the rat spleen the potency of these agonists was not altered in the presence of cocaine and beta-oestradiol, and their order of potency was the same as in the vas deferens. 3. The non subtype selective alpha 1-adrenoceptor antagonist prazosin (up to 1 x 10(-7) M) was found to antagonize contractions to noradrenaline in the vas deferens competitively (pA2 9.2), but only in a non competitive manner in the spleen. Contractions to phenylephrine in the spleen however were competitively antagonized by prazosin (up to 1 x 10(-7) M) with a pA2 of 9.2. This suggests that there is an alpha 1- and a non alpha 1-adrenoceptor response to noradrenaline in the rat spleen. 4. Pretreatment with chlorethylclonidine (10(-4) M for 30 min) did not alter the noradrenaline contractions in the vas deferens, but contractions to noradrenaline and phenylephrine in the spleen were shifted 30 and 300 fold to the right of the control curve, respectively. This suggests that only the contractions in the spleen were mediated by alpha 1B-adrenoceptors. 5. The noradrenaline contractions in the vas deferens were competitively antagonized by WB 4101 (pA29.6), 5-methyl-urapidil (pA2 8.7), phentolamine (pA2 8.3), benoxathian (pA2 9.4), spiperone (pA2 7.5),indoramin (pA2 8.4) and BMY 7378 (pA2 6.7), consistent with the affinities of these antagonists in binding studies on tissue alpha 1A-adrenoceptors. These values correlated best with their published affinities on the expressed alpha 1c-adrenoceptor clone and poorly with those at either the expressed alpha lb- or alpha 1d adrenoceptor clones. Therefore the classical alpha 1A-adrenoceptor appears to be the same as the expressed alpha lc-adrenoceptor clone.6. The phenylephrine contractions in the spleen were competitively antagonized by WB 4101 (pA2 8.1),5-methyl-urapidil (pA2 7.1), phentolamine (pA2 7.3), benoxathian (pA2 7.4), spiperone (pA2 7.9),indoramin (pA2 7.5) and BMY 7378 (pA2 7.4), consistent with the affinities of these antagonists in binding studies on tissue alB-adrenoceptors. The pA2 values correlated best with the published affinities of these compounds on the expressed alb-adrenoceptor clone and poorly with those at either the expressed alpha ld- or alpha lc-adrenoceptor clones. Therefore the alpha lB-adrenoceptor appears to be the same as the expressed alpha lb-adrenoceptor clone.7. The results provide pharmacological evidence that the alpha1-adrenoceptor mediating noradrenaline contractions in the epididymal portion of the rat vas deferens is the alpha 1A-(alpha lC) subtype and that contractions to phenylephrine in the rat spleen are mediated by the alpha 1B-subtype.

Adrenergic alpha-Agonists↗
PubMed1993

Effects of contraction level on the changes of surface electromyogram during fatiguing static contractions.

Changes of the surface electromyogram (EMG) during a fatiguing static contraction were studied at contraction levels of 5, 10, 15, 20, 30, 40, and 50% of the maximum voluntary contraction (MVC). Seven subjects performed the static contractions of the elbow flexion and 6 subjects performed those of the planter flexion. Bipolar surface EMG was led from biceps brachii (BB) in the elbow flexion and from soleus in the planter flexion. Power spectra, mean amplitudes of EMG (AEMG) and durations of averaged waves classified by amplitude (AWCA) were calculated from EMG. The AWCA was calculated by averaging EMG waves separately for the 5 amplitude ranges of the trigger points. Relative power increased below 50 Hz in BB and 120 Hz in soleus during the contractions with time. Relative power in low frequencies (RPWL) increased with time even at the low contraction levels during one third part of the contraction from the start. But the RPWL decreased with time in some cases below and equal to 20% MVC. The increase in the RPWL was larger at 20-50% MVC than at 5-15% MVC contraction. The duration of AWCA increased with time at 30-50% MVC and decreased at 5-20% MVC. The duration, however, correlated positively with RPWL in part even at 5-20% MVC. The changes in the AWCA duration were attributed to the changes in conduction velocity (CV) of muscle action potential, since the relation between the changes in the duration by fatigue and the contraction levels was the same with the reported relation between changes in CV and the contraction levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Phorbol ester (PMA)-induced biphasic contraction of the rat aorta and effects of sodium nitroprusside and forskolin on the contraction.

