Pathophysiology

The pharmacological activates of the ergot alkaloids

and their semi synthetic derivatives are extremely
varied and complex

The ergot alkaloid have the ability to interfere with

more than one type includes:

1.

Alpha-adrenergic receptor interference (both agonist and

antagonist) ergotamine and dihydroergotamine process the
most potent vasoconstrictor activity of the ergot alkaloids;
producing constriction of both veins and arteries (pressor
effect lead to hypertension with cerebral and peripheral
ischemia)

Due to mediation by alpha-adrenergic receptors and tryptaminergic receptors

or both

Also, may inhibit receptor reuptake of norepinephrine at sympathetic

nerve endings which
increases the vasoconstrictive action.
May cause bradycardia as a result of their effects of increasing vagal
activity, possibly decreasing sympathetic tone and causing direct
myocardial depression
2.

A Potent emetic effect through stimulation of the

chemoreceptor trigger zone may cause nausea and
vomiting

3.

Dopaminergic effect

4.

Serotonin
antagonist)

5.

Ecbolic action(lead to abortion)

6.

hyper or hypothermia

receptor

activity(agonist

and

Treatment

1.

Stomach wash using a local alkaloidal antidote e.g. activated charcoal

2.

Safe-guard respiration

3.

Physiological antidotes are vasodilators:

Phentolamine (regitin) 5mg slowly I.V.

Nitrites as amyl-nitrite inhalation, or Na-nitrite I.V.

Papaverine I.V.

4.

If convulsions are not controlled by vasodilators, diazepam 5-10 mg I.V.

is given with O2 inhalation.

5.

I.V. heparin as anticoagulant.

6.

Nitroglycerine injection I.V. and intra-arterial for coronary vasospasm

7.

Na-nitroprusside for severe spasm (it has direct action on smooth

muscles).