This study is the high contraction processing conditions set by the method of the CPB process. And the ultimate goal of this study is the high contraction of the CPB processing test method that can solve the problems of the high-contraction fabric processing method of the current jet dyeing machine. Non-coating process(CPB process) developed by the expression of a soft touch, light weight, functional and to develop excellent breathable nylon fabric. The nylon fabrics established the optimum processing conditions through the high contraction of the various test conditions, the CPB system.(The benzyl alcohol was used as the main constrictor.) At this time, the warp and weft contraction of nylon fabric was about 20%. And it established the constrictor concentration, the treatment temperature, time of a variety of tests. Also non-coating process(CPB process) can develop soft touch, lightweight, excellent air permeability. As a result, we developed a high contraction nylon fabric having a uniform surface. Manufactured fabric is used for Wind-proof and Down-proof.
Effects of pH, $PCO_2$, and adenosine on the vascular contractility were investigated in the pig coronary arteries. The helical strips of isolated coronary arteries were immersed in the HEPES or $HCO_3^-/CO_2$-buffered Tyrode's solution equilibrated with 100% $O_2\;or\;95%\;O_2-5%\;CO_2\;at\;35^{\circ}C$. The contraction was recorded isometrically using a force transducer. The amplitudes of contraction induced by ACh, high $K^+$, and electrical Held stimulation (EFS) were decreased by elevating extracellular pH (pHo) and were increased by lowering pHo. A shift from $0%\;CO_2\;to\;5%\;CO_2$ at constant pHo (pH 7.4) reduced the contractions induced by ACh, high $K^+$, EFS. However the contraction induced by 100mM $K^+$ was less influenced by the change of pHo or $CO_2$. The contraction induced by ACh in $Ca^{2+}$free Tyrode's solution as well as the contraction developed by the addition of extracellular of $Ca^{2+}$ were decreased by lowering pHo and were increased by elevating pHo. High $K^+$ (25mM) induced contraction at pH 6.8 was not returned to the level of the contraction at pH 7.4 by the elevation of extracellular. calcium $[Ca^{2+}]_o$. Adenosine-induced relaxation was more significant with 5% $CO_2$ than 0% $CO_2$ in the high $K^+$-induced contraction and was more significant with low pHo than high pHo in the contraction induced by EFS. From the above results, it is suggested that $H^+$ and $CO_2$ inhibit $Ca^{2+}$ influx as well as $Ca^{2+}$ release from intracellular $Ca^{2+}$ storage sites and enhance the relaxing effect of adenosine in the pig coronary artery.
The aim of present study was to investigate the possible influence and related mechanism of alcohol on the arterial contraction. Vascular contraction involves the activation of thick or thin filament pathway. However, there are no reports addressing the question whether this pathway is involved in alcohol-induced regulation. We hypothesized that alcohol plays a role in vascular contraction evoked by a vasoconstrictor in rat aortae regardless of endothelial function. Denuded arterial rings from male rats were used and isometric contractions were recorded using a computerized data acquisition system. Interestingly, alcohol at a low concentration (3% v/v) inhibited thromboxane $A_2$ or phorbol ester-induced contraction with endothelial function but at a high concentration (10%) didn't inhibit and rather increased the contraction in the denuded muscle. Therefore, alcohol at a low concentration decreases the contraction and alcohol at a high concentration increases the contraction suggesting that additional pathways different from endothelial nitric oxide synthesis might be involved in the regulation of contractility. In conclusion, alcohol has some effect on the regulation of contractility regardless of endothelial function.
Effect of noradrenaline and endothelium on the high K+ or Ach-induced contraction were investigated in the pig myocardial coronary artery. The helical strip of isolated pig myocardial coronary artery was immersed in the Tris-buffered Tyrode`s solution equilibrated with 100% O2 at 37oC and its isometric tension was measured. High K+ and Ach-induced contraction were dose-dependent. By denuding the endothelium, dose-contraction curve of K+ was not shifted significantly to the left and upward, but that of Ach was shifted significantly to same direction 25 mM K+ - and Ach-induced contraction were relaxed by norepinephrine[NE]. NE-induced relaxation was blocked by the pretreatment of propranolol, which was known as b-adrenoceptor blocker. And, phenylephrine known as a-adrenoceptor agonist, and clonidine known as a-adrenoceptor agonist increased the 25mM K+ - induced contraction respectively. Denuding of endothelium did not show any significant effects on NE-induced relaxation and contraction increased by phenylephrine and clonidine. Tyramine increased 25mM K+ - induced contraction further. The contractile response by tyramine on the 25mM K+ - induced contraction was not blocked by the pretreatment of phentolamine, but was partially blocked by the pretreatment of atropine. From the above results, it is suggested that activation of a1-and a2-adrenoceptors induce the contraction, activation of b-adrenoceptors induce the relaxation, and NE-induced relaxation is mainly due to activation of b-adrenoceptors. Also it is suggested that denudation of endothelium did not influence NE-induced relaxation, but influence Ach-induced contraction in the pig myocardial coronary artery.