Effects of sodium nitroprusside (SNP) and forskolin on the contractile responses of aortic strips to phorbol 12-myristate 13-acetate (PMA) were investigated in the present study. PMA produced biphasic contraction in the rat aorta, i.e. sustained, slowly developing contraction followed by phasic contraction superimposed on the sustained contraction. Both sustained contraction and phasic response were completely abolished by treatment with staurosporine. Phasic contraction was completely inhibited by nicardipine or removal of external Ca2+, whereas sustained contraction was not affected by nicardipine. Both SNP and forskolin inhibited sustained contraction. Ca(2+)-induced contraction of the aorta which had been treated with PMA in Ca(2+)-free medium was completely inhibited by nicardipine and was partially inhibited by forskolin, but SNP had no effect on the Ca(2+)-contracture. These results suggest that 1) PMA contacts the rat aorta through stimulation of protein kinase C and activation of voltage-dependent Ca2+ channels; 2) there may be great differences in the effects of cyclic GMP and cyclic AMP on the protein kinase C-induced sustained and phasic contractions.

Adenylyl Cyclases↗
PubMed1993

Frequency of acoustic myography during isometric contraction of fresh and fatigued muscle and during dynamic contractions.

The frequency of the acoustic myographic (AMG) signal was examined during fresh and fatigued isometric contractions of quadriceps and during dynamic contractions of biceps brachii (BB) in healthy subjects. Recordings were obtained from quadriceps over a range of forces between 10% and 100% maximal voluntary contraction prior to, and 15 minutes after, a fatiguing exercise. Recordings from BB were obtained over a range of submaximal forces (0-8.5 kg) during concentric and eccentric contractions. The mean power frequency (MPF) of the AMG signal was analyzed during each of these contractions by fast-Fourier transform (FFT). The MPF was not significantly different (P > 0.05) during fresh and fatigued contractions of quadriceps and increased quadratically with force in both states (r = 0.81, fresh; r = 0.77, fatigued). During concentric contractions of BB the MPF initially increased with force, but then decreased at the heavier loads (> 5.5 kg). The MPF of eccentric contractions did not significantly (P > 0.05) alter with force. The AMG MPF was within a similar low frequency range for both muscles, during different types of contraction, and was unaltered with fatigue.

Adolescent↗
PubMed1991

Effects of hypoxia and reoxygenation on regular contractions and postrest contraction in rat papillary muscles.

The effects of hypoxia and reoxygenation on regular contractions and postrest contractions (PRC) of papillary muscle of rats were studied. Isometric tension was measured during two cycles of hypoxia and reoxygenation. Trains of 80 externally continuous stimulations at 40/min were applied. PRCs were evoked by a stimulus train after a 60 sec resting interval. After 90 min of hypoxia (the first hypoxia period), regular contractions and PRCs decreased to 5.6 +/- 2.0% and 23.4 +/- 2.4% of baseline values, respectively (p less than 0.001; n = 18). After 90 min of reoxygenation, the recovery of the PRCs (44.4 +/- 3.4%) was better than that of the regular contractions (23.3 +/- 3.3%) (p less than 0.01; n = 18). After 30 min of hypoxia (the second hypoxic period), regular contractions and PRCs decreased to 2.2 +/- 0.6% and 13.6 +/- 1.6% of baseline values, respectively (p less than 0.001; n = 18). However, the recovery from the second hypoxic injury was not significant for either regular contractions or PRCs. The % diastolic tension, which was normalized to the baseline for regular contractions, increased to 113.2 +/- 6.9% and 133.6 +/- 8.4% at the end of the first and the second hypoxic periods, respectively. There was statistically significant correlation between the % diastolic tension and the % hypoxic injury of PRCs (p less than 0.002; n = 18). There was no significant relationship between % diastolic tension and % hypoxic injury of regular contractions. There was no statistically significant correlation between % diastolic tension and % recovery from the hypoxic injury of either regular contractions or PRCs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

The trilateral opioid contract. Bridging the pain clinic and the primary care physician through the opioid contract.

We have extended the traditional use of opioid contracts to involve the primary care physician (PCP). The PCP was asked to collaborate with the pain specialist's decision to use opioids by cosigning an opioid contract. Explicit in the agreement was the understanding that the primary care physician would assume prescribing the refills for these medications once the opioid regimen had become stabilized. The present study was a retrospective chart review of the first 81 patients with non-malignant chronic pain who received an opioid agreement requiring the participation of the primary care physician. Sixty-nine of the 81 patients (85%) agreed to the terms of the contract initially, but only 50 of these 69 individuals (72%) successfully obtained their PCP's written agreement for the prescribing of opioids for chronic pain management. Despite expecting reluctance on the part of the PCP to enter into this agreement, the low compliance rate was due to lack of commitment on the part of the patient, who either refused to sign the contract outright or, after initially agreeing to sign the contract, did not have it signed by the PCP. If the PCP did not agree to sign the opioid contract, the patient was tapered off the medication. If the contract was approved and signed by the PCP, there were no subsequent reversals by this physician in terms of agreeing to continue to prescribe opioids. In all cases in which a contract was completed, the patient was successfully stabilized on an appropriate opioid regimen and then discharged back to the care of the PCP for long-term opioid treatment. The opioid contract may be an effective tool for networking specialty and primary care services in the delivery of chronic opioid therapy.

