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Results for “Muscle Contraction”

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At least 595 records · Page 33Linked to original sources

PubMed1994

Muscle contraction increases the strength of healing tibial fracture in the rat.

Tibial fractures in 7-week-old rats were fixed with intramedullary nails. After 25 days of healing the nails were removed and the tibiae loaded in vivo with intact soft tissues until refracture. The animals were tested in three-point anterior cantilever bending either during muscle contraction (n 8) or with relaxed muscles (n 8). Muscle contraction increased the ultimate bending moment by 84 percent, energy absorption by 108 percent, bending stiffness by 21 percent, and ultimate deflection by 49 percent.

Animals↗

PubMed1984

Effect of tubocurarine on static and dynamic muscle contractions in man.

The effect of a bolus injection of tubocurarine (0.1 mg X kg-1 i.v.) was followed in six young subjects by registration of static, and slow (30 degrees X s-1) and fast (150 degrees X s-1) dynamic (isokinetic) maximal voluntary leg extensions. Mechanograms from both unblocked and curarized muscle contractions showed a "notch" after about 440 ms separating two relative maxima. The mechanograms were divided by an arbitrary straight line connecting the starting point of the contraction curve and the notch. The line separated an area (Nm X s) above and to the left (alpha-component) from an area below and to the right (beta-component) of the line. Tubocurarine affected the beta-component selectively until about 70% reduced in the static contractions. With further curarization the alpha-component was also reduced in size. The alpha-component was equally affected during the three types of contractions, while the faster the contraction the more the beta-component was reduced. The results suggest that static as well as dynamic human muscle contractions can be divided into two parts with a different sensitivity for tubocurarine, one of which seems to have a sensitivity which depends on the contraction velocity.

Adult↗

PubMed2002

Ionic mechanisms and Ca(2+) regulation in airway smooth muscle contraction: do the data contradict dogma?

In general, excitation-contraction coupling in muscle is dependent on membrane depolarization and hyperpolarization to regulate the opening of voltage-dependent Ca(2+) channels and, thereby, influence intracellular Ca(2+) concentration ([Ca(2+)](i)). Thus Ca(2+) channel blockers and K(+) channel openers are important tools in the arsenals against hypertension, stroke, and myocardial infarction, etc. Airway smooth muscle (ASM) also exhibits robust Ca(2+), K(+), and Cl(-) currents, and there are elaborate signaling pathways that regulate them. It is easy, then, to presume that these also play a central role in contraction/relaxation of ASM. However, several lines of evidence speak to the contrary. Also, too many researchers in the ASM field view the sarcoplasmic reticulum as being centrally located and displacing its contents uniformly throughout the cell, and they have focused almost exclusively on the initial single [Ca(2+)] spike evoked by excitatory agonists. Several recent studies have revealed complex spatial and temporal heterogeneity in [Ca(2+)](i), the significance of which is only just beginning to be appreciated. In this review, we will compare what is known about ion channels in ASM with what is believed to be their roles in ASM physiology. Also, we will examine some novel ionic mechanisms in the context of Ca(2+) handling and excitation-contraction coupling in ASM.

Animals↗

PubMed1992

Output power and metabolic input power of skeletal muscle contracting linearly to compress a pouch in a mock circulatory system.

Output power and metabolic input power values were determined for unconditioned canine latissimus dorsi (two), gastrocnemius (seven), and triceps (three) muscles contracting linearly to cause compression of a doubly valved pouch in a hydraulic model of the circulation. The motor nerves to the muscles were stimulated tetanically with 450 msec trains of 0.1 msec pulses having a frequency of 50/sec. The muscles were contracted 10, 20, 30, and 40 times per minute and pouch output in milliliters per minute was measured directly for each muscle at each contraction (train) rate. The output power in milliwatts was determined by two methods: (1) by using the pouch output and the pressure rise imparted to the stroke volume (average power) and (2) by using the pressure-volume loop. Metabolic input power in milliwatts was determined from the oxygen consumption in milliliters per minute of the working muscle. It was found that as the pouch output was increased, the pouch output power and the metabolic input power both increased. The average power output was slightly less than that computed from the pressure-volume loop. The mean output power values, when pumping at L liters per minute, were 0.62 L (average) and 0.75 L mW/gm (pressure-volume loop) for the latissimus dorsi muscles; 0.83 L (average) and 1.16 L mW/gm (pressure-volume loop) for the gastrocnemius muscles; and 0.55 L (average) and 0.66 L mW/gm (pressure-volume loop) for the triceps muscles. The percent efficiency of energy conversion ranged from 9.2% to 17.8% for the latissimus dorsi muscles, from 5.1% to 19.5% for the gastrocnemius muscles, and from 10.5% to 27.3% for the triceps muscles. However, it should not be concluded that one muscle type is better than another on the basis of percent efficiency because efficiency does not take endurance into account. An important observation in this study relates to the large output obtained with the three linearly contracting muscle types. All were capable of pumping in excess of 1.5 L/min. A second observation relates to the absence of fatigue, although determination of endurance was not an objective in these studies.

Animals↗

PubMed1997

Ketamine relaxes airway smooth muscle contracted by endothelin.

Endothelins (ETs) are synthesized not only in vascular endothelial cells but also in airway epithelial cells. Increased ET-1 has been demonstrated in bronchial epithelium of asthmatic patients, and, in severe asthma attacks, ET-1 increases in plasma and bronchoalveolar lavage fluid. In this study, we investigated whether ketamine (KET) relaxes ET-induced tracheal contractions. Female guinea pigs were killed with an overdose of pentobarbital. The trachea was removed and cut spirally into two strips that were mounted in an organ bath filled with Krebs-bicarbonate buffer. The response of each strip to 10(-7) M carbachol was taken as 100% contraction to which the response to ET was referred. The contribution of the epithelium to the relaxant effect of KET was studied in denuded tracheae or in the presence of 5 x 10(-5) M indomethacin. ET-1 (3 x 10(-8) M) induced contractions that were 76 +/- 3% of those induced by carbachol. KET reversed the response to ET-1 in a dose-dependent fashion. Similarly, ET-2 (3 x 10(-8) M) induced contractions that were 74 +/- 5% of those induced by carbachol, and KET also reversed this response in a dose-dependent manner. In epithelium-denuded strips, ET-1 induced contractions that were 104 +/- 3% of those induced by carbachol, and KET still reversed this response. The tonic phase of the response to ET-1 was equal (100 +/- 6%) to the response to carbachol, and KET did not affect it significantly. In the presence of ryanodine, KET reduced the ET-1-induced contraction from 67 +/- 2% to 36 +/- 3.%, P < 0.01. In the presence of nicardipine, KET also inhibited the ET-1-induced contraction. We conclude that KET relaxes the tracheal smooth muscle contracted by ETs via a mechanism that is independent of the tracheal epithelium. The relaxant effect of KET on the ET-induced contraction of the trachealis muscle is not dependent upon blockade of 1) sarcolemma influx of Ca2+ through the dihydropyridine Ca2+ channel or 2) the release of intracellular Ca2+ through the ryanodine-sensitive intracellular Ca2+ channel. It is likely that the action of KET relaxing ET-induced tracheal contractions is at some point of the inositol 1,4,5-trisphosphate signaling pathway.

Anesthetics, Dissociative↗

PubMed1951