• Title/Summary/Keyword: contractile states

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An Estimating Method of Contractile State Changes Come From Continuous Isometric Contraction of Skeletal Muscle (골격근의 지속적인 등척성 수축 시 발생하는 수축상태변화 추정 방법)

  • Park Hyung-Jun;Lee Seung-Ju
    • The Transactions of the Korean Institute of Electrical Engineers D
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    • v.52 no.1
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    • pp.55-63
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    • 2003
  • In this study was proposed that a new estimating method for investigation of contractile state changes which generated from continuous isometric contraction of skeletal muscle. The physiological changes(EMG, ECG) and the psychological changes by CNS(central nervous system) were measured by experiments, while the muscle of subjects contracted continuously with isometric contraction in constant load. The psychological changes were represented as three-step-change named 'fatigue', 'pain' and 'sick(greatly pain)' from oral test, and the method which compared physiological change with psychological change on basis of these three steps was developed. The result of analyzing the physiological signals, EMG and ECG signal changes were observed at the vicinity of judging point in time of psychological changes. Namely, it is supposed that contractile states have three kind of states pattern (stable, fatigue, pain) instead of two states (stable, fatigue).

An Analysis of Multichannel EMG in Continuous Isometric Contraction of Human Muscle (근육의 지속적인 등척성 수축시의 다 채널 근전도 해석)

  • Lee, Seung-Ju;Kim, Ki-Young;Yoon, Chae-Hyun;Lee, Hyun-Chul;Yoon, Yang-Woung;Park, Hyung-Jun
    • Proceedings of the KIEE Conference
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    • 2002.07d
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    • pp.2696-2698
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    • 2002
  • In this study, the comparison of the contractile states change at prime mover muscle with that at synergist muscle was executed, while the muscle contracted continuously with isometric contraction. The contractile states of muscle becomes to change when the voluntary contraction of skeletal muscle is progressed continuously. Such the contractile states change is divided into three states in consideration for not only physiological change but also the psychological change by CNS(central nervous system) as "stable state", "fatigue state" and "pain state". As a result of this study, the prime mover muscle is reached "pain state" but the synergist muscle is not reached. Namely the synergist muscle is delayed state than the prime mover muscle. This result judged that although the prime mover muscle have reached a limit when contraction is continued, owing to effect of delayed state of the synergist muscle, the prime mover muscle is endured some more contraction.

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Characteristics of Diprophylline-Induced Bidirectional Modulation on Rat Jejunal Contractility

  • Liu, Fang-Fei;Chen, Da-Peng;Xiong, Yong-Jian;Lv, Bo-Chao;Lin, Yuan
    • The Korean Journal of Physiology and Pharmacology
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    • v.18 no.1
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    • pp.47-53
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    • 2014
  • In this study, we propose that diprophylline exerts bidirectional modulation (BM) on the isolated rat jejunal segment depending on its contractile state. The results supported the hypothesis. Diprophylline ($20{\mu}M$) exerted stimulatory effects on the contractility of jejunal segment in six low contractile states while inhibitory effects in six high contractile states, showing the characteristics of BM. Diprophylline-induced stimulatory effect was significantly blocked by atropine, indicating the correlation with cholinergic activation. Diprophylline-induced inhibitory effect was partially blocked by phentolamine, propranolol, and L-N-Nitro-Arginine respectively, indicating their correlation with sympathetic activation and nitric oxide-mediated relaxing mechanisms. Diprophylline-induced BM was abolished by tetrodotoxin or in a $Ca^{2+}$ free condition or pretreated with tyrosine kinase inhibitor imatinib, suggesting that diprophylline-induced BM is $Ca^{2+}$ dependent, and that it requires the presence of enteric nervous system as well as pacemaker activity of interstitial cells of Cajal. Diprophylline significantly increased the reduced MLCK expression and myosin extent in constipation-prominent rats and significantly decreased the increased MLCK expression and myosin extent in diarrhea-prominent rats, suggesting that the change of MLCK expression may also be involved in diprophylline-induced BM on rat jejunal contractility. In summary, diprophylline-exerted BM depends on the contractile states of the jejunal segments, requires the presence of $Ca^{2+}$, enteric nervous system, pacemaker activity of interstitial cells of Cajal, and MLCK-correlated myosin phosphorylation. The results suggest the potential implication of diprophylline in relieving alternative hypo/hyper intestinal motility.