Contracts↗
PubMed1993

Functional study on the effects of nifedipine, cromakalim, and the absence of extracellular Ca2+ on alpha 1-adrenoceptor-mediated excitation-contraction coupling in isolated rat portal vein: comparison with depolarization-mediated excitation-contraction coupling.

The effects of Ca(2+)-entry blockade by nifedipine, K+ channel opening by cromakalim, and of omitting extracellular Ca2+ on the contractile response elicited by a supramaximum concentration of the "full" and selective alpha 1-adrenoceptor agonist phenylephrine (10(-4) M) were compared with those elicited by a supramaximal concentration of KCl (50 mM) in isolated rat portal vein. The contractile response to phenylephrine appeared to be biphasically composed of an early "transient" phase and a slowly developing "sustained" phase that reached maximum values after 30 s and 5 min after initiation of contraction, respectively. The contractile response to KCl (50 mM) exhibited a triphasic pattern consisting of "spike," "transient", and "sustained" components that peaked after 8 s, 25 s, and 10 min, respectively. Nifedipine was able to eliminate all components of the contractions in response to both phenylephrine and KCl almost completely. Nifedipine was approximately 10 times more potent at suppressing the slowly developing sustained components of the contractions in response to both stimuli than the early transient components. The spontaneous myogenic contractions were inhibited by nifedipine with intermediate potency. Cromakalim, in contrast to nifedipine, selectively eliminated the early transient components of the contractions in response to both phenylephrine and KCl. The sustained components of the contractions in response to both stimuli were relatively resistant to K+ channel opening, although higher concentrations (> 1 microM) of cromakalim were capable of antagonizing the sustained response to phenylephrine accompanied by oscillations in tone. Cromakalim was most potent in counteracting spontaneous myogenic contractions. When phenylephrine and KCl were added with or without external Ca2+ after different periods of equilibration in nominally Ca(2+)-free medium, different washout kinetics for the different components of the contractions in response to both stimuli were observed. The early transient phases of tension development in response to both stimuli were completely lost after approximately 6 min of equilibration in nominally Ca(2+)-free medium, whereas the slowly developing sustained components of the contractions were immediately lost after the change to nominally Ca(2+)-free medium. Externally added Ca2+, when administered together with phenylephrine or KCl after the preparations had been exposed for different times to nominally Ca(2+)-free medium, could not restore the early transient components.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2001

Nitric oxide contracts longitudinal smooth muscle of opossum oesophagus via excitation-contraction coupling.

1. The effects of sodium nitroprusside (SNP) and diethylenetriamine/nitric oxide adduct (DETA/NO), putative nitric oxide (NO) donors, on opossum oesophageal longitudinal smooth muscle were investigated using isometric tension and intracellular micro-electrode recordings. 2. SNP produced concentration-dependent contractions of oesophageal longitudinal smooth muscle with an EC(50) of 239.6 +/- 78.2 microM (mean +/- S.E.M., n = 10). Maximal contraction induced by SNP (1 mM) was about 75.5 +/- 8.5 % (n = 10) of the 60 mM KCl-induced contraction. The SNP-induced contraction was resistant to tetrodotoxin (TTX; 1 microM), but abolished by nifedipine (1 microM), as well as by niflumic acid (300 microM) and 9-anthroic acid (9-AC; 1 mM), Ca(2+)-activated Cl(-) channel blockers. 3. DETA/NO at concentrations of 100 and 500 microM induced 83.1 +/- 24.4 and 104.1 +/- 34.9 % of the 60 mM KCl-induced contraction (n = 4), respectively, which was abolished by nifedipine (1 microM), niflumic acid (300 microM) and 9-AC (1 mM). 4. Pre-application of 1H-[1,2,4]oxidiazolo[4,3,-alpha]quinoxalin-1-one (ODQ) (10 microM), a guanylate cyclase inhibitor, significantly inhibited the SNP-induced contraction, whereas 8-bromo-cGMP (1 mM), a membrane-permeable analogue of cGMP, mimicked the SNP-induced contraction. 5. Intracellular recordings revealed that SNP (300 microM) depolarized resting membrane potentials (RMPs) and increased the frequency of spontaneous spike-like action potentials. However, these electrical alterations were eliminated by pretreatment with niflumic acid (300 microM). 6. These results suggest that NO produces an excitation-contraction coupling in opossum oesophageal longitudinal smooth muscle via a cGMP-dependent signalling pathway. This contraction depends on extracellular Ca(2+) entry through activation of L-type Ca(2+) channels.

