Cholinergic drugs

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Cholinergic drugs

Post  counselor on Mon Oct 15, 2012 11:57 am

Cholinergic drugs



AUTONOMOUS NERVOUS SYSTEM

The autonomic nervous system (ANS) regulates the activities of the body are not subject to voluntary or normally operate below the level of consciousness.
Are under the control of the ANS:
or Breathing
or Circulation
or Digestion
or body temperature
or metabolism
or sweating, etc..

Section afferent autonomic
E 'consists of fibers for the most part not coated with myelin. Starting in vague, in the pelvic nerves, the splanchnic nerves in the autonomic nerves, as well as somatic nerves.
Sensors are neurotransmitters substance P, vasoactive intestinal peptide (VIP), colecistokinina (CCK), calcitonin gene-related peptide (CGRP), glutamate, etc..

Connections autonomous central
Autonomic reflexes can be evoked in the spinal cord without the influence of the higher centers. Autonomic reflexes are frequently supplemented by higher centers such as:
Marrow-stretched (blood pressure and respiration)
-Hypothalamus (body temperature, water balance, blood pressure, sexual reflexes)
-Limbic system (emotional state integration with motor activity and visceral)
-Bark (additional level of integration of these functions)

Section efferent autonomic
1) Section thoraco-lumbar sympathetic or
The cells are located in columns intermediolaterali of the spinal cord (from T1 to L2-L3).
Axons shall run in nerve roots front and form synapses in various types of ganglia:

Paravertebral: 22 pairs at the sides of the spine.
They have a branch communicating white (myelinated preganglionic) and a branch communicating gray (postganglionic fibers) that goes to the spinal nerves.

Prevertebral: are located in the abdomen and pelvis: celiac, superior mesenteric and inferior aortic-renal.

Terminals: there are not many. They are located close to the bladder and rectum.
The postganglionic fibers innervate the effector structures.
The substance adrenal medulla is embryologically and anatomically similar to the sympathetic ganglia.



2) Section parasympathetic or craniosacral

Midbrain:
Edinger-Westphal nucleus of the third nerve brain.

Medulla oblongata:
fibers which run in the seventh, ninth and tenth cranial nerve.

The sacral spinal cord:
II, III, IV sacral segment. The preganglionic fibers form the pelvic nerves.
The parasympathetic ganglia are close to or within the organs innervated. Therefore, the parasympathetic influences exercised more limited.

Sympathetic-parasympathetic interactions
1) physiological antagonism:
for example at the level of the heart and of the 'iris
2) Complementarity:
male genital organs
3) Lack of interaction:
such as the control of peripheral resistance is mainly due to sympathetic.






TRANSMISSION neurohumoral

Cholinergic fibers

Acetylcholine (ACh) is the first substance that has been assigned the role of neurotransmitter (Dale 1914).
Are cholinergic fibers:

1) preganglionic fibers (both sympathetic and parasympathetic)
2) Fibre directed to the adrenal
3) postganglionic parasympathetic fibers
4) postganglionic sympathetic fibers to the sweat glands and some direct sympathetic fibers vasodilatory
5) somatic motor neurons
6) neurons in the central nervous system.
Major cholinergic nuclei:
- Magnocellular nucleus basalis of Meynert (cortical projections) and the nucleus of the band of Broca (projections to the hippocampus) that are important in the control of cognitive functions
- Interneurons in the striatum (motor control)


FIBRE adrenergic

1) sympathetic postganglionic fibers (noradrenaline)
2) Neurons of the central nervous system
(Epinephrine, dopamine, norepinephrine)



Moments of neurotransmission

1) Genesis of an action potential (AP)
2) axonal conduction.
3) Transmission Junctional Liberation
neurotransmitter.

The non-peptide transmitters are synthesized in axonal terminals and accumulated in synaptic vesicles.
The peptides are synthesized in the soma and axon migrate to the termination, where they are deposited into granules.

The liberation of the neurotransmitter is under the control of car-and heteroreceptors:
-  2 adrenergic receptors on adrenergic fibers
inhibit the release of noradrenaline
- 2 adrenergic receptors  promote the liberation of
noradrenaline
- Muscarinic receptors reduce the release of
acetylcholine from cholinergic fibers and norepinephrine
adrenergic fibers.

