Indication |
Used for the induction and maintenance of general anaesthesia
during surgery and cesarean section and also used for analgesia during
vaginal delivery. |
Pharmacodynamics |
Enflurane is an extremely stable halogenated ether inhalation
anesthetic that allows rapid adjustments of anesthesia depth with little
change in pulse or respiratory rate. Enflurane induces muscle
relaxation and reduces pains sensitivity by altering tissue
excitability. Induction of and recovery from anesthesia with enflurane
are rapid. Enflurane may provide a mild stimulus to salivation or
tracheobronchial secretions. Pharyngeal and laryngeal reflexes are
readily obtunded. In the cardiovascular system, enflurane is a mild
negative inotrope, causing a marked decrease in systemic vascular
resistance, thus leading to a decrease in mean arterial pressure. This
results in a reflex tachycardia. Enflurane also decreases coronary
vascular resistance and sensitizes the myocardium to circulating
catecholamines. Enflurane is a strong respiratory depressant. It
decreases tidal volume but may increase respiratory rate. It also causes
bronchodilatationa and inhibits pulmonary macrophage activity and
mucociliary activity. Enflurane principle action in the CNS is general
anaesthesia with little analgesic effect. It causes increased cerebral
blood flow in concentrations and may induce tonic/clonic muscle activity
and epileptiform EEG traces. It also causes a marked decrease in
skeletal muscle tone. Actions in the genitourinary system include a
decreased renal blood flow and glomerular filtration rate and the tone
of pregnant uterus is decreased. |
Mechanism of action |
Enflurane induces a reduction in junctional conductance by
decreasing gap junction channel opening times and increasing gap
junction channel closing times. Enflurane also activates calcium
dependent ATPase in the sarcoplasmic reticulum by increasing the
fluidity of the lipid membrane. It also appears to bind the D subunit of
ATP synthase and NADH dehydogenase. Enflurane also binds to and
angonizes the GABA receptor, the large conductance Ca2+
activated potassium channel, the glycine receptor, and antagonizes the
glutamate receptor receptor. These yield a decreased depolarization and
therefore, tissue excitability which results in anesthesia. |
Absorption |
Rapidly absorbed into the circulation via the lungs. |
Volume of distribution |
Not Available |
Protein binding |
97% |
Metabolism |
2.4% of the dose is slowly metabolized hepatically via oxidation
and dehalogenation (primarily through the actions of cytochrome P450
2E1). Leads to low levels of serum fluoride (15 µmol/L). |
Route of elimination |
Not Available |
Half life |
Not Available |
Clearance |
Not Available |
Toxicity |
LD50=5.4 ml/kg (oral, rat). Symptoms of acute overdose
include nausea, vomiting, irritation to the eyes, skin and nose/throat,
headache, dizziness, and drowsiness. Symptoms of chronic overdose
include hypotension, cardiac arrhythmias, respiratory depression, and
liver/kidney dysfunction. |