Early changes of muscle membrane properties in porcine faecal peritonitis

Abstract Purpose In neuropathic postural tachycardia syndrome, peripheral sympathetic dysfunction leads to excessive venous blood pooling during orthostasis. Up to 84% of patients report leg pain and weakness in the upright position. To explore possible pathophysiological processes underlying these symptoms, the present study examined muscle excitability depending on body position in patients with neuropathic postural tachycardia syndrome and healthy subjects. Methods In ten patients with neuropathic postural tachycardia syndrome and ten healthy subjects, muscle excitability measurements were performed repeatedly: in the supine position, during 10 min of head-up tilt and during 6 min thereafter. Additionally, lower leg circumference was measured and subjective leg pain levels were assessed. Results In patients with neuropathic postural tachycardia syndrome, muscle excitability was increased in the supine position, decreased progressively during tilt, continued to decrease after being returned to the supine position, and did not completely recover to baseline values after 6 min of supine rest. The reduction in muscle excitability during tilt was paralleled by an increase in lower leg circumference as well as leg pain levels. No such changes were observed in healthy subjects. Conclusions This study provides evidence for the occurrence of orthostatic changes in muscle excitability in patients with neuropathic postural tachycardia syndrome and that these may be associated with inadequate perfusion of the lower extremities. Insufficient perfusion as a consequence of blood stasis may cause misery perfusion of the muscles, which could explain the occurrence of orthostatic leg pain in neuropathic postural tachycardia syndrome.

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Vascular Muscle Membrane Properties in Hypertension

Physiology and Pathophysiology of the Heart - Developments in Cardiovascular Medicine ◽

10.1007/978-1-4613-0873-7_41 ◽

1989 ◽

pp. 847-854

Author(s):

Kent Hermsmeyer

Keyword(s):

Membrane Properties ◽

Muscle Membrane ◽

Vascular Muscle

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Glucocorticoid-induced atrophy is not due to impaired excitability of rat muscle

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1982.243.6.e512 ◽

1982 ◽

Vol 243 (6) ◽

pp. E512-E521 ◽

Cited By ~ 2

Author(s):

R. L. Ruff ◽

D. Martyn ◽

A. M. Gordon

Keyword(s):

Membrane Potential ◽

Muscle Weakness ◽

Cortisone Acetate ◽

Membrane Properties ◽

Muscle Membrane ◽

Membrane Excitability ◽

Glucocorticoid Treatment ◽

Tetanic Tension

We explored the possibility that glucocorticoid-induced muscle weakness and atrophy resulted from impaired muscle membrane excitability. Male Sprague-Dawley rats received intramuscular injections of dexamethasone, cortisone acetate (equivalent anti-inflammatory doses), or saline for up to 28 days. Temporal patterns of change in muscle mass, twitch and tetanic tension, and membrane potential, cable parameters, and excitability were studied in vitro in the extensor digitorum longus (EDL), soleus (SOL), omohyoid (OMO), caudofemoralis (CF), and the sternomastoid muscles (membrane potential only). the membrane properties of EDL fibers were also studied in vivo (pentobarbital anesthesia). The relative severity of atrophy was OMO greater than CF greater than EDL greater than SOL. Reduction in twitch or tetanic tension never preceded atrophy. The twitch and tetanic tension (per g muscle) increased with glucocorticoid treatment. There were no significant changes in the time course of the twitch or tetanus. Dexamethasone produced more severe atrophy and force reduction than did cortisone acetate. Glucocorticoid treatment produced a depolarization of EDL muscle fibers measured in vitro at 23 degrees C, but this did not appear to be physiologically significant because EDL fibers studied in vivo were not depolarized and had normal action potential amplitudes and thresholds. Glucocorticoid treatment did not change the membrane resistance or capacitance. We conclude that glucocorticoid treatment did not produce muscle weakness by impairing sarcolemmal excitability or excitation-contraction coupling, but that the weakness resulted from muscle atrophy.

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Length-dependent electromechanical coupling in single muscle fibers.

The Journal of General Physiology ◽

10.1085/jgp.68.6.653 ◽

1976 ◽

Vol 68 (6) ◽

pp. 653-669 ◽

Cited By ~ 16

Author(s):

A M Gordon ◽

E B Ridgway

Keyword(s):

Membrane Potential ◽

Calcium Release ◽

Muscle Fibers ◽

Membrane Properties ◽

Constant Current ◽

Equilibrium Potential ◽

Muscle Membrane ◽

Single Muscle ◽

Fiber Membrane ◽

Length Dependence

In single muscle fibers from the giant barnacle, a small decrease in muscle length decreases both the calcium activation and the peak isometric tension produced by a constant current stimulus. The effect is most pronounced if the length change immediately precedes the stimulation. In some cases, the decrease in tension with shortening can be accounted for almost entirely by a decrease in calcium release rather than changes in mechanical factors such as filament geometry. During the constant current stimulation the muscle membrane becomes more depolarized at longer muscle lengths than at the shorter muscle lengths. Under voltage clamp conditions, when the membrane potential is kept constant during stimulation, there is little length dependence of calcium release. Thus, the effect of length on calcium release is mediated through a change in membrane properties, rather than an effect on a subsequent step in excitation-contraction coupling. Stretch causes the unstimulated fiber membrane to depolarize by about l mV while release causes the fiber membrane to hyperpolarize by about the same amount. The process causing this change in potential has an equilibrium potential nearly 10 mV hyperpolarized from the resting level. This change in resting membrane potential with length may account for the length dependence of calcium release.

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