4) Combination of neurotransmitter receptors with postgiunzionali.
5) Login postgiunzionale.
6) Destruction or dissipation of the transmitter.
a) metabolizing enzymes (ACh, Peptides)
b) reuptake (norepinephrine, serotonin)
c) release into the synaptic cleft



Cholinergic transmission

Summary of ACh

Choline acetyltransferase is synthesized in the soma and then migrate into the nerve ending.
Choline is taken up from extracellular fluid (rate limiting step). The emicolinio-3 blocks the transporter for choline. Choline is generated mainly by hydrolysis of phosphatidylcholine.
Nerve endings in the mitochondria synthesize acetylcholine dall'acetilcoenzima A.
L 'acetylcholine is deposited in vesicles in which enters by active transport.

Release of ACh

Upon arrival of the AP is has input of Ca + + from voltage-gated channels, vesicular membrane fusion with that axonal and liberation of acetylcholine.
The release of ACh is modulated by autoreceptors (muscarinic and nicotinic inhibitor-stimulatory)
Botulinum toxin and -bungarotoxin block exocytosis.
Toxin Black Widow has the opposite effect.




Receptors for ACh

There are 2 main types of receptors:

1. Nicotinic
There are 3 subtypes: ganglion cells, muscle, neuronal
It is eteropentameri which differ for the aggregation of different subunits:
• 9 types of 
• 4 types of 
• 1 type of 
• 1 type of 
• 1 type of 
The nicotinic receptor identifies a membrane ion channel that controls the permeability to Na + and K +; the receptor ( 7) neuronal controls the entry of Ca + +.
The activation of the receptor occurs when 2 molecules of ACh bind to  2 subunit of the receptor

2. Muscarinic
They are located in structures and autonomous effector in the CNS.
Have been cloned five subtypes of muscarinic receptors (m1-m5), however the pharmacological characterization is good only for 3 subtypes (M1-M3).
The M1 or increase gastric secretion
o M2 mediate the vagal effects on the heart and act as autoreceptors on cholinergic terminals
The M3 have excitatory or functions of glands and muscle fibers
or The function of M4 and M5 (found mainly in the brain) is the subject of study.


Actions dell'ACh released from peripheral nerves (Table A)

• Eye:
iris (sphincter of the pupil) miosis.
Ciliary muscle contraction, near vision, intraocular pressure reduction
• Salivary glands, lacrimal,
Increased sweat secretion
• Bronchi tightness, increased secretion
• Heart chronotropic effect,
dromotropic and isotropic
negative
• Release of NO from the vascular tree
endothelium, vasodilatation
• Stomach and intestinal secretions and increase
tone, relaxation
sphincters
• Urinary bladder detrusor contraction,
sphincter relaxation
• Erection Male Reproductive System
• Skeletal muscle contraction
• Adrenals liberation epinephrine
• Activation of peripheral ganglia ganglia
sympathetic and parasympathetic





Acetylcholine metabolism
o The acetylcholinesterase is present in the cholinergic neuron and into the synaptic space. And 'present in large quantities in the neuromuscular junction.
or The butyrylcholinesterase is present in the liver and in plasma and to a lesser extent in the CNS (both in glial cells that in neurons).
Both break down ACh. Choline is 105 less active ACh.



Muscarinic agonists DIRECT

Compounds of synthesis
These are esters of choline (methacholine, carbachol, bethanechol)

Pharmacodynamics
They have activities both on muscarinic receptors that nicotinic
Exert the effects shown in Table A

TOXICITY '
or Bronchoconstriction.
or hypotension
o Increased gastric acid secretion.
o Risk of atrial fibrillation in hyperthyroidism.

THERAPEUTIC USES:
• glaucoma
• bladder atony
• adynamic ileus

Natural alkaloids
Muscarine
Amanita muscaria and alkaloid Pantherina, fungi widespread in Europe, Asia and America.
It 'selective for muscarinic receptors.
It 's just toxicologically relevant

Arecoline
Alkaloid of the seeds of Areca catehu tree of Malaysia.
Has both muscarinic action that nicotine.

Pilocarpine
Imidazole alkaloid of the leaves of shrubs of the genus Pilocarpus.
E 'used as eye drops to treat glaucoma open-angle glaucoma.
It 'also used in xerostomia by anticancer radiotherapy or Sjogren's disease, in order to stimulate salivary secretion.