Ameliorative effects of atractylodin on intestinal inflammation and co-occurring dysmotility in both constipation and diarrhea prominent rats

  • Yu, Changchun;Xiong, Yongjian;Chen, Dapeng;Li, Yanli;Xu, Bin;Lin, Yuan;Tang, Zeyao;Jiang, Chunling;Wang, Li
    • The Korean Journal of Physiology and Pharmacology
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    • v.21 no.1
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    • pp.1-9
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    • 2017
  • Intestinal disorders often co-occur with inflammation and dysmotility. However, drugs which simultaneously improve intestinal inflammation and co-occurring dysmotility are rarely reported. Atractylodin, a widely used herbal medicine, is used to treat digestive disorders. The present study was designed to characterize the effects of atractylodin on amelioration of both jejunal inflammation and the co-occurring dysmotility in both constipation-prominent (CP) and diarrhea-prominent (DP) rats. The results indicated that atractylodin reduced proinflammatory cytokines TNF-${\alpha}$, IL-$1{\beta}$, and IL-6 in the plasma and inhibited the expression of inflammatory mediators iNOS and NF-kappa B in jejunal segments in both CP and DP rats. The results indicated that atractylodin exerted stimulatory effects and inhibitory effects on the contractility of jejunal segments isolated from CP and DP rats respectively, showing a contractile-state-dependent regulation. Atractylodin-induced contractile-state-dependent regulation was also observed by using rat jejunal segments in low and high contractile states respectively (5 pairs of low/high contractile states). Atractylodin up-regulated the decreased phosphorylation of 20 kDa myosin light chain, protein contents of myosin light chain kinase (MLCK), and MLCK mRNA expression in jejunal segments of CP rats and down-regulated those increased parameters in DP rats. Taken together, atractylodin alleviated rat jejunal inflammation and exerted contractile-state-dependent regulation on the contractility of jejunal segments isolated from CP and DP rats respectively, suggesting the potential clinical implication for ameliorating intestinal inflammation and co-occurring dysmotility.

The Modulation of Motility of Pyloric Antral Smooth Muscles of Rat by Melatonin

  • Han, Sang-Hoon;Lee, Da-Woon;Cho, Soo-Hyun;Kim, June-Sun
    • Biomolecules & Therapeutics
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    • v.18 no.2
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    • pp.166-170
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    • 2010
  • Recently some researches have established that the melatonin, secreted by pineal gland, may evoke the changes of contractile responses on smooth muscles. We examined the effects of melatonin on the motility of rat pyloric antrum and which mechanism might be involved in the effects. Pyloric antral strips from the stomach of 20 Sprague-Dawley rats were prepared for isometric tension recording in organ bath. The strips were precontracted by acetylcholine and high-KCl solutions. In precontracted conditions the tensions were increased by accumulative application of melatonin ($10^{-8}-10^{-4}$ M) dose-dependently, even in resting states. And the effects were almost disappeared when the concentrations of ACh were over than 10 ${\mu}M$. The effects of melatonin were inhibited by pretreatment of 10 mM TEA and/or 10 ${\mu}M$ 4-AP and rarely affected by pretreatment of 1 mM TEA, 10 ${\mu}M$ glibenclamide and 10 ${\mu}M$ verapamil respectively. From these results it is concluded that the contractile responses of smooth muscles of rat pyloric antrum were enhanced by melatonin application and the mechanism might be concerned with the inhibition of some voltage-dependent potassium channels.

