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Maximal Contraction (maximal + contraction)
Selected AbstractsIn vitro tracheal hyperresponsiveness to muscarinic receptor stimulation by carbachol in a rat model of bleomycin-induced pulmonary fibrosisAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 3 2006J. Barrio Summary 1 Bleomycin-induced lung injury is widely used as an experimental model to investigate the pathophysiology of pulmonary fibrosis but the alterations in the pharmacological responsiveness of airways isolated from bleomycin-exposed animals has been scarcely investigated. The aim of this study was to examine the in vitro tracheal responses to muscarinic receptor stimulation with carbachol in a rat bleomycin model. 2 Concentration,response curves to carbachol (10 nm to 0.1 mm) were obtained in tracheal rings isolated from Sprague,Dawley rats 14 days after endotracheal bleomycin or saline. The intracellular calcium signal in response to carbachol (10 ,m) was measured by epifluorescence microscopy using fura-2 in primary cultures of tracheal smooth muscle cells from bleomycin- and saline-exposed rats. Circulating plasma tumour necrosis factor (TNF)- ,/interleukin (IL)-1, levels were measured by enzyme-linked immunosorbent assay. 3 Maximal contraction in response to carbachol was significantly greater in tracheal rings from bleomycin-exposed rats compared with controls (15.8 ± 1.3 mN vs. 11.8 ± 1.4 mN; n = 19, P < 0.05). 4 Carbachol (10 ,m) elicited a transient increase of intracellular calcium with greater increment in tracheal smooth muscle cells from bleomycin-exposed rats compared with controls (372 ± 42 nmvs. 176 ± 20 nm; n = 7, P < 0.01). 5 Circulating plasma levels of TNF- ,/IL-1, were augmented in bleomycin-exposed rats compared with controls. Tissue incubation with TNF- , (100 ng ml,1)/IL-1, (10 ng ml,1) increased in vitro tracheal responsiveness to carbachol. 6 In conclusion, tracheal contraction in response to muscarinic receptor stimulation with carbachol was increased in bleomycin-exposed rats. This in vitro cholinergic hyperresponsiveness may be related to the augmented levels of inflammatory cytokines in bleomycin-exposed rats. [source] Long-lasting contractile action and the inhibitory action of cupric ions on ileal longitudinal muscleAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 4 2004K. Miyazaki Summary 1 Cupric ions (Cu2+), at concentrations above 0.03 mm, induced a progressive increase in the tonic contraction of guinea-pig ileal longitudinal muscle. Maximal contraction of 0.1 mm Cu2+ attained a level above that of the 60-mm K+ -induced tonic response, within 20 min of application. The tension induced by Cu2+ persisted for more than several hours. Tetrodotoxin (3 × 10,6 m) had no effect on the contraction induced by 0.1 mm Cu2+. 2 After incubation in a Ca2+ -free medium, the ileal response to 0.1 mm Cu2+ was lost. Nifedipine, a L-type Ca2+ channel blocker, dose-dependently inhibited contractions induced by Cu2+. 3 As the duration of the first application of 0.1 mm Cu2+ increased above 30 min, after washing with normal medium, the contractile response to a second application of 0.1 mm Cu2+ decreased gradually. After 150 min of the first application of 0.1 mm Cu2+, a second application of Cu2+ could not evoke any contraction. 4 After the application of 0.1 mm Cu2+ for 150 min, when muscles were washed with a medium containing 1 mm EDTA, the response to 0.1 mm Cu2+ returned to a greater extent in the normal Ca2+ medium. 5 In conclusion, Cu2+ (0.1 mm) induced a maximal ileal tension above that of the K-induced tonic response within 20 min. The ileal contraction to Cu2+ persisted for more than several hours and depended on extracellular Ca2+ concentrations. It is possible that a part of Cu2+, bound to a EDTA-inaccessible site, also has a tension inhibitory effect. [source] Spasmogenic action of endothelin-1 on isolated equine pulmonary artery and bronchusEQUINE VETERINARY JOURNAL, Issue 2 2003A. E. M. BENAMOU Summary Reasons for performing study: There is currently little published information about the effects of endothelin-1 (ET-1), a potent endogenous spasmogen of vascular and airway smooth muscle, on pulmonary vasculature and airways or which ET receptor