MUSHROOM POISONING
1) Mushrooms of the species Inocybe and Clitocybe are rich muscarine. Damage salivation, lacrimation, visual disturbances, abdominal colic, bronchospasm, bradycardia, hypotension, and shock.
Treatment with atropine intramuscularly.

2) The poisoning by Amanita muscaria is mainly due to isoxazole compounds different from muscarine.
Produces restlessness, ataxia, hallucinations.
Atropine is not indicated, as are appropriate benzodiazepines.

3) Poisoning by Amanita verna, virosa, or phalloides mushrooms of the genus Galerina.
The major toxins are the    amanitin and which block the RNA-polymerase II.
You can die after 4-7 days for renal and hepatic failure.



Cholinergic agonists INDIRECT (cholinesterase inhibitors or anti-cholinesterase)

The acetylcholinesterase exist in various molecular forms,

The active center of the 'enzyme contains a:
1) anionic site with a group glutamic acid that attracts the quaternary group of the choline
2) esterasico site containing serine, which operates OH nucleophilic attack at the acyl carbon, removing the acyl group dall'Ach.

The acetylcholinesterase can be inhibited by:
A) Quaternary Compounds as edrophonium, which gives reversible inhibition for 2-10 min.
B) Compounds carbamilici as neostigmine and physostigmine, damage reversible inhibition lasting 4-6 hours.
C) reversible inhibitors able to traverse well the blood brain barrier (donepezil, rivastigmine and galantamine)
D) organophosphorus inhibitors (such as diisopropilfluoro-phosphate, malathion, sarin, soman, tabun, etc.) that produce irreversible inhibition.


Pharmacodynamics
Act as indirect agonists of muscarinic receptors. For their pharmacological effects see Table A

PHARMACOKINETICS

• Oral absorption is good for physostigmine, but not for the neostigmine and quaternary compounds.
The organophosphates are absorbed very well through the different routes of administration.
• Physostigmine (tertiary amine) penetrates enough in the brain. Neostigmine and pyridostigmine do not cross the blood-brain barrier.
Donepezil, rivastigmine and galantamine well through the barrier
• Elimination mostly metabolic by esterases.


FATAL POISONING BY INHIBITORS

Acute intoxication
May be due to suicidal or homicidal purposes and inappropriate use of insecticides.
It is manifested by:
- Miosis (especially for exposure to vapors)
- Profuse salivation
- Bronchoconstriction and bronchial secretion
- Bradycardia and hypotension
- Central effects (ataxia, confusion, convulsions)
- Weakness and muscle paralysis then
It has death from respiratory failure device (bronchospasm and paralysis of respiratory muscles).
Treatment should be done with atropine and reactivators of acetylcholinesterase, such as pralidossima.
If treatment with pralidossima is not timely it has "aging" of the enzyme, which can not be reactivated.

It 'also need:
• Prevent further absorption of toxic
• Use artificial respiration
• diazepam to control seizures
• Pharmacological treatment of shock

Chronic intoxication
Causes severe polyneuritis

THERAPEUTIC USES
1) Paralytic ileus and atony of the urinary bladder.
2) Glaucoma. Respond well to the anticolinesterasicici open-angle glaucoma.
In angle-closure glaucoma using drugs that reduce the production of aqueous humor and infusion of mannitol (acute in the attack). It requires surgery.
3) Symptomatic treatment of Myasthenia gravis, autoimmune disease that affects the cholinergic receptors of the plate.
4) Physostigmine (which penetrates well enough in the CNS) is used in intoxication by atropine, fenotiazione, antidepressants.
5) donepezil, rivastigmine and galantamine are used in Alzheimer's disease, characterized by neurodegeneration of cholinergic neurons that project to the frontal cortex.


Antimuscarinic

Are antagonists of muscarinic receptors on:
- Self-effectors innervated by cholinergic fibers
- Muscarinic receptors in neuronal
- Ganglionic muscarinic receptors
Have little effect on nicotinic receptors, though similar quaternary ammonium have a certain affinity for nicotinic receptors.

Atropine is the prototype of antimuscarinic drugs.
And 'the ester of tropic acid and tropanolo (hyoscyamine) and is the racemate of d-and l-hyoscyamine.
It is made dall'Atropa belladonna and Datura stramonium (Solanaceae).
The scopolamine (hyoscine-l) presents a different alcohol, the scopina. Is extracted from Hyosciamus niger.



