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PubMed1998

Evoked isometric muscle contractions in myopathies: analysis of pathophysiological properties by different stimulus patterns.

Isometric twitches of the adductor pollicis muscle following ulnar nerve stimulation were investigated in healthy subjects (n = 35) and patients with different types of myopathies (myotonic dystrophy, n = 19; limb girdle muscular dystrophy, n = 10; metabolic myopathy, n = 6). The changes within the rising part (i.e. within the contraction time, CT) of the isometric twitches after single stimuli were similar in myotonic and limb girdle dystrophies: the first part of CT, which lasts until the maximal contraction rate is achieved, was shortened, whereas the following second part of CT, which lasts until the maximal twitch force is achieved, was normal. In metabolic myopathies the first part was normal, whereas the second part was prolonged. The relaxation was prolonged in all types of myopathies, particularly in metabolic myopathies. Using double stimuli with short interstimulus intervals (ISI), the absolute refractory period of the muscle contraction (healthy subjects: 1.35 +/- 0.16 ms) was shortened in patients with myotonic dystrophy (1.02 +/- 0.11 ms). In the other types of myopathies, the absolute refractory period was only shortened provided that the single twitch force was clearly reduced. A similar dependence on a reduced single twitch force was also found with regard to the maximal force development with two stimuli and the corresponding ISI: the force contributed by a second stimulus was pathologically enhanced if the single twitch force was clearly reduced. The ISI related to the maximal force with two stimuli was shifted towards very short values (healthy subjects: 10.5 ms, myotonic dystrophy: 4.6 ms, limb girdle dystrophies: 5.0 ms). Our results can be attributed to altered kinetics of calcium release and uptake by the sarcoplasmic reticulum in myopathies.

Adolescent↗
PubMed1997

Inhibition of antigen-induced muscle contractions by inhibitors of thromboxane pathway in rat small intestine.

Rats were sensitized against egg albumin and the response of the longitudinal muscle from the proximal small intestine to the antigen was tested. Egg albumin (1-100 micrograms/ml) concentration-dependently induced a contraction of the longitudinal muscle in tissues from sensitized animals but not from nonsensitized animals. The response to the antigen was resistant to neuronal blockers like tetrodotoxin, atropine and hexamethonium. Inhibitors of thromboxane synthesis such as the cyclooxygenase inhibitor, indomethacin, the thromboxane synthase blocker, 1-benzylimidazole, or the combined cyclooxygenase/lipoxygenase/thromboxane synthase inhibitor, sulfasalazine, inhibited the contraction evoked by egg albumin. A similar concentration-dependent inhibition of the antigen response was observed with two thromboxane A2 receptor blockers, SK&F 88046 and KW-3635. None of these blockers affected the response to the muscarinic agonist, carbachol, excluding unspecific effects of the drugs on smooth muscle contractility. The effect of antigen was reduced by the mast cell stabilizing agent, quercetin, and by the histamine H1 receptor blocker, mepyramin. These drugs, however, also inhibited the response to carbachol. When contractions were stimulated directly by the stable thromboxane derivative, carbocyclic thromboxane A2, the smooth muscle proved to be more than three orders of magnitude more sensitive to this agonist of the thromboxane pathway compared to histamine. Consequently, thromboxane A2 seems to be one of the main mediators of anaphylactically induced longitudinal muscle contractions in the rat small intestine.

Animals↗
PubMed2004

Decreased aortic smooth muscle contraction in a rat model of multibacterial sepsis.

We investigated whether blockade of the smooth muscle cell (SMC) inducible nitric oxide synthase (iNOS)-soluble guanylyl cyclase (sGC) vasodilator pathway would restore the fall in vasoreactivity produced by sepsis following cecal ligation and perforation (CLP) in rats. Contraction of adjacent aortic rings paired for the presence or absence of endothelial cells (EC) was recorded following high [K(+)](e) (40 mm) or norepinephrine (NE, 10(-8) to 10(-5) m) in the presence of the nitric oxide synthase inhibitor (NOS), N(G)-nitro-l-arginine methyl ester (l-NAME, 0.3 mm) or the sGC inhibitor, 1H-[1,2,4]oxadiazolo[4,3-alpha]quinoxalin-1-one (ODQ, 5 mum). In EC-denuded rings, sepsis halved SMC contraction induced by high [K(+)](e) or NE; neither l-NAME nor ODQ produced an increase in NE E(max) or high [K(+)](e)-evoked contraction. In conclusion, SMC contractility is globally reduced in CLP; this reduction does not appear to be explained by induction of SMC NOS in this CLP model.

Animals↗
PubMed2002

Octopamine modulates spermathecal muscle contractions in Locusta migratoria.