subtypes mediate ET-1-induced vasoconstrictive and bronchoconstrictive action in the horse. Objectives: To investigate the effect of endothelin-1 (ET-1) on smooth muscle from isolated equine pulmonary artery and bronchus. In addition, the roles of ETA and ETB receptors in ET-1 mediated contraction in these tissues were assessed. Methods: The force generation of ring segments from pulmonary arteries or third-generation airways (obtained from horses subjected to euthanasia fororthopaedic reasons) were studied in an organ bath at 37°C in response to exogenous endothelin and selective endothelin A (BQ123) or B receptor (BQ788) antagonists. Results: ET-1 produced concentration-dependent contractions of the equine pulmonary artery and bronchus. The threshold for contraction was 10,10 and 10,9 mol/l ET-1 for pulmonary artery and bronchus, respectively. The maximal contraction induced by the highest ET-1 concentration (10,7 mol/l) was 173 and 194% of the contraction obtained with 100 mmol/l KCl in pulmonary artery and bronchus, respectively. ET-1 potency was 25 times greater in equine pulmonary artery than in equine bronchus (concentration of ET-1 producing 50% of maximal contraction [EC50] = 5.6 10,9 mol/l and 2.2 10,8 mol/l, respectively). In pulmonary artery, ET-1 induced contractions were significantly inhibited by the ETA receptor antagonist BQ123 (1 ,mol/l; dose-response curve to ET-1 was shifted to the right by 5.4-fold), but not by the ETB antagonist BQ788. In bronchus, dose-responses curves to ET-1 were shifted to the right by BQ123 (1 ,mol/l; 2.5-fold), but not by BQ788 (1 ,mol/l). In the presence of both antagonists, the dose-response curve to ET-1 was shifted to the right by 4.5-fold. Conclusions: These functional studies demonstrate that ET-1 is a potent spasmogen of equine third generation pulmonary artery and bronchus, and that contractions are mediated via ETA receptors in the former and both ETA and ETB receptors in the latter. Potential clinical relevance: Endothelin receptor antagonists may have potential for treating equine pulmonary hypertension or bronchoconstriction. [source] Evidence from proprioception of fusimotor coactivation during voluntary contractions in humansEXPERIMENTAL PHYSIOLOGY, Issue 3 2008Trevor J. Allen In experiments on position sense at the elbow joint in the horizontal plane, blindfolded subjects were required to match the position of one forearm (reference) by placement of their other arm (indicator). Position errors were measured after conditioning elbow muscles of the reference arm with an isometric contraction while the arm was held either flexed or extended. The difference in errors after the two forms of conditioning was large when the conditioned muscles remained relaxed during the matching process and it became less when elbow muscles were required to lift a load during the match (10 and 25% of maximal voluntary contraction, respectively). Errors from muscle conditioning were attributed to signals arising in muscle spindles and were hypothesized to result from the thixotropic property of passive intrafusal fibres. Active muscle does not exhibit thixotropy. It is proposed that during a voluntary contraction the errors after conditioning are less, because the spindles become coactivated through the fusimotor system. The distribution of errors is therefore seen to be a reflection of fusimotor recruitment thresholds. For elbow flexors most, but not all, fusimotor fibres appear to be recruited by 10% of a maximal contraction. [source] Postcontraction changes of muscle architecture in human quadriceps muscleMUSCLE AND NERVE, Issue 4 2004Konrad Mahlfeld MD Abstract Maximal voluntary contraction changes the mechanical properties of skeletal muscle. Using ultrasound, we investigated whether these changes are reflected by changes in muscle architecture in the vastus lateralis muscle of 8 healthy volunteers. The mean pennation angle during the time interval from 3 to 6 min after maximal voluntary contraction (late postcontraction state) was 14.4 ± 1.11° (mean ± SEM) and differed significantly from the precontraction state (16.2 ± 1.39°), but the pennation angle in the early postcontraction state did not change statistically from the precontraction angle. Thus, postcontraction