Pharmacodynamics
Competitively blocking muscarinic receptors, evoke antimuscarinic drugs:
• Eye:
iris (sphincter of the pupil) mydriasis.
Ciliary muscle relaxation, vision
far
• Salivary glands, lacrimal,
reduced sweat secretion
• Bronchi dilatation, reduced secretion
• Heart chronotropic and dromotropic effect positive
• Reduce Stomach and intestinal secretions and peristalsis
• Urinary bladder detrusor relaxation, relaxation sphincters

Order of sensitivity to atropine
1) saliva, bronchial and sweat
2) iris, ciliary muscle, heart
3) urinary bladder and gastrointestinal tract
4) secretion and gastric motility

At therapeutic doses, atropine has little effect central
A toxic doses produce central excitation (restlessness, hallucinations and delirium), followed by depression (respiratory arrest and circulatory collapse).
Scopolamine depresses the CNS at therapeutic doses.

Ganglia M1 receptors mediate the excitatory postsynaptic potential generation.
The inhibition of gastric secretion by pirenzepine appears mostly mediated by receptors M1 ganglion

PHARMACOKINETICS
• Good oral absorption of atropine, scopolamine and tertiary amines. Quaternary compounds such as ipratropium are not absorbed
• trihexyphenidyl and benztropine are distributed well to the CNS.
• The elimination is both metabolic excretory

TOXICITY '
Side effects:
Dry mouth or
or Constipation
or difficulty in urination
or mydriasis, blurred vision
Tachycardia or

Acute intoxication can occur for:
- Ingestion of berries containing atropine (children)
- Overdose of pharmaceutical preparations
- Interaction with compounds acting antimuscarinic (phenothiazines, antidepressants, antihistamines).

The intoxication is manifested by:
or Mydriasis
Cute or hot and dry. Hyperthermia unresponsive to NSAIDs
or restlessness, hallucinations, delirium, convulsions.
o In severe cases, coma, circulatory collapse and death from respiratory paralysis.

Treatment consists of:
- To promote heat loss (sponge soaked in alcohol, bags of ice).
- Administration of physostigmine.
- Administration of diazepam for seizures.

HEAVY THERAPEUTIC

• In ophthalmology the antimuscarinics are used to induce mydriasis (for eye examination for diagnosis refractive defects or to break adhesions iris-lens). Atropine has very prolonged action, you prefer homatropine, tropicamide, cyclopentolate
• Treatment of cramps and intestinal colic.
Using scopolamine butylbromide that has low systemic absorption and therefore little effect
• Treatment of renal colic and urinary incontinence. You would use tolderodina or oxibu-tinina that have more affinity for M3 receptors kidney
• The pirenzepine (M1 selective antagonist) is used in the treatment of gastro-duodenal ulcers. The effect is mediated by M1 ganglion and those on gastric glands
• Ipratropium is used in chronic obstructive pulmonary disease inhaled (very little is absorbed being a compound with a quaternary nitrogen and does not affect the bronchial ciliated epithelium). Little effect on bronchial asthma
• Treatment of Parkinson's disease. Using trihexyphenidyl and benztropine, especially reduce the tremor.
• The scopolamine is used in the prevention of cinetopatie.
• Treatment of intoxication by anticholinesterase agents or direct muscarinic





Ganglionic neurotransmission

Ganglionic transmission involves different receptors:

1) nicotinic acetylcholine receptors
Mediate rapid depolarization postsynaptic, due to the current of Na +. It generates a ready potential excitatory postsynaptic (EPSP) that may give rise to an action potential.

2) muscarinic receptors
Postsynaptic receptors M1 median decrease of conductance for the K +. This produces an EPSP, which is slower and lasting (30-60 sec.) Than that evoked by nicotinic receptors.

3) PEPTIDE RECEPTORS: Receptors for substance P, angiotensin, VIP, enkephalins, neuropeptide Y and RH LH give a slow EPSP and late that lasts for several minutes.