Octopamine was identified in the spermathecal tissue of Locusta migratoria using HPLC and immunohistochemical techniques. Octopamine-like immunoreactive unpaired median neurons were identified in the VIIth and VIIIth (terminal) abdominal ganglia and octopamine-like immunoreactive axons were present in the ventral ovipositor nerve (branches from this nerve innervate the spermatheca). Stimulatory actions of octopamine on myogenic and neurogenic contractions were observed. Dose-dependent increases in the frequency of myogenic contractions and the amplitude of neurogenic contractions were elicited by the application of octopamine to the spermathecal muscle. Non-sustained basal tension increases were noted in some preparations, although these were not found to be dose-dependent. SchistoFLRFamide (PDVDHVFLRFamide) inhibited octopamine-induced contractions by a maximum of about 30%. In the presence of 3-isobutyl-1 -methylxanthine, octopamine increased cAMP levels in all regions of the spermathecal. The largest increase in cAMP content was found in the spermathecal sac, followed by the straight duct and coil duct. Phentolamine blocked octopamine-induced increases in cAMP levels and abolished the actions of octopamine on myogenic contractions.

1-Methyl-3-isobutylxanthine↗
PubMed2003

PDE4D plays a critical role in the control of airway smooth muscle contraction.

The airways of mice deficient in the cAMP phosphodiesterase PDE4D gene are refractory to muscarinic cholinergic stimulation. This study was undertaken to determine whether altered smooth muscle contractility causes the PDE4D-/- phenotype. A major disruption in contractility was observed in isolated PDE4D-/- tracheas, with a 60% reduction in maximal tension and a fivefold decrease in sensitivity to muscarinic cholinergic agonists. Conversely, responses to KCl or arginine vasopressin were unaffected. PDE4D is the predominant PDE4 form in tracheal extracts and PDE4D mRNA is expressed in smooth muscle where muscarinic binding sites are most abundant. Cyclic AMP accumulation in response to acute G(s)alpha-coupled receptor stimulation was increased up to fourfold in the airway of PDE4D-/- mice when compared with wild-type. This increase in cAMP was associated with an increased sensitivity to PGE2-induced relaxation of the PDE4D-/-tracheas. Furthermore, a blockade of prostanoid accumulation in PDE4D-/- tracheas restored the response to muscarinic cholinergic stimulation in vitro and in vivo. These results demonstrate that PDE4D plays a key role in balancing relaxant and contracting cues in airway smooth muscle, suggesting that natural mutations in the PDE4D gene have profound effects on airway tone.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2006

Short- and long-latency contributions to reciprocal inhibition during various levels of muscle contraction of individuals with cerebral palsy.

Deficits in reciprocal inhibition likely contribute to excessive antagonist muscle cocontraction during voluntary movements of individuals with cerebral palsy. This study examined neural contributions to reciprocal inhibition of the soleus motoneurons of individuals with spastic, diplegic cerebral palsy and nondisabled individuals during various levels of voluntary tibialis anterior contraction. A condition-test H-reflex paradigm examined short- and long-latency contributions to reciprocal inhibition of soleus neural pools during changing levels of voluntary tibialis anterior contraction. Electrically induced short- and long-latency inhibition was similar between healthy, neurologically intact control subjects and subjects with cerebral palsy during rest. With increasing levels of tibialis anterior contraction, control subjects experienced increasing levels of soleus motoneuron inhibition, especially of long-latency inhibitory responses. In contrast, there was no evidence of modulation of short- or long-latency inhibition with increasing levels of tibialis anterior contraction among subjects with cerebral palsy. Deficits in long-latency (presynaptic) inhibition appear to contribute prominently to voluntary movement impairment of individuals with cerebral palsy.

Adult↗
PubMed2000

Inhibition of isolated rat and human detrusor muscle contraction by disopyramide.

1. The aim of this study was to investigate the effect of in vitro and in vivo disopyramide treatment on human and rat isolated detrusor muscle contractile response. Muscle strips were suspended in an organ bath chamber containing Kreb's solution at 37 degrees C aerated with 95% oxygen and 5% carbon dioxide. 2. Disopyramide antagonized significantly the contractile response of isolated human detrusor muscle to carbachol stimulation, shifting the concentration-response curve to the right in a parallel manner. The pA2 for competitive inhibition was estimated to be 6.4 with a slope of 0.64 for disopyramide. 3. Rat detrusor muscle contractile response to electrical field stimulation (EFS) was inhibited by 28% (P < 0.01) after in vitro administration of disopyramide (7.5 x 10(-6) M). Disopyramide had no effect on the atropine-resistant component of the response to EFS or on spontaneous contractions of isolated rat detrusor muscle strips. The concentration-response curve to carbachol was competitively antagonized by disopyramide with a pA2 of 6.3 and a Schild curve a slope of 0.85. 4. Disopyramide (7.5 x 10(-6) M) had no effect on rat detrusor contractile response to low concentrations of KCl but at high concentrations contraction was reduced significantly by 16% (P < 0.01). 5. In vivo treatment of rats with disopyramide for 8 days or with a single dose had a significant inhibitory effect on the contractile response of detrusor muscle strips. 6. In conclusion, disopyramide had a significant anticholinergic effect on isolated human and rat detrusor muscle contraction.

Aged↗

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