Skeletal muscle necrosis following membrane-active drugs plus serotonin

  title={Skeletal muscle necrosis following membrane-active drugs plus serotonin},
  author={Herbert Y. Meltzer},
  journal={Journal of the Neurological Sciences},
  • H. Meltzer
  • Published 1 May 1976
  • Biology
  • Journal of the Neurological Sciences

The influence of ketanserin, a new S2 receptor antagonist on experimentally induced skeletal muscle myopathy in the rat

Oral pretreatment with ketanserin effectively inhibited this skeletal muscle myopathy promoted by serotonin in the femoral artery ligated rats: skeletal muscle lesions appeared to be absent or significantly reduced in severity as well as in extent.

Serotonin accumulation by skeletal muscle

Serotonin Metabolism in the Normal and Failing Hamster Heart

Both the stores and synthesis of serotonin are reduced in the failing myopathic hamster heart, indicating significant stores of serotonin synthesized within the heart.

Pre-clinical study of 21 approved drugs in the mdx mouse

Nerve, muscle, and serotonin.

  • M. Takamori
  • Biology, Medicine
    Journal of neurology, neurosurgery, and psychiatry
  • 1977
Effects of serotonin one neuromuscular transmission and muscle contraction were studied in the tibialis anterior of rabbits; pharmacological mechanisms are discussed in comparison with those of adrenaline and isoprenaline.

5-Hydroxytryptamine potentiates post-tetanic twitch responses in the rat phrenic nerve diaphragm preparation.

It is demonstrated that 5-hydroxytryptamine does have significant effects upon the neuromuscular junction under conditions of physiological compromise (following tetanus) and these observations are the first step, therefore, in a series of studies aimed at identifying the resident 5-HydroxyTryptamine receptors within the neuron junction which will subsequently enable us to predict therapeutic effect or toxicity.

Serotonin uptake in blood platelets of duchenne muscular dystrophy patients

There was a significant negative correlation between serum creatine kinase activity and Km of 5‐HT uptake in blood platelets of patients with Duchenne‐type muscular dystrophy, but no correlation was found between Km or Vmax and ambulatory status of DMD.



Proximal Myopathy induced by 5-HT-Imipramine simulates Duchenne Dystrophy

Support for this hypothesis of skeletal muscle damage is found in the observation that skeletal muscle from biopsies of Duchenne dystrophy patients has shown the presence of an abnormal intrafibrillar fluorescence presumed to be a monoamine-like substance.

Serotonin and platelet function in Duchenne muscular dystrophy.

The major finding was a markedly reduced initial rate of accumulation of serotonin 14 C into platelets from DMD patients, which may be of significance to the proposed vascular pathogenesis for DMD in raising the possibility of an alteration in biogenic amine deactivation at the microvascular level.

Calcium as mediator of isoproterenol-induced myocardial necrosis.

It was concluded that ISO-induced myocardial necrosis is not mediated exclusively by flooding of heart muscle with plasma-derived calcium, although this is undoubtedly an important factor, and was further supported by experiments showing that propranolol, at doses which completely suppressed the increase in [Ca] due to ISO, did not completely prevent necrosis.

Increased Plasma Enzyme Concentrations in Rats with Functional Ischaemia of Muscle provide a Possible Model of Duchenne Muscular Dystrophy

During the early and mid-stage histopathological lesions of Duchenne muscular dystrophy, serum enzyme levels of creatine phosphokinase (CPK), glutamic-oxaloacetic transaminase (GOT), glutamysial connective tissue between muscle fibres that are small, enlarged and sometimes with internal nuclei are markedly increased.

An experimental myopathy secondary to excessive acetylcholine release

The results suggest that excessive acetylcholine can induce skeletal muscle necrosis even when the cholinesterase system is intact, and that the myopathy is not just the result of excessive depolarization and contraction but more likely is related to a disturbance in the trophic effect mediated by acetylCholine.