Ardipusilloside-I stimulates gastrointestinal motility and phosphorylation of smooth muscle myosin by myosin light chain kinase

  • Xu, Zhili;Liang, Hanye;Zhang, Mingbo;Tao, Xiaojun;Dou, Deqiang;Hu, Liping;Kang, Tingguo
    • The Korean Journal of Physiology and Pharmacology
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    • v.21 no.6
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    • pp.609-616
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    • 2017
  • Ardipusilloside-I is a natural triterpenoid saponin, which was isolated from Ardisia pusilla A. DC. The aim of the study was to evaluate the stimulation of ardipusilloside-I on gastrointestinal motility in vitro and in vivo. The experiment of smooth muscle contraction directly monitored the contractions of the isolated jejunal segment (IJS) in different contractile states, and the effects of ardipusilloside-I on myosin were measured in the presence of $Ca^{2+}$-calmodulin using the activities of 20 kDa myosin light chain ($MLC_{20}$) phosphorylation and myosin $Mg^{2+}$-ATPase. The effects of ardipusilloside-I on gastro emptying and intestinal transit in constipation-predominant rats were observed, and the MLCK expression in jejuna of constipated rats was determined by western blot. The results showed that, ardipusilloside-I increased the contractility of IJS in a dose-dependent manner and reversed the low contractile state (LCS) of IJS induced by low $Ca^{2+}$, adrenaline, and atropine respectively. There were synergistic effects on contractivity of IJS between ardipusilloside-I and ACh, high $Ca^{2+}$, and histamine, respectively. Ardipusilloside-I could stimulate the phosphorylation of $MLC_{20}$ and $Mg^{2+}$-ATPase activities of $Ca^{2+}$- dependent phosphorylated myosin. Ardipusilloside-I also stimulated the gastric emptying and intestinal transit in normal and constipated rats in vivo, respectively, and increased the MLCK expression in the jejuna of constipation-predominant rats. Briefly, the findings demonstrated that ardipusilloside-I could effectively excite gastrointestinal motility in vitro and in vivo.

Changes in the Endothelin-1-induced Contraction of Aorta in Streptozotocin-induced Diabetic Rats

  • Cheong, Hyun-Joo;Kim, Eun-Jin;Kim, Su-Jin;Lee, Sun-Hee;Rhim, Byung-Yong
    • The Korean Journal of Physiology and Pharmacology
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    • v.4 no.3
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    • pp.185-195
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    • 2000
  • Vascular diseases are significant complications of diabetes mellitus (DM), and the endothelial cells may play a pivotal role in the development of vascular disease in DM. Endothelin-1 (ET-1) released from endothelium is a potent vasoconstrictor peptide and circulating level of ET-1 is increased in a variety of disease states. The purpose of this study was to determine the changes of responsiveness to ET-1 in DM, and we experimented on the changes in the ET-1-induced contraction, levels of nitrite and lipid peroxidation, and ET-1 immunoreactivity in aorta from streptozotocin-induced DM rats. DM was induced by single injection of streptozotocin (55 mg/kg, i.p.). The immunoreactive ET-1 levels in endothelial layer of thoracic aorta were much higher in DM rats than control rats. Nitrite in tissue homogenate was decreased and plasma nitrite was increased in DM rats. Malondialdehyde (MDA) was significantly increased in DM rats and cGMP was not significantly different between control and DM rats. ET-1 produced concentration- dependent contractile responses that are significantly attenuated in DM rats compared to controls. In the presence of selective $ET_A$ receptor antagonist BQ610, the maximum contraction was decreased and the concentration ratios for BQ610 yielded $pA_2$ values of 7.3 (slope, 0.65) in control rats, whereas BQ610 had no antagonistic effect on ET-1-induced contraction in DM rats. However, pretreatment with BQ788, an $ET_B$ receptor antagonist, maximum response was decreased and the dose-response curves for ET-1 were shifted to the right in both groups and $pA_2$ values were 7.9 and 7.7 (slope, 1.05 in control and DM rats), respectively. IRL 1620 and sarafotoxin S6c, $ET_B$ agonists, induced relaxation in control rats but not in DM rats. These results indicate that endothelial cell dysfunction and enhanced immunoreactivity of ET-1 have been found in DM rat and ET-1-induced contraction was attenuated in DM rat. These attenuated responses might be at least in part caused by the alteration of $ET_A$ receptor properties (e.g. desensitization), and partly related with an alteration in intracellular mechanism for contraction to ET-1.

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