4) -ADRENERGIC RECEPTORS: They are located on the postsynaptic membrane. Are activated by dopamine or norepinephrine that is released by cells SIF (small cell immunofluorescent).
Once activated generate an IPSP





STIMULANTS ganglion

NICOTINE
E 'was isolated for the first time in 1828 from the leaves of Nicotiana tabacum.
Lobeline, EPIBATIDINA
are orgine plants and animals, respectively
Tetramethylammonium, DIMETILFENILPIPERAZINIO
are of experimental interest


PHARMACOLOGICAL ACTIONS OF NICOTINE

Peripheral nervous system
Nicotine acts on:
Ganglia-
-Adrenal medulla (free catecholamines)
-Adrenergic terminations (free catecholamines)
-Neuromuscular junction
Chemoreceptors of the carotid body-

Nicotine has biphasic action:
1) Low doses stimulate the ganglion cells.
2) At high doses, the initial stimulation is followed by blocking the transmission.
3) All ganglia respond to nicotine, the effect depends on the predominant control (parasympathetic or sympathetic) of that function


Cardiovascular system
The effect of nicotine is predominantly sympathomimetic of the heart and blood vessels:
a) stimulates the sympathetic ganglia
b) It stimulates the adrenal medulla
c) Royalty catecholamines from nerve endings
d) Enable aortic and carotid chemoreceptors of the glomus

Gastrointestinal tract
Parasympathomimetic effect of ganglionic origin (increased tone and intestinal motor activity).

Exocrine glands
Stimulation and then block the salivary glands and bronchial.

Central nervous system
There are two subtypes of neuronal nicotinic receptors:
- One high affinity receptor ( 4) 2 ( 2) 3, and
- One low affinity, the receptor ( 7) 5

Nicotine has a clear action reinforcement (ie induces the subject to summarize it), even if its power of gratification is modest.
Nicotine increases the firing and dopamine release in mesolimbic dopaminergic neurons ventral tegmental area, as do other drugs of abuse. These effects could explain the Charges of abuse of nicotine.


Induces in the CNS:
- Stimulation of the central (tremors and convulsions)
- Stimulation of respiration (both by direct and reflected)
- Vomiting for action on the chemoreceptor trigger zone (CTZ) + peripheral actions
The stimulation is followed by depression to death from respiratory failure.

Its power to generate drug reinforcement with:
Tolerance
The tolerance and 'mostly of origin pharmacodynamics. It istaura tolerance to nausea, vomiting and dizziness.
Dependence
The withdrawal syndrome is manifested by:
anxiety, restlessness, insomnia, craving tobacco,
increased appetite

PHARMACOKINETICS
Good absorption from the gut, skin and lungs.
Elimination mostly metabolic.

ACUTE INTOXICATION
May have been due to accidental ingestion of insecticide sprays or ingestion of tobacco in children.
Acute lethal dose: 60 mg about.

It is manifested by:
• salivation and vomiting,
• abdominal pain,
• mental confusion and weakness, then
• a decrease in pressure and
• difficulty breathing.
• Possible seizures.
• Death due to respiratory failure.

Treatment:
• Gastric lavage,
• artificial respiration,
• treatment of shock.


PROBLEMS OF SMOKING
The mortality rate of smokers is about 2.0 times higher than that of non-smokers due to:
1) Cardiovascular disease (coronary artery disease, cerebrovascular disease, peripheral vascular disease). Combined effects of CO and nicotine.
2) neoplasms (lung, larynx, oral cavity, esophagus, pancreas, bladder). Are due to the many carcinogens present in smoke (nitrosamines, polycyclic aromatic hydrocarbons).
3) Broncopnenmopatia chronic obstructive lung clearance mechanisms for inhibition.
4) Smoking in pregnancy decreases the birth weight of the baby and increases the risk of perinatal death



DRUG DEPENDENCE OF NICOTINE

- Therapy patches or gum containing nicotine
- Trattameno with the antidepressant bupropion. This probably works by blocking the reuptake of dopamine and norepinephrine.



BLOCKERS ganglion (GANGLIOPLEGICI)

Powerful non-depolarizing ganglion blocker hexamethonium are the pentolinio, mecamylamine and Trimethaphan.

In the past were used as antihypertensives.

It is currently available only Trimethaphan to induce controlled hypotension in surgery or in severe hypertensive crisis.


Neuromuscular blocking agents

- The nicotinic receptor of the neuromuscular junction is a pentamer with 4 types of subunits (2   + 1 + 1 + 1  ), outlining an ion channel.
- Only the subunits  have the recognition sites for the 'ACh.
- The combination of 2 molecules of agonists on units  gives rise to opening of the channel with a rapid movement of Na + to 'internal and K + to' external.
- Block a unit  is sufficient to hinder the 'opening of the channel.
- The ACh released from motor nerve produces depolarization of the neuromuscular junction; if the depolarization reaches the amplitude of an AP (action potential), this is propagated in the muscle fiber.

