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  • Arner, Anders, et al. (författare)
  • Metabolism and force in hypertrophic smooth muscle from rat urinary bladder
  • 1990
  • Ingår i: American Journal of Physiology. - American Physiological Society. - 0002-9513. ; 258:5 Pt 1, s. 923-932
  • Tidskriftsartikel (refereegranskat)abstract
    • Ten days of urinary outlet obstruction in the rat induced a threefold increase in bladder weight. Active force of control and hypertrophic bladder muscle strips was measured at varying PO2 levels after high-K+, carbachol, or electrical field stimulation. Highest force output was obtained with carbachol. Force per muscle area was lower in the hypertrophic muscles. The basal rates of oxygen consumption and lactate formation were similar in the two groups. The metabolic tension cost (ATP turnover/active force) was similar in the two groups for activation with high K+ and carbachol. In anoxia the active force decreased, but this was less pronounced in the hypertrophied muscle. Hypertrophied muscle could, in contrast to the controls, maintain a sustained K+ contracture in anoxia. Basal metabolic rates and tension cost were markedly reduced in anoxia for both groups. The lower force per area with unaltered tension cost, in hypertrophic muscles under all experimental conditions, may reflect unaltered intrinsic properties of the contractile system, although the amount of contractile material has decreased relative to cell volume. The increased resistance to anoxia may reflect a metabolic adaptation to impaired oxygen supply to the hypertrophied tissue.
  • Aronson, D., et al. (författare)
  • Extracellular-regulated protein kinase cascades are activated in response to injury in human skeletal muscle
  • 1998
  • Ingår i: American Journal of Physiology. - HighWire Press. - 0002-9513 .- 2163-5773. ; 275:2, s. C555-C561
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>The mitogen-activated protein (MAP) kinase signaling pathways are believed to act as critical signal transducers between stress stimuli and transcriptional responses in mammalian cells. However, it is not known whether these signaling cascades also participate in the response to injury in human tissues. To determine whether injury to the vastus lateralis muscle activates MAP kinase signaling in human subjects, two needle biopsies or open muscle biopsies were taken from the same incision site 30-60 min apart. The muscle biopsy procedures resulted in striking increases in dual phosphorylation of the extracellular-regulated kinases (ERK1 and ERK2) and in activity of the downstream substrate, the p90 ribosomal S6 kinase. Raf-1 kinase and MAP kinase kinase, upstream activators of ERK, were also markedly stimulated in all subjects. In addition, c-Jun NH2-terminal kinase and p38 kinase, components of two parallel MAP kinase pathways, were activated following muscle injury. The stimulation of the three MAP kinase cascades was present only in the immediate vicinity of the injury, a finding consistent with a local rather than systemic activation of these signaling cascades in response to injury. These data demonstrate that muscle injury induces the stimulation of the three MAP kinase cascades in human skeletal muscle, suggesting a physiological relevance of these protein kinases in the immediate response to tissue injury and possibly in the initiation of wound healing.</p>
  • Ask, Per, et al. (författare)
  • Effect of time interval between swallows on esophageal peristalsis.
  • 1980
  • Ingår i: American Journal of Physiology. - 0002-9513 .- 2163-5773. ; 238:6, s. G485-90
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Esophageal peristaltic pressure amplitude, peristaltic incidence, speed of peristalsis, and wave duration were investigated as a function of swallow interval. In the distal half of the esophagus, the amplitude decreased at swallow intervals of 8 s and shorter. At intervals of 8 and 4 s, dropouts of contractions that were obtained were most frequent in the distal esophagus and for the 4-s interval. At continuous swallows no contractions were obtained below the upper esophageal sphincter until the end of the swallow sequence, after which a peristaltic wave of high amplitude propagated along the esophagus. The peristaltic speed increased toward a level 5 cm above the lower esophageal sphincter. The peristaltic wave duration was approximately the same in different parts of the esophagus and at different swallow intervals. The findings indicate an impairment of esophageal transport function by short swallow intervals.</p>
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