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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    European journal of clinical pharmacology 49 (1996), S. 335-339 
    ISSN: 1432-1041
    Keywords: Migraine ; Histamine ; nitric oxide ; glyceryl trinitrate ; cerebral arteries ; transcranial Doppler
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract It has previously been shown that in migraine sufferers infusion of glyceryl trinitrate (GTN) and histamine causes an immediate headache during the infusion and a genuine migraine attack one to several hours after the infusion. This identical time profile indicates a common mechanism of action. To evaluate whether GTN causes headache via liberation of histamine, we studied the effect of GTN 0.5 ώg · kg−1·min−1 for 20 min in seven migraine sufferers, once after pretreatment with the histamine-1(H1)-receptor blocker mepyramine (0.5 mg · kg−1) and once without pretreatment. This mepyramine dose is known to completely abolish histamine-induced headache. After pretreatment with mepyramine five patients experienced migraine, and without pretreatment six patients did so. The median peak headache score was 7 on a 0–10 scale with and without mepyramine pretreatment. The arterial responses, evaluated with transcranial Doppler, were also unaffected by the mepyramine pretreatment. Our results demonstrate that neither headache nor arterial dilatation due to GTN infusion is caused by histamine release. In all likelihood the common mediator of migraine induction by GTN and histamine is nitric oxide.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Clinical autonomic research 5 (1995), S. 243-250 
    ISSN: 1619-1560
    Keywords: migraine ; sympathetic ; parasympathetic ; nitric oxide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Abnormal regulation of the large cranial arteries seems to play a significant role in the mechanisms of migraine pain. Thus, vasodilatation of extra- and intracranial conductance arteries has been described both during spontaneous migraine attacks and during experimentally provoked vascular headaches. The regulation of the diameter of these arteries is complex and involves autonomic, trigeminovascular, endothelial and humoral mechanisms. Studies concerned with the function of the autonomic nervous system in migraine suggest that a mild parasympathetic dysfunction may be present. Cerebral arteries in migraineurs are hypersensitive to nitric oxide, which may induce migraine attacks. As the enzyme responsible for nitric oxide synthesis is present in parasympathetic nerve endings around cerebral arteries, this supports a role for the parasympathetic nervous system in migraine. In addition, vasoactive transmitters released from perivascular trigeminal nerve endings may be implicated. Several of these aspects are closely linked to the presumed mechanisms of action of modern migraine therapeutics.
    Type of Medium: Electronic Resource
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