Skeletal muscle relaxants-Mechanism of Action.pptx

Skeletal Muscle Relaxants
Mechanism of Action

1. Skeletal Muscle Relaxants Presented by: J. Amos Babu Associate Professor SIMS College of Pharmacy Acharya Nagarjuna University, Guntur

2. 1.Introduction 1. These are also called Spasmolytic. 2. These are Reduced spasticity. 3. These Relax skeletal and smooth muscle. 4 . These agents reduced the Post Anesthetic Recovery Period. 5 . These are Block the Post synaptic actions at motor End plate. 6 . These are Adjuvant to Anesthetics.

3. 2.Classification of Skeletal Muscle Relaxants 1.Peripheral Skeletal Muscle Relaxants : These act on NMJ 1.Non-Depolarising Blockers (Nm) 1.Long Acting eg . Tubocurarine, Doxacuronium. 2.Intermediate acting eg . Atracurium , Cistracurium . 3.Short acting eg . Mivacurium , Rapacuronium 2. Depolarizing Blockers eg . Succinylcholine 2.Central acting Skeletal Muscle Relaxants. 1.Mephesin Group eg . Carisoprodol , Chlormezanone . 2.Benzodizipine Group eg.Diazepam , clonazepam. 3.GABA Derivative eg . Baclofen 4.Central alpha-2 agonist eg Tizanidine 3.Directly acting Skeletal Muscle Relaxants Eg . Dantrolene 4.Miscellaneous agents Eg Riluzole , Progabide .

4. 1.Non-Depolarising Blockers (Nm) 1.These are first Neuromascular blocking agents found in plants like Strychnos , Chondrodendron genera. 2.Tubocuraine first inreoduced in Clinical Practice 1940s 1.Mechanism of Action 1.These agents are Quaternary compounds with two positive charge nitrogen. 2.These agents block Nm type Receptors at motor end plate. 3.These agents prevent and opening of Sodium Channels. 4.The absence of EPP relaxation of Skeletal muscle. 5. The block is reversible. Tubocurarine 2.Pharmacokinetic actions. 1. These are Polar ionized at physiological pH. 2.These are not absorbed orally. 3. LA agents are more potent and given less doses. 4.These agents Cross BBB. 5.These are Excreated by Kidney (35-100 min)

5. 3.Pharmacodynamic actions 1.Skeletal muscle : Flaccid Paralysis. 2.Histamine Release 3.Heart : M2 receptor Blockage. 4.Lungs: Bronchospasm 5. GIT : Reduced the Motility and Tone. 4.Adverse Effects Hypoxia Respiratory Paralysis. Hypotension & Bradycardia. Constipation . 2. Depolarizing Blockers 1.Mechanism of Action 1.S.Ch is Analogue of A.Ch . 2.It bind Nm of receptors and produced Transient muscle fasciculation 3. It not metabolized by A.ChE 4.It desensitization of Nm receptors 5. Sodium channels are prolonged closed state.

6. 2.Pharmacokinetics 1.It not absorbed orally 2.It dose not Cross BBB. 3.Duration of Action (5-10min ) 3.Pharmacodynamics actions 1.Faciculations occurred in Abdomen and chest. 2.Complete relaxation occurred in 1-2 min. 3.Paralysis effect passed to neck and face. 4.Aponea occurred in 1min. 5.Histamin Release lesser 4.Adverse Effects 1.Hyperkelemia 2.Hyperthermia 3. Rise IOP

7. 2.Central acting Skeletal Muscle Relaxants. 1.These agents act on Cerebro -spinal axis without alter the Consciousness. 2.These are improved in Spasticity. 3.These agents are activation the Internuncial Neurons. 4.These agents directly bind with contracting proteins inhibit muscle contraction . 3.Adverse effects Drowsiness (Desire to sleep) Muscle weakness. Hallucinations. Sedative. 3.Directly acting Skeletal Muscle Relaxants Reduced Ca+2 Oriented depolarization in Skeletal muscle. Muscle Fiber are responsive but contractile mechanism reduced. These agents stimulate GABA release in brain stem depress the Motor activity. It is also used spasticity. It also block release of Ca+2 in sarcoplasmic Reticulum.

8. 4.Miscellaneous agents It Suppress the Neuromuscular Transmission by Motor end plate. These are block VAMP by presynaptic terminal It treat myotonia congentia. Nocturnal leg cramps. Treatment of strabismus Wrinkles in face are suppressed. Adverse Effects Dry mouth ( Xerostomia ) Speech Disorders. Local Injection produced more pain. Dry Eyes. Corneal ulceration.