Anesthetics, Local↗
PubMedDate not supplied

Calmodulin-myosin light chain kinase inhibition changes fibroblast-populated collagen lattice contraction, cell migration, focal adhesion formation, and wound contraction.

Wound healing requires fibroblast migration, synthesis of new extracellular matrix, and organization of that matrix, all of which depend upon myosin ATPase activation and subsequent cytoplasmic actin-myosin contraction. Myosin ATPase activity is optimized by phosphorylation of myosin light chain at serine 19. Several different signaling pathways can perform that phosphorylation, the focus here is calcium saturated calmodulin dependent -myosin light chain kinase (CaM-MLCK). It is proposed that CaM-MLCK phosphorylation of myosin light chain and subsequent myosin ATPase activation affects granulation tissue fibroblast behavior and contributes to wound contraction. Myosin ATPase activity generates actin-myosin contraction within fibroblasts. Myosin ATPase activity is involved in ATP-induced cell contraction, the generation of focal adhesions, fibroblast migration, fibroblast populated collagen lattice (FPCL) contraction, and wound contraction. The MLCK inhibitors ML-9 and ML-7 inhibited ATP-induced cell contraction, fibroblast migration, FA formation, and FPCL contraction. The calmodulin inhibitors W7 and fluphenazine blocked rat open wound contraction. In addition, fluphenazine delayed re-epithelialization. These findings support the idea that fibroblast CaM-MLCK activity is essential for tissue repair. We speculate that inhibition of CaM-MLCK may reduce or prevent detrimental fibrotic contracture.

Animals↗
PubMed2005

Fluctuations in motor output during steady contractions are weakly related across contraction types and between hands.

The presence of differences in motor unit activity across contraction types and between hands suggests that the magnitude of fluctuations in motor output is only weakly related when these conditions are compared. Twenty right-handed young (24.1 +/- 5.3 years) and old (72.5 +/- 4.9 years) adults performed three levels (</=40% of maximal force) of isometric and anisometric contractions with the first dorsal interosseous muscle of each hand. The fluctuations in motor output were quantified by the coefficient of variation for force during isometric contractions, and as the standard deviations of acceleration and position during anisometric contractions. There was no effect of age on fluctuations in motor output. The magnitude of the fluctuations in motor output was weakly related across contraction types (r(2) < 0.325) and between hands (r(2) < 0.262). Furthermore, the standard deviations of acceleration and position during shortening and lengthening contractions were largely unrelated to one another. Because the activity in a motor unit population differed across contraction types and hands during steady contractions, the central nervous system likely employed distinct strategies to accomplish these different tasks.

Acceleration↗
PubMed1999

Effects of eicosapentaenoic acid on the contraction of intact, and spontaneous contraction of chemically permeabilized mammalian ventricular myocytes.

The n-3 polyunsaturated fatty acids appear to protect the heart from ischaemia-induced arrhythmias. We have used single adult guinea-pig and rat ventricular myocytes to investigate the effects of the n-3 polyunsaturated fatty acid eicosapentaenoic acid on, (i) the l -type Ca2+current, (ii) twitch contraction, and (iii) the spontaneous mechanical activity induced in chemically skinned myocytes by an elevation of the superfusing [Ca2+]. Eicosapentaenoic acid reduced the size of the l -type Ca2+current in a dose-dependent manner in myocytes from both species. Inclusion of delipidated bovine serum albumin (BSA) to the Tyrode, which binds eicosapentaenoic acid, completely reversed the inhibition of the Ca2+current in both guinea-pig and rat cells. The effects of eicosapentaenoic acid on contraction were species dependent. In guinea-pig myocytes it produced a reduction in contraction size which was complex, being described by three phases. In rat cells there was an initial increase in the size of contractions, followed by a simple reduction in contraction strength. Delipidated BSA completely reversed these effects in rat cells but only partially restored twitch contraction in guinea-pig cells (60%). In saponin permeabilized cells, the frequency of the spontaneous activity evoked by elevation of [Ca2+] was reduced by micromolar concentrations of eicosapentaenoic acid in cells from both species. The reduction in the amplitude of contractions caused by eicosapentaenoic acid can be explained by an inhibition of the l -type Ca2+current, and by a reduction in Ca2+released from the sarcoplasmic reticulum (SR). The inhibition of the release of Ca2+from the SR reduces the frequency of [Ca2+] dependent spontaneous contractions in chemically skinned guinea-pig and rat ventricular myocytes.

Animals↗