Neuromuscular Blocking Drugs
Overview
Neuromuscular blocking drugs (NMBDs), referred to as peripheral muscle relaxants, in contrast to centrally acting muscle relaxants such as guaifenesin or diazepam, interfere with or block neuromuscular transmission at the motor end plate. They are useful adjuncts to general anesthesia because they provide short-term or reversible skeletal muscle relaxation. NMBDs do not provide analgesia, sedation, amnesia, or hypnosis, and they predispose the animal to hypothermia. Animals are unable to breathe, necessitating controlled ventilation and constant monitoring.
General Considerations
I The primary pharmacologic effect of peripheral NMBDs is to produce skeletal muscle (SM) relaxation
II NMBDs are potentiated by many other drugs
III Other factors that may influence the effects of NMBDs
IV Potential mechanisms of SM relaxation
A NMBDs interfere with cholinergic (nicotinic) neuromuscular transmission in the peripheral somatic nervous system
B Some NMBDs enhance the activity of endogenous inhibitory mechanisms in the central nervous system, which normally modulate SM tone
V NMBDs are used adjunctively during anesthesia to produce controlled muscle relaxation
VI NMBDs produce muscle relaxation but do not produce analgesia or unconsciousness
VII NMBDs produce respiratory paralysis, which necessitates manual or mechanical ventilation support
VIII Hypothermia is an important secondary effect of prolonged SM relaxation
IX NMBDs are positively charged (ionized) and therefore do not pass the blood-brain barrier or cross the placenta in significant amounts
X Various electrical stimulators and stimulation protocols can be used to determine the degree of neuromuscular blockade (Figs. 10-1 and 10-2)

Normal Neuromuscular Function
I Acetylcholine (ACh) is released in small amounts, even in resting muscles
A Random ACh release causes mini-endplate potentials at the postsynaptic muscle membrane, which help to maintain muscle tone but are insufficient to evoke muscle contraction
II Action–potential-dependent ACh release
A Nerve impulses (action potentials) cause large depolarization in nerve terminals of α-motor neurons
B Depolarization in the presence of extracellular Ca++ causes simultaneous fusion of many ACh-containing vesicles with the terminal nerve membrane (Fig. 10-3)

C Release of ACh packets (quanta) evokes a large endplate potential, leading to muscle contraction
III Combination of ACh with postjunctional nicotinic receptors (Nm receptors)
A Receptors on the muscle endplates are nicotinic, type IV cholinergic (Nm) receptors
B Strength of muscle contraction is proportional to the number of receptors activated by ACh
IV The duration of ACh activity at any cholinergic synapse is limited by the action of acetylcholinesterase (ACh esterase); ACh is metabolized to acetic acid plus choline at the synaptic cleft
Types of Neuromuscular Blocks
I Phase I block: depolarizing block (succinylcholine)
II Phase II block: nondepolarizing block (atracurium)
III Mixed block: any combination of I and II
IV Dual block: excessive amounts of depolarizing agents producing phase II block
V Nonacetylcholine block (procaine, botulinum, decreased Ca++, increased Mg++, increased K+, decreased K+)
Muscle Relaxation Sequence
I First to last: Oculomotor muscle (m.) → palpebral m., facial m. → tongue and pharynx → jaw and tail → limbs → pelvic m.→ caudal abdominal m. → cranial abdominal m. → intercostal m. → larynx → diaphragm
A The sequence of motor blockade is highly variable
1. Intercostal and diaphragmatic muscles are thought to be affected last but the clinical return of functional motor function is highly variable
B Motor activity to the limbs may appear to return (twitching, jerking) before the diaphragm is fully functional
II Recovery is generally in the reverse order of paralysis
III It is possible but difficult to titrate the dose of a specific NMBD to paralyze the muscles of the eye while maintaining diaphragmatic function
Specific Neuromuscular Blocking Drugs (Tables 10-1 and 10-2)
TABLE 10-1
Dose Of Neuromuscular Blocking Drugs with Side Effects and Contraindications
Agent | Species | Dose Intravenously (mg/kg) | Duration of Action (min) | Side Effects | Contraindications |
Succinylcholine chloride | Dog | 0.3-0.4 | 1-38 | Little cardiovascular effect; muscarinic effect is bradycardia; nicotinic effects are hypertension, increased intraocular pressure; hyperpyrexia | Organophosphate anthelmintics, chronic liver disease, malnutrition, high-K+, glaucoma, penetrating eye injury |
Cat | 3-5 (total) | 2-6 | |||
Pig | 0.75-2 | 1-3 | |||
Horse | 0.1-0.33 | 1-10 | |||
Pancuronium bromide | Dog | 0.02-0.06 | 15-108 | Negligible | Liver or kidney disease |
Cat | 0.02-0.06 | 14-15 | |||
Pig | 0.07-0.12 | 7-30 | |||
Horse | 0.08-0.14 | 16-35 | |||
Cattle | 0.1 | 30-40 | |||
Calf | 0.04 | 26 | |||
Sheep | 0.005 | 21 | |||
Vecuronium | Dog | 0.01-0.2 | 10-42 | Negligible | |
Cat | 0.02-0.04 | 5-9 | |||
Pig | 0.1-0.2 | 5-20 | |||
Horse | 0.1 | 20-40 | |||
Sheep | 0.004 | 14 | |||
Atracurium | Dog | 0.1-0.4 | 10-30 | ||
Cat | 0.1-0.25 | 10-15 | Negligible | ||
Pig | 0.5-2.5 | 10-60 | |||
Horse | 0.07-0.09 | 8-24 | Negligible | ||
Sheep | 6 µg/kg/hr | ||||
Llama | 0.15 | 6 | |||
Cisatracurium | Dog | 0.02-0.1 | 10-30 | Negligible | |
Rocuronium | Dog | 0.3-0.6 mg/kg | 20-30 min | Negligible | |
Pipecuronium | Dog | 70-90 µg/kg | 16-81 | Occasional hypotension | |
Cat | 40-60 µg/kg | 17-24 |

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