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Biomedical subjects

M G Buzzi

Publications and source records attributed to M G Buzzi.

At least 55 records · Page 3Linked to original sources
PubMed1990

The antimigraine drug, sumatriptan (GR43175), selectively blocks neurogenic plasma extravasation from blood vessels in dura mater.

1. We describe the actions of GR43175, a 5-hydroxytryptamine1 (5-HT1)-like receptor agonist, on neurogenically-mediated plasma protein extravasation within an important pain-sensitive intracranial tissue, the dura mater. 2. GR43175 markedly attenuated extravasation of 125I-albumin from blood vessels within ipsilateral dura mater when administered to rats (100 micrograms kg-1) fifteen minutes before unilateral electrical trigeminal stimulation (1.2 mA, 5 Hz, 5 ms, 5 min); the ratio (stimulated/unstimulated sides) decreased from 1.81 to 1.23, P less than 0.005). 3. GR43175 (100 micrograms kg-1, i.v., rats; 30 micrograms kg-1, guinea-pigs) decreased the leakage of radiolabelled albumin from 163% to 119% (P less than 0.005, guinea-pig) or from 174 to 118% (P less than 0.05, rat) above vehicle-treated controls when injected ten minutes before systemic capsaicin treatment (0.5 or 1 mumol kg-1, i.v.). 4. GR43175 (30-300 micrograms kg-1) did not block plasma protein extravasation within extracranial tissues of rats and guinea-pigs innervated by the trigeminal nerve (conjunctiva, eyelid and lip). 5. The protein leakage which followed the i.v. administration of 5-HT (1 mumol kg-1) or neuropeptides which mediate neurogenic plasma extravasation, substance P (0.3 nmol kg-1 or 1 nmol kg-1) and neurokinin A (1 nmol kg-1), was not blocked by GR43175 (100, 300 micrograms kg-1) despite the presence of leakage in amounts equivalent to that following neurogenic stimulation. 6. GR43175 (100 micrograms kg-1) decreased bradykinin (10 mumol kg-1)-induced extravasation from 142 to 115% above vehicle-treated animals (P less than 0.05). 7. These results demonstrate an important action of GR43175 on neurogenic mechanisms in dural blood vessels. Since the ergot alkaloids possess a similar profile of drug activity, it is suggested that drugs useful in the treatment of acute vascular headaches may share a similar mechanism of action.

Animals↗
PubMed1989

Indomethacin and acetylsalicylic acid block neurogenic plasma protein extravasation in rat dura mater.

Leakage of 125I-bovine serum albumin was measured in rat dura mater, conjunctiva, eyelid and lip, after unilateral electrical stimulation of the trigeminal ganglion. In one animal, 99Tc-human serum albumin leakage was imaged in ipsilateral facial tissues. Pretreatment with indomethacin 1 mg/kg i.p. decreased leakage in dura mater but not in extracranial tissues. When extravasation was expressed as a ratio of stimulated to unstimulated sides, indomethacin 1 mg/kg, or acetylsalicylic acid 50 mg/kg decreased this ratio from 1.80 to 1.27 (P less than 0.01) or from 1.84 to 1.21 (P less than 0.01), respectively. Dexamethasone (1 mg/kg i.p. tid X 1 day) caused only a very small decrease. Only large doses of indomethacin (10 mg/kg) or acetylsalicylic acid (50 mg/kg) reduced substance P (SP)-induced leakage in the dura. The latter results suggest that both drugs block plasma extravasation by acting on neuropeptides-induced changes in vascular permeability and/or smooth muscle contractility. However, inhibition of SP release from sensory axons cannot be excluded at concentrations which block neurogenic plasma extravasation but not SP-induced plasma leakage. Together, these results provide a possible mechanism for the therapeutic effects of indomethacin and acetylsalicylic acid in headache.

Animals↗
PubMed1989

The development of neurogenic plasma extravasation in the rat dura mater does not depend upon the degranulation of mast cells.

Mast cells were visualized in stretch preparations of the rat dura mater and were found mostly in relation to small and large blood vessels. The overall number of dural mast cells was unaffected by electrical trigeminal or chemical deafferentation. As in other tissues, mast cell degranulation increased at sites of local injury (electrode penetration) or after systemic treatment with compound 48/80. However, mast cells did not degranulate following electrical trigeminal stimulation, or after injection of drugs (capsaicin or substance P) which promote plasma extravasation in the dura. Furthermore, pretreatment with a mast cell stabilizer (sodium dicromoglycate) or with large doses of H1 and H2 histamine receptor blockers (mepyramine and cimetidine), did not block electrically- or chemically-induced neurogenic plasma extravasation (NPE). Daily pretreatment with 48/80 however completely attenuated or abolished NPE. Taken together these data suggest that as assessed by the extrusion of metachromatic granules, mast cells are not essential to the development of neurogenic inflammation within the rat dura mater. However, these findings cannot exclude the possibility that mast cells may amplify or modulate this process.

Animals↗
PubMed1989

Preproenkephalin mRNA expression in nucleus caudalis neurons is enhanced by trigeminal stimulation.

Electrical stimulation of trigeminal afferents increases expression of preproenkephalin mRNA in neurons of laminae I and II of the trigeminal nucleus caudalis in animals sacrificed 6 hours after the end of stimulation. More neurons express, and positive cells express at higher levels. These neurons thus express the mRNA corresponding to a major pain-modulating neurotransmitter gene with significant input-related plasticity.

Animals↗
PubMed1989

Postocclusive cerebral hyperemia is markedly attenuated by chronic trigeminal ganglionectomy.

