Indication |
For the treatment of depression and depression accompanied by anxiety, agitation or sleep disturbance |
Pharmacodynamics |
Trimipramine is a tricyclic antidepressant. It was thought that
tricyclic antidepressants work by inhibiting the re-uptake of the
neurotransmitters norepinephrine and serotonin by nerve cells. However,
this response occurs immediately, yet mood does not lift for around two
weeks. It is now thought that changes occur in receptor sensitivity in
the cerebral cortex and hippocampus. The hippocampus is part of the
limbic system, a part of the brain involved in emotions. Presynaptic
receptors are affected: a1 and b1 receptors are sensitized, a2 receptors
are desensitised (leading to increased noradrenaline production).
Tricyclics are also known as effective analgesics for different types of
pain, especially neuropathic or neuralgic pain. A precise mechanism for
their analgesic action is unknown, but it is thought that they modulate
anti-pain opioid systems in the CNS via an indirect serotonergic route.
They are also effective in migraine prophylaxis, but not in abortion of
acute migraine attack. The mechanism of their anti-migraine action is
also thought to be serotonergic. |
Mechanism of action |
Trimipramine's mechanism of action differs from other tricyclic
antidepressants. Trimipramine acts by decreasing the reuptake of
norepinephrine and serotonin (5-HT). |
Absorption |
Rapid absorption |
Volume of distribution |
Not Available |
Protein binding |
93%-96% (to plasma proteins) |
Metabolism |
Hepatic |
Route of elimination |
Not Available |
Half life |
11-18 hrs |
Clearance |
Not Available |
Toxicity |
Side effects include agitation, coma, confusion, convulsions,
dilated pupils, disturbed concentration, drowsiness, hallucinations,
high fever, irregular heart rate, low body temperature, muscle rigidity,
overactive reflexes, severely low blood pressure, stupor, vomiting |
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