Competitive neuromuscular blocking agents or stabilizers
Agents are competitive:
- D-tubocurarine is the active ingredient of curare (soft extract unpurified obtained from the bark and roots of Strychnos Toxifera and Condrodendron Tomentosun). E 'was used by the natives along the Amazon and Orinoco as a poison for arrows.
- -eritroidina and tossiferine (of natural origin)
- Gallamina
- Mivacurium
- Pancuronium
- Atracurium etc.
Apart from the -eritroidina are all quaternary compounds, characterized by a cyclic structure rather rigid.

MECHANISM OF ACTION
- Combine with the nicotinic receptors of the membrane postgiunzionale, without activating it.
- They block competitively the action of ACh. The block is selective for the response to Ach (it maintains the muscle response to electrical stimulation and exposure to K +).

These drugs induce muscle paralysis:
- Flaccid (also abolish muscle tone)
- Primary (not preceded by excitation)



Depolarizing blockers
-Decametonio and
Succinylcholine-(the only depolarizing in use)

MECHANISM 'ACTION
There are two distinct phases of the block that correspond to 2 different mechanisms:
Phase I:
Persistent depolarization of the membrane postgiunzionale the endplate and the surrounding membrane of the muscle fiber.
The channels for Na +, which are voltage sensitive become inactivated and will not generate more action potentials
Phase II:
For prolonged exposure to succinylcholine replaces desensitization of the nicotinic receptor.
The Anti-AChE enhance the blocking phase I, while reducing that of phase II.

Although these drugs produce flaccid paralysis. However with depolarizing agents paralysis is secondary to an excitation phase. Before dell'istaurarsi of paralysis may occur painful muscle fasciculations initials.



Pharmacodynamics OF TWO CLASSES OF BLOCKING NEUROMUSCULAR

Muscles
Sequence of paralysis
- Muscles of the fingers and eyes
- Muscles of the limbs, neck, trunk
- Intercostal muscles
- Diaphragm
The restoration of muscle activity occurs in reverse order.

Central Nervous System
The blockers in quaternary structure do not exert effects on the central nervous system, because it does not cross the barrier.

Autonomic Ganglia
• The-tubocurarine also exerts a certain block of nicotinic receptors ganglia and adrenal capsules, with consequent decrease in systemic blood pressure and tachycardia.
• Lower blood pressure is caused by pancuronium, still less to atracurium, vecuronium, mivacurium, rocuronium.
•-The vecuronium but produces tachycardia per share antimuscarinic quite pronounced.
•-Succinylcholine has no action of ganglionic blocking agents.


PHARMACOKINETICS
- The quaternary compounds are absorbed very little by mouth.
- The effect of tubocurarine runs out in 20 min, that of succinylcholine in just 5 min.
- The mivacurium has a short duration of action because it is degraded by butyrylcholinesterase.

TOXICOLOGY
The main risks are:
1. Respiratory paralysis. The paralytic agents is reduced by competitive inhibitors of acetylcholinesterase.
2. Bronchospasm and hypotension for histamine release from mast cells.
3. Tubocurarine produces intense release of histamine. Succinylcholine, mivacurium, atracurium give liberation of histamine to a lesser extent.
4. Atropine and antihistamines are useful to reduce the effects of histamine released.
5. Malignant hyperthermia for excessive release of Ca + + from the sarcoplasmic reticulum. The treatment consists in the administration of dantrolene, dispersion of heat, oxygen administration and control of acidosis.
6. Depolarizing agents can quickly clear K + from the cells and cause dangerous hyperkalemia in patients treated with digitalis
7. In subjects with low plasma cholinesterase activity succinylcholine prolonged apnea can lead to increased effect of succinylcholine

Pharmacodynamic Interactions
Inhalational anesthetics (halothane, isoflurane) synergize with competitive blockers.
Aminoglycosides, tetracycline, colistin, polymyxin B potentiate neuromuscular blockade.
For Ca + + channel blockers potentiate neuromuscular blockade.

THERAPEUTIC USES
• in anesthesia surgical adjuvants to enhance relaxation of skeletal muscle.
• Nell'elettroshock therapy.
• For clinical examinations (laryngoscopy, bronchoscopy, etc.).
• Other diagnostic purposes (pain by compression of the nerve roots for muscle spasms, diagnosis myasthenia gravis).
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