Velocity recovery cycles of human muscle action potentials in chronic renal failure

Z'Graggen, Werner Josef; Aregger, Fabienne; Farese, Stefan; Humm, Andrea M.; Baumann, Corina; Uehlinger, Dominik E.; Bostock, Hugh

doi:10.1016/j.clinph.2010.01.024

Cited by 43 publications

(36 citation statements)

References 17 publications

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“…Similar changes of muscle membrane properties have already been shown in critically ill patients diagnosed with probable CIM [20], during ischaemia [15,17] and in patients with chronic renal failure [16]. In probable CIM, we found a significant relationship between membrane dysfunction (that is fall in ESN and rise in MRRP) and potassium.…”

Section: Discussionsupporting

confidence: 86%

“…In probable CIM, we found a significant relationship between membrane dysfunction (that is fall in ESN and rise in MRRP) and potassium. Compared to patients with chronic renal failure, this relationship was much steeper in patients with probable CIM, suggesting that additional factors besides the expected dependence of membrane properties on potassium were involved [16,20]. The changes in our earlier studies during ischaemia were interpreted as a result of membrane depolarization, which was assumed to occur in ischaemia following ATP depletion and, therefore, failing of the Na + /K + pump [15].…”

Section: Discussionmentioning

confidence: 98%

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Early changes of muscle membrane properties in porcine faecal peritonitis

et al. 2014

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IntroductionSepsis-induced myopathy and critical illness myopathy (CIM) are possible causes of muscle weakness in intensive care patients. They have been attributed to muscle membrane dysfunction. The aim of this study was to investigate membrane properties in the early stage of experimental sepsis by evaluating muscle excitability.MethodsIn total, 20 anaesthetized and mechanically ventilated pigs were randomized to either faecal peritonitis (n = 10) or to non-septic controls (n = 10). Resuscitation with fluids and vasoactive drugs was started 3 hours after peritonitis induction. Muscle membrane properties were investigated by measuring muscle velocity recovery cycles before induction of peritonitis as well as 6, 18 and 27 hours thereafter. Muscle relative refractory period (MRRP) and early supernormality (ESN) were assessed.ResultsPeritonitis lasting 27 hours was associated with an increase of MRRP by 28% from 2.38 ± 0.18 ms (mean ± SD) to 3.47 ± 1.79 ms (P <0.01) and a decrease of ESN by 31% from 9.64 ± 2.82% to 6.50 ± 2.64% (P <0.01). ESN reduction was already apparent 6 hours after induction of peritonitis. Values in controls did not show any significant alterations.ConclusionsMuscle membrane abnormalities consistent with membrane depolarization and/or sodium channel inactivation occurred within 6 hours of peritonitis induction. This indicates that changes that have been described in established sepsis-induced myopathy and/or CIM start early in the course of sepsis. Muscle excitability testing facilitates evaluation of the time course of these changes.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-014-0484-2) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 98%

Early changes of muscle membrane properties in porcine faecal peritonitis

et al. 2014

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“…We previously demonstrated that ischaemia progressively prolongs RRP and reduces ESN, confirming that these parameters are sensitive to membrane depolarisation 6. In addition, we found evidence that muscle membranes are depolarised in patients with chronic renal failure7 and in patients with critical illness myopathy 8…”

Section: Introductionsupporting

confidence: 75%

Muscle ischaemia in patients with orthostatic hypotension assessed by velocity recovery cycles

Humm

Bostock

Troller

et al. 2011

Journal of Neurology, Neurosurgery & Psychiatry

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“…In ATS the extra late supernormality due to trains of impulses is reduced and delayed (Fig. 2), as also occurs in muscle fibers depolarized by ischemia and chronic renal failure 29, 35…”

Section: Discussionmentioning

confidence: 91%

“…The early afterpotential, like the negative afterpotential in nerve,33 is attributed to a slight excess of inward over outward charge movement during the action potential, leaving a charge on the membrane capacitance which decays passively 34. The balance between inward Na + and outward K + movements during the action potential depends on membrane potential, so that ESN, like superexcitability in nerve, is a sensitive indicator of the depolarization occurring during ischemia or uremia 29, 35. Membrane depolarization also prolongs MRRP, because it slows the recovery from sodium inactivation.…”

Section: Discussionmentioning

confidence: 99%