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Biomedical subjects

M Fanciullacci

Publications and source records attributed to M Fanciullacci.

107 records · Page 6Linked to original sources
PubMedDate not supplied

Possible non-muscarinic miotic action of echothiophate iodide in humans.

The proposed non-muscarinic pupillary action of echothiophate iodide (EI) was investigated in humans. In 10 healthy volunteers the variations of the pupillary area, induced by EI eye drops, were evaluated by using an electronic pupillometer. When instilled alone, as well as after homatropine, EI caused pupillary constriction. The reduction of the homatropine-induced mydriasis by EI was not accompanied by any increase in the almost abolished pupillary response to light, thus excluding that an enhancement of the parasympathetic activity contributes to pupillary constriction. These findings suggest a non-muscarinic component in the EI-induced miosis, the nature of which remains to be elucidated.

Adolescent↗
PubMedDate not supplied

[The pathogenetic bases of hemicrania].

Studies of regional cerebral blood flow in migraine with aura have shown that the aura phase is associated with hypoperfusion in the cortical area which relates topographically to the clinical symptoms. Thus, the previously hypoperfused area becomes hyperperfused. However, there is no strict association between hyperperfusion and headache. The mode of hypoperfusion propagation recalls the circulatory manifestations of experimental cortical spreading depression. In addition, there are no focal cerebral blood flow abnormalities in migraine without aura. During the headache phase of migraine, dilation of both the large extra- and intracranial arteries takes place. A bulk of biochemical evidence has suggested that the pain in migraine is caused by blood vessels which are dilated and sensitized by circulating pain-producing substances e.g. bradykinin, serotonin and histamine (sterile inflammation). Recently, perivascular trigeminal fibres (trigeminovascular system) which, when stimulated, release sensory peptides (substance P and the calcitonin gene-related peptide) capable of provoking marked vasodilation and plasma extravasation (neurogenic inflammation) have been identified. Thus, the activation of the trigeminovascular system is probably involved in the vasodilatative and nociceptive phenomena of the migraine attack. The finding of a reduced endorphinergic brain tonus in migraine patients supports the hypothesis of a central nociceptive derangement in migraine. Nonetheless, the exact relationship between vasodilation and headache remains to be defined. However, the potent antimigraine effectiveness of sumatriptan--an agonist of the serotonin receptors which selectively constricts dilated arteries during the migraine attack--once again stresses the fact that serotonin is probably the crucial factor in the link between vasodilation and headache.

Cerebrovascular Circulation↗
PubMedDate not supplied

Non-vascular action of calcium blockers in migraine: pupillopharmacological study.

A pupillopharmacological study has been carried out to evaluate the influence of two calcium blockers (CBs), flunarizine and nimodipine, on iris neurotransmission in migraine patients. Pretreatment with an oral dose of flunarizine or nimodipine markedly decreased the mydriasis induced by instillation of tyramine, a noradrenaline releaser. On the contrary, both drugs did not change the mydriasis by conjunctival phenylephrine, a postsynaptic adrenoceptor stimulant. In addition, nimodipine abolished the miosis caused by echothiophate iodide eye drops, a putative releaser of substance P from trigeminal sensory nerve endings. These findings suggest the idea that CBs treatment in migraine syndromes acts at presynaptic level by attenuating calcium-dependent release of monoaminergic and peptidergic neurotransmitters.

Echothiophate Iodide↗