Skeletal muscle drugs causing relaxation

SKELETAL MUSCLE RELAXANTS. These drugs may cause drowsiness. Because of the risk of injury, the nurse evaluates the patient carefully before allowing the patient to ambulate alone. If drowsiness does occur, assistance with ambulatory activities is necessary. If drowsiness is severe, the nurse notifies the primary health care provider before the next dose is due... 

Dantrolene is a drug that causes spastic muscle contraction. Unlike other muscle relaxants, it has a direct effect on the contractile mechanism by interfering in the process of calcium ion release from the sarcoplasmic reticulum. This results in a lack of coordination in the mechanism of excitation—contraction of skeletal muscle, which has a greater effect on fast muscle fibers than on slow muscle fibers. Dantrolene is used for controlling the onset of clinical spasticity resulting from serious clinical cases such as wounds, paralysis, cerebral palsy, and disseminated sclerosis. Synonyms of this drug are dantrium and danlen. 

Isoxsuprine is a vasodilator that also stimulates p-adrenergic receptors. It causes relaxation of vascular and uterine smooth muscles, and its vasodilating action is greater on the arteries supplying skeletal muscles than on those supplying skin. The drug also produces positive inotropic and chronotropic effects [39]. 

Geriatric Considerations - Summary Carisoprodol is a skeletal muscle relaxant that at higher doses can cause CNS depression. It appears to have more use with acute muscle discomfort as compared to chronic use. Carisoprodol s metabolite is meprobamate and therefore may have abuse potential and cause sedation in older adults. The risks of fhis drug outweigh benefits in treating older adults. 

Chlorzoxazone (Paraflex, Parafon Forte DSC, Others) [Skeletal Muscle Relaxant/ANS Drug] Uses Adjunct to rest physical therapy to relieve discomfort associated w/ acute, painful musculoskeletal conditions Action Centrally acting skeletal muscle relaxant Dose Adults. 250-500 mg PO tid-qid Peds. 20 mg/kg/d in 3-4 + doses Caution [C, ] Avoid EtOH CNS depressants Contra Severe liver Dz Disp Tabs SE Drowsiness, tach, dizziness, hepatotox, angioedema Interactions T Effects W/ antihistamines, CNS depressants, MAOIs, TCAs, opiates, EtOH, watercress EMS Use of CNS depressants and concurrent EtOH use can T sedation urine may turn reddish purple or orange OD May cause N/V/D, dizziness, HA, X deep tendon reflexes, hypotension and resp depression symptomatic and supportive, activated charcoal may be effective... 

On the other hand, these compounds have a general depressant effect on the CNS that is, they cause a global decrease in CNS excitability that results in generalized sedation. It therefore seems possible that some of their muscle relaxant effects are caused by their sedative powers rather than a selective effect on specific neuronal reflex pathways.11,92 This observation is not to say that they are ineffective, because clinical research has shown that these drugs can be superior to a placebo in producing subjective muscle relaxation.8 20 80 97 However, the specific ability of these drugs to relax skeletal muscle remains doubtful, and it is generally believed that their muscle relaxant properties are secondary to a nonspecific CNS sedation. 

Only drugs causing skeletal muscle relaxation are used for clinical purposes... 

Used mainly in anesthesia protocols or in the ICU to afford muscle relaxation and/or immobility. Occasionally used to treat tetanus. These muscle relaxants interact with nicotinic receptors at the skeletal muscle end plate. Nicotinic receptors are comprised of five subunits, two of which (alpha) bind ACh, a requirement for opening of the Na+ channel. Most drugs in this class bind competitively to one of the alpha subunits to prevent depolarization (receptor antagonists) one drug (succinylcholine) binds noncompetitively and opens the Na+ channel, causing excessive depolarization and desensitization. 

Musck Halothane causes some relaxation of skeletal muscle via its central depressant effects and potentiates the actions of nondepolarizing muscle relaxants (curariform drugs see Chapter 9), increasing both their duration of action and the magnitude of their effect. Halothane and the other halogenated inhalational anesthetics can trigger malignant hyperthermia this syndrome frequently is fatal and is treated by immediate discontinuation of the anesthetic and administration of dantrolene. 

Minoxidil (loniten) is efficacious in patients with the most severe and drug-resistant forms of hypertension. A small fraction of minoxidil is metabolized by hepatic sulfotransferase to the active molecule, minoxidil N-O sulfate. Minoxidil sulfate activates the ATP-modulated channel in smooth muscle, causing hyperpolarization and relaxation of arteriolar smooth muscle. Minoxidil produces arteriolar vasodilation with essentially no effect on capacitance vessels. Minoxidil preferentially increases blood flow to skin, skeletal muscle, the GI tract, and the heart. The disproportionate increase in blood flow to the heart may have a metabolic basis, in that administration of minoxidil is associated with a reflex increase in myocardial contractility and in cardiac output. The cardiac output can increase by as much as three- to fourfold, primarily due to enhanced venous return to the heart. The increased venous return probably results from enhanced flow in vascular beds with a fast response for venous return to the heart. The adrenergic increase in myocardial contractility contributes to the increased cardiac output, but is not the predominant factor. The renal effects of minoxidil are complex it dilates renal arteries, but systemic hypotension produced by the drug actually can decrease renal blood flow. Renal function usually improves in patients who take minoxidil for the treatment of hypertension, especially if renal dysfunction is secondary to hypertension. Minoxidil potently stimulates renin secretion, an effect mediated by renal sympathetic stimulation. 

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