The properties of cytosolic $Ca^{2+}$ level$([Ca^{2+}]_i)$ movement of high KCl, carbachol and oxytocin were examined with myometrium isolated from non-pregnant rat(estrus cycle). High concentration of KCl$({\leq}23.3mM)$ induced rhythmic increases in $[Ca^{2+}]_i$ and muscle contraction. However, sustained $[Ca^{2+}]_i$ and contracion were obtained at higher KCl concentration $({\geq}30.3mM)$ The rhythmic and sustained contraction closely associated with changes in $[Ca^{2+}]_i$ induced by high KCl. Carbachol $(3{\sim}30{\mu}M$ generated rhythmic increases with tonic component in $[Ca^{2+}]_i$ and muscle contraction. Myometrial contraction stimulated by carbachol was also closely correlated with change in $[Ca^{2+}]_i$. And the $[Ca^{2+}]_i/contraction$ relationships were similar when muscle strips were stimulated by high KCl and carbachol. Maximal concentration of carbachol $(10{\mu}M)$ and oxytocin(100 nM) increased $[Ca^{2+}]_i$ and contraction which were slightly greater than that of high KCl in non-pregnant myometrium, respectively. However, the $[Ca^{2+}]_i$ and contraction were strongly inhibited by verapamil $(10{\mu}M)$, a 1-type $Ca^{2+}$ channel blocker, as in the case of high KCl. Additionally, although carbachol further increased $[Ca^{2+}]_i$ and contraction induced by high KCl, these changes also strongly inhibited by application of verapamil. These results suggest that uterotonic agents, carbachol and oxytocin, induced contraction by increase in $[Ca^{2+}]_i$ through $Ca^{2+}$ influx than by a regulation of $Ca^{2+}-sensitization$ in non-pregnant myometrium.
Purpose: Leg length discrepancy causes the posture deformation, gait asymmetry, and lower back pain. The purpose of this study is to investigate the correlation among functional leg length discrepancy (FLLD), muscle activity, muscle contraction onset time and vertical ground reaction force (vGRF) during simple lifting task. Methods: Thirty-nine subjects participated in this study. FLLD was measured from the umbilicus to medial malleolus of left and right leg using a tape. The subjects performed to lift a 10 kg box from the floor to chest. The muscle activity and muscle contraction onset time of rectus abdominis, erector spinae and rectus femoris was measured using EMG system and vGRF was measured by two force plate. Pearson correlation was used to fine out the correlation among FDDL, muscle activity, muscle contraction onset time and vGRF during simple lifting task. Results: Correlation between FLLD and difference of muscle activity of short-long side was very high (r>0.9) during simple lifting task. Correlation between FLLD and difference of muscle contraction onset time of short-long side was very high (r>0.9) during simple lifting task. And correlation between FLLD and difference of vGRF of short-long side was high (r>0.7) during simple lifting task. Conclusion: This study suggests that there is high correlation between FLLD and muscle activity, muscle contraction onset time, and ground reaction force during simple lifting task. Therefore, FLLD could negatively affect the postural balance.
Hyperglycemia is associated with an increased risk of cardiovascular diseases. It has been demonstrated that chronic exposure to high glucose impaired endothelial functions. However, specific effects of short-term exposure to high glucose on vascular reactivity are controversial. Moreover, the combined effects of other metabolic substrates such as free fatty acids (FFA) on vascular reactivity remain poorly understood. Here we investigate the effects of short-term exposure to high glucose with or without other metabolic substrates including FFAs termed "nutrition full" (NF) solution, on mesenteric (MA) and deep femoral arteries (DFA) of rats. Arterial ring segments were mounted in a double-wire myograph. Contraction in response to phenylephrine (PhE) was determined in control (5 mM) and high glucose (23 mM, HG) environments over a 30 min period. In both arteries, PhE-inducedvasocontraction was enhanced by pre-incubation of HG solution. A combined incubation with HG and palmitic acid ($100{\mu}M$) induced similar sensitization of PhE-contractions in both arteries. In contrast, high $K^+$-induced contractions were not affected by HG. Interestingly, pre-incubation with NF solution decreased PhE-induced contraction in MA but increased the contraction in DFA. In NF solution, the HG-induced facilitation of PhE-contraction was not observed in MA. Furthermore, the PhE-induced contraction of DFA was attenuated by HG in NF solution. Our results demonstrate that the sensitization of PhE-induced arterial contraction by HG is differentially affected by other metabolic substrates. The conversation of skeletal arterial contractility by HG in NF solution requires careful interpretation of the previous in vitro studies where only glucose is included in physiological salt solutions. Further studies are required to elucidate the mechanism underlying the inconsistent effect of NF solution on MA and DFA.