changes of the muscle,tendon interface appeared for 6 min after a maximal contraction, which may be important for biomechanical optimization of force transmission in vivo. Muscle Nerve 29: 597,600, 2004 [source] Interleukin-1, attenuates endothelin B receptor-mediated airway contractions in a murine in vitro model of asthma: roles of endothelin converting enzyme and mitogen-activated protein kinase pathwaysCLINICAL & EXPERIMENTAL ALLERGY, Issue 9 2004Y. Zhang Summary Background Asthma is a chronic airway disease, known to involve several inflammatory mediators. Little is known about how these mediators interact in order to produce or attenuate even basic features of the disease, like airway hyper-reactivity and remodelling. Endothelin-1 (ET-1) and IL-1, are two mediators suggested to play important roles in the induction of airway inflammation. Objective To investigate the interactions between ET-1 and IL-1,, using a novel in vitro model of asthma, focusing on airway smooth muscle contractility. Methods Isolated murine tracheal segments were cultured from 1 to 8 days in the absence and presence of IL-1,. The subsequent contractile responses to sarafotoxin 6c (S6c) (selective agonist for ETB receptor) and sarafotoxin 6b (S6b) (ETA and ETB receptor agonist) were recorded by a myographs system. In all experiments, ETB receptors were desensitized before the contractile response to S6b was recorded. Thus, the response to S6b is only mediated by ETA receptors in the present study. The mRNA expressions for ET-1 and endothelin (ET) receptors were quantified by real-time PCR. Results Organ culture in the presence of IL-1, attenuated the maximal contraction induced by S6c, but not S6b. This reduction was concentration-dependent and was significant after 2, 4 and 8 days of culture. To investigate the mechanisms behind this, inhibitors for endothelin converting enzyme (ECE) phosphoramidon, c-JUN N-terminal kinase (JNK) SP600125, extracellular-signal-regulated kinase 1/2(ERK 1/2) PD98059 and p38 pathway SB203580 were used. Individually, SP600125 and PD98059, but not SB203580, could partly reverse the reduction induced by IL-1,. An additional effect was obtained when SP600125 and PD98059 were combined. The mRNA expressions for ET-1 and ETB receptor were up- and down-regulated, respectively, by IL-1,. Conclusion Presence of IL-1, in the airways attenuate the contractile response mediated via ETB receptors, an effect dependent on ECE, JNK and ERK 1/2 pathways. [source] COMPARATIVE EFFECTS OF TRAMADOL ON VASCULAR REACTIVITY IN NORMOTENSIVE AND SPONTANEOUSLY HYPERTENSIVE RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2008Juliana M Raimundo SUMMARY 1The aim of the present study was to determine the effects of tramadol on vascular reactivity in aortic rings from Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). 2Aortic rings, with or without endothelium, were obtained from male WKY rats and SHR (15,20 weeks old) and prepared for isometric tension recording. Aortic rings were precontracted with phenylephrine (10 µmol/L) or 40 mmol/L KCl and then exposed to cumulative concentrations of tramadol (0.1,1 mmol/L). 3Tramadol produced a concentration-dependent relaxation of precontracted aortic rings from WKY rats and SHR, which was not dependent on functional endothelium. Vascular relaxation was significantly greater in rings from SHR than WKY rats. 4The concentration of tramadol necessary to produce a 50% reduction of the maximal contraction to phenylephrine (IC50) in rings with and without endothelium from SHR was 0.47 ± 0.08 and 0.44 ± 0.03 mmol/L, respectively (P = 0.76). 