Early Lipid Raft-Related Changes: Interplay between Unilateral Denervation and Hindlimb Suspension.

Muscle disuse and denervation leads to muscle atrophy, but underlying mechanisms can be different. Previously, we have found ceramide (Cer) accumulation and lipid raft disruption after acute hindlimb suspension (HS), a model of muscle disuse. Herein, using biochemical and fluorescent approaches the influence of unilateral denervation itself and in combination with short-term HS on membrane-related parameters of rat soleus muscle was studied.

Changes in Membrane Ceramide Pools in Rat Soleus Muscle in Response to Short-Term Disuse.

Lipid raft disruption is an early event during skeletal muscle unloading. Ceramide (Cer) serves as a signaling lipid that can contribute to lipid raft disturbance and muscle atrophy. Using biochemical and fluorescent approaches, the distribution of Cer and related molecules in the rat soleus muscle subjected to 12 h of hindlimb suspension (HS) was studied.

Clomipramine counteracts lipid raft disturbance due to short-term muscle disuse.

Disuse-induced skeletal muscle dysfunction is a serious consequence of long-term spaceflight, numerous diseases and conditions for which treatment possibilities are still strictly limited. We have previously shown that acute hindlimb suspension (HS)-mediated disuse disrupts membrane lipid rafts in the unloaded muscle. Here, we investigated whether pretreatment of rats with the inhibitor of acid sphingomyelinase, clomipramine (1.

Water balance of lung and nitrogen oxide in blood at experimental autoimmune encephalomyelitis after capsaicin blockade of vagus nerve.

The Purpose Of The Research: To study the water balance of lung and NO level in blood in experimental autoimmune encephalomyelitis combined with capsaicin blockade of vagus nerve.

Methods: Experiments were conducted on 47 adult (16-week-old) male rats weighing 220-280 g. To simulate the experimental autoimmune encephalomyelitis (EAE) rats were subcutaneously injected with encephalitogenic mixture in complete Freund's adjuvant (0.

[BINDING OF CELL-DERIVED MICROPARTICLES WITH FIBRIN IN BLOOD CLOTTING].

Direct effects of circulating blood microparticles on fibrin formation and structure were studied. Clots made from platelet-free plasma and from microparticle-depleted plasma obtained by filtration was studied in parallel, including clots from the microparticle-depleted plasma replenished with phospholipids. Fibrin formation was induced by exogenous thrombin without Ca2+ to prevent formation of endogenous thrombin and exclude indirect kinetic effects of microparticles related to thrombin generation.