The present study was conducted to evaluate the effect of phorbol 12,13-dibutyrate (PDBu) on the contraction of rabbit jugular vein in vitro. PDBu concentrations of greater than 10 nM induced a periodic contraction which was composed of rapid contraction, plateau and slow relaxation. The frequency of periodic contraction increased as PDBu concentration increased. The PDBu-induced contraction was inhibited by staurosporine (100 nM), it was not changed by tetrodotoxin $(1\;{\mu}M).$ In $Ca^{2+}$-free medium, PDBu induced a sustaining contraction, but not periodic contraction. Addition of $Ca^{2+}$ to medium evoked periodic contraction which was inhibited by nifedipine, PDBu concentrations of greater than $0.1\;{\mu}M$ increased ^{45}Ca^{2+}$ uptake without changing $^{45}Ca^{2+}$ efflux. Charybdotoxin and apamin, $Ca^{2+}$-activated K^{+}$ channel blockers, did not affect the PDBu-induced periodic contraction, whereas tetraethylammonium (TEA) abolished the periodicity. Pinacidil $(10\;{\mu}M).$, a potassium channel activator, blocked PDBu induced periodic contraction, which was recovered by glybenclamide $(10\;{\mu}M).$. In high potassium solution, PDBu did not produce the periodic contraction. These results suggest that the PDBu-induced periodicity of contraction is modulated by voltage dependent $Ca^{2+}$ channel and ATP-sensitive $K^{+}$ channel.
Present paper is attempted to introduce the phenomenon of 'after contraction' in isolated cardiac-muscle. Papillary muscles were removed from cat right ventricle and were used as a preparation. The muscle strip was Placed in tissue bath which is kept in steady temperature of around $25^{\circ}C$ and was perfuced by Tyrode solution, saturated with 95% $O_2$ and 5% $CO_2.$ under the condition of high calcium (8.2-10.0 mM/l), low sodium (72.4-70.0 mM/l) perfusion with the administration of epinephrine (1-2 mg/l) into tile tissue bath normally triggered muscle contraction was followed by oscillatory, repetitive contractions - after contraction. The phenomenon of after contraction was augumented by decrease in tissue bath temperature and by increase in number of preceding beats and in driving rate. Authors were able to maintain the phenomenon in prominent and steady state giving proper experimental conditions such as fixed bath temperature (ranged from $22^{\circ}C\;to\;27^{\circ}C$), suitable driving rate (20 per minute in average) and perfusion of high calcium, loll sodium and 1-2 mg/l of epinephrine. In some preparations, the strength of after contraction (second contraction) reached up-to 80% of normally triggered contraction and five repetitive contractions were observed as largest number of after contractions. Intracellular action potential measured in the muscle which was beating regulary showing steady after contraction revealed no oscillating after potential in most parts of the muscle but in few cases oscillating changes of after potentials were detectable. In electrogram of the muscle preparation recorded by means of contact electrode prominent, oscillating after potentials were observable when the recorder was set at highest sensitivity. It still is not clear that whether after contraction is the phenomenon which corresponds to those changes in action potential, oscillating after potential, of the muscle preparation. Possible mechanism of the phenomenon of after contraction relating with after potential changes was proposed. Detailed results obtained from further studies on after contraction and concrete discussion on the phenomenon will be reported by authors.
The purpose of this study was to investigate the changes of muscle power by transcutaneous electrical nerve stimulation(TBNS), low frequency-low intensity(20pps, invisible muscle contraction intensity), low frequency-high intensity(20pps, visible muscle contraction), high frequency-low intensity(100pps, invisible muscle contraction intensity) and high frequency-high intensity(100pps, visible muscle contraction). The results were as follows. 1. Increased muscle power after 30 minutes of treatment by low frequency-low intensity TENS, and post-treatment 30 minutes muscle power were increased more than pre-treatment power(p<0.05). 2. Decreased muscle power after a 30 minute treatment by low frequency-high intensity TENS, and after the 30 minute treatment was terminated muscle power didn't recover to pre-treatment levels. 3. Decreased muscle power after 30 minute treatment by high frequency-low intensity TENS, but post-treatment 30 minute, muscle power didn't recover to pre-treatment levels. 4. The muscle power was remarkably decreased by high frequency-high intensity TENS after 30 minute treatment, in addition treatment terminated after 30minutes didn,t recover to pre-treatment power(p<0.05). 5. Lower frequency-low intensity TENS are good methods for preventing muscle fatigue, buty high intensity (TENS) are increased muscle fatigue. 6. Traditional TENS by high frequency-low intensity is a good method for preventing muscle fatigue.
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