5Tramadol attenuated the contracture elicited by Ca2+ in depolarized tissue, suggesting that it may inhibit L-type Ca2+ channels. However, pretreatment with nicardipine (1 µmol/L) prevented the relaxation induced by tramadol in aortic rings from WKY rats and partially reduced its inhibitory effect in aortic rings from SHR. 6Pretreatment of endothelium-denuded aorta with glybenclamide (3 µmol/L), 4-aminopyridine (3 mmol/L), tetraethylammonium (3 mmol/L) and naloxone (100 µmol/L) did not affect tramadol-induced vasodilation of aortic rings from either WKY rats or SHR. 7Intravenous administration of tramadol (10 mg/kg) to conscious SHR significantly reduced both systolic and diastolic blood pressure from 171.4 ± 5.3 to 129.3 ± 5.3 (P = 0.002) and from 125.0 ± 6.5 to 57.8 ± 8.9 mmHg (P = 0.003), respectively. [source] The energetic cost of activation in mouse fast-twitch muscle is the same whether measured using reduced filament overlap or N -benzyl- p -toluenesulphonamideACTA PHYSIOLOGICA, Issue 4 2008C. J. Barclay Abstract Aim:, Force generation and transmembrane ion pumping account for the majority of energy expended by contracting skeletal muscles. Energy turnover for ion pumping, activation energy turnover (EA), can be determined by measuring the energy turnover when force generation has been inhibited. Most measurements show that activation accounts for 25,40% of isometric energy turnover. It was recently reported that when force generation in mouse fast-twitch muscle was inhibited using N -benzyl- p -toluenesulphonamide (BTS), activation accounted for as much as 80% of total energy turnover during submaximal contractions. The purpose of this study was to compare EA measured by inhibiting force generation by: (1) the conventional method of reducing contractile filament overlap; and (2) pharmacological inhibition using BTS. Methods:, Experiments were performed in vitro using bundles of fibres from mouse fast-twitch extensor digitorum longus (EDL) muscle. Energy turnover was quantified by measuring the heat produced during 1-s maximal and submaximal tetanic contractions at 20 and 30 °C. Results:,EA measured using reduced filament overlap was 0.36 ± 0.04 (n = 8) at 20 °C and 0.31 ± 0.05 (n = 6) at 30 °C. The corresponding values measured using BTS in maximal contractions were 0.46 ± 0.06 and 0.38 ± 0.06 (n = 6 in both cases). There were no significant differences among these values. EA was also no different when measured using BTS in submaximal contractions. Conclusion:, Activation energy turnover is the same whether measured using BTS or reduced filament overlap and accounts for slightly more than one-third of isometric energy turnover in mouse EDL muscle. [source] The role of antenatal pelvic floor muscle exercises in prevention of postpartum stress incontinence: a randomised controlled trialJOURNAL OF CLINICAL NURSING, Issue 19-20 2010Linda Mason Aim., This article reports a randomised controlled trial to determine the efficacy of antenatal pelvic floor muscle exercises in the primary prevention of postpartum stress incontinence in primiparous women. Background., Pelvic floor muscle exercises are effective in treating stress incontinence, yet prevention studies demonstrate equivocal findings. Design., Randomised controlled trial. Method., Pregnant women recruited from two hospitals in North-west England were randomised to an intervention (n = 141) or control group (n = 145). Data were collected from 2005,2006. The intervention comprised four sessions of taught pelvic floor muscle exercise training during pregnancy and 8,12 maximal contractions repeated twice daily at home. A modified Bristol Female Lower Urinary Tract Symptom questionnaire, Leicester Impact Scale and Three Day Diary were administered at 20 and 36 weeks of pregnancy and three months postpartum. Results., The intervention group was more likely to exercise their pelvic floor muscles compared to controls at 36 weeks (p = 0·019) and three months (0·022), reporting fewer episodes of incontinence and a lower score on the Leicester Impact Scale. However, these differences were not statistically significant. Conclusion., Significant differences were not demonstrated between the groups in relation to incontinence episodes and degree of bother of symptoms postpartum, although trends indicate a positive effect. Further research is necessary to address issues of adherence and the effect of pelvic floor muscle exercise undertaken during pregnancy on postpartum stress urinary incontinence. Relevance to clinical practice., A proportion of women did not meet the required attendance at antenatal class, furthermore, few exercised their pelvic floor muscles during pregnancy according to instructions. Health professionals need to find ways to instruct and motivate women to perform pelvic floor muscles exercises regularly during pregnancy and the postpartum. [source] | |||||||||||||