Marked hyperemia may develop in brain following temporary cessation of blood flow and is associated with the morbidity following cardiac arrest, stroke, and head injury. Regional cerebral blood flow was measured using radiolabeled microspheres and compared in 10 symmetrical regions after chronic unilateral trigeminal ganglionectomy (n = 8), trigeminal rhizotomy (n = 4), or sham operation (n = 4) following 10 min of combined brachiocephalic-left subclavian occlusion and hypotension (mean arterial blood pressure less than 50 mmHg) in cats. Blood flow was symmetrical at rest in the three groups and was undetectable during the ischemic period. Within 30 min after re-establishing flow, values in cortical gray matter increased symmetrically to approximately 250 ml.100 g-1.min-1 in the rhizotomy and the sham groups. Increases of similar magnitude were measured on the intact side following trigeminal ganglionectomy but flow was attenuated by greater than 50% ipsilateral to the ganglionectomy. Marked hyperemia developed during reperfusion in thalamus, caudate, deep cortical white matter, midbrain, and pons, but no asymmetries were present in the three groups. These data suggest that cortical hyperemia is mediated by trigeminal neurogenic mechanisms via axonal reflexlike mechanisms and suggest the importance of therapeutic strategies based on blockade of this nerve or its constituent neuropeptides.

Animals↗
PubMed1989

Pain mechanisms underlying vascular headaches. Progress Report 1989.

Vascular headaches are among the most prevalent yet poorly understood problems in clinical neurology. Headaches may develop in association with hypertension, seizures, stroke or without a recognizable pathophysiology such as during migraine and cluster headaches. Cephalic blood vessels (pial and dural vessels) are implicated as the most important source for all headaches and are innervated by sensory fibers which arise from ganglia innervating the forehead, scalp and neck. Sensory fibers contain vasoactive neuropeptides which become released from peripheral (perivascular) and central terminations to mediate vasodilation and pain, respectively. The presence of vascular headache implies activation of this final common pain pathway which we have termed the trigeminovascular system. The presence of vascular headache implies activation of this final common pain pathway which we have termed the trigeminovascular system. The existence of such a system a) clarifies certain pain patterns which develop following stimulation of cephalic blood vessels, b) suggests a mechanism to explain the referral of pain to the forehead, c) provides a mechanism to explain the action of certain antimigraine drugs, d) suggests a local mechanism which enhances blood flow under certain pathological conditions. Hence, this review will update existing knowledge about the trigeminovascular system and its role in headache pathophysiology.

Animals↗
PubMed1986

Flunarizine-pizotifen single-dose double-blind cross-over trial in migraine prophylaxis.

The results of a double-blind cross-over clinical trial involving 27 patients with classical or common migraine are described to compare the prophylactic effect of the calcium entry blocker flunarizine with that of pizotifen. Duration of the treatment was two months, with an evening single-dose administration of both drugs. For most parameters, there was no definite difference between flunarizine and pizotifen in migraine prophylaxis. It has been demonstrated previously that pizotifen is an effective drug in migraine prophylaxis, and these results suggest that flunarizine is effective, too. Weight gain as a side effect was less frequent and less severe with flunarizine than with pizotifen; other side effects showed the same incidence with both drugs.

Calcium Channel Blockers↗
PubMed1986

Neuroendocrine effects of setoperone: a new neuroleptic drug.

Setoperone (R 52245), a serotonin S2 and dopamine D2 receptor blocker, was tested on eight healthy male volunteers, receiving 5 or 40 mg orally, in order to assess the modifications of plasma prolactin levels, as an index of receptor blocking activity. Both doses significantly increased plasma levels, confirming the dopamine blocking activity. In vitro and in vivo studies have shown serotonin S2 receptor blockade and lysergic acid diethylamide antagonist activity. Setoperone is proposed as a possible new neuroleptic drug.

Adolescent↗
PubMedDate not supplied

Assessing the relative incidence of mitochondrial DNA A3243G in migraine without aura with maternal inheritance.

OBJECTIVE: To determine whether patients with migraine without aura with maternal "inheritance" are affected by a monosymptomatic form of the MELAS syndrome (mitochondrial encephalomyopathy, lactic acidosis, and strokelike episodes) or carry the most common mitochondrial DNA (mtDNA) mutation associated with MELAS, namely the A3243G transition in the transfer RNA (tRNA)Leu(UUR) gene. BACKGROUND: The association between migraine and abnormal mitochondrial function has been suggested on clinical, biochemical, and neuroradiological grounds. Migraine attacks with vomiting and cerebral infarctions, most often in the posterior cerebral regions, which are reminiscent of complicated migraine, are typical features of MELAS. The observation that migrainous patients have affected mothers more often than affected fathers suggests a possible role for maternally transmitted genetic factors. METHODS: We studied 25 patients with migraine with aura whose mothers were also affected. A sensitive polymerase chain reaction restriction fragment length polymorphism analysis was used to detect mutated genomes. CONCLUSIONS: We failed to detect the MELAS mutation, but migraine may still be associated with point mutations of mtDNA other than A3243G or with as-yet-unidentified nuclear DNA factors related to mitochondrial function.

Adolescent↗
PubMedDate not supplied

[Double-blind clinical study: flunarizine versus pizotifen in a single nightly dose in hemicrania patients].

In this double-blind clinical trial we compared the prophylactic efficacy of the calcium-entry blocker flunarizine (15 mg nocte) with that of pizotifen (1,5 mg nocte). In 30 patients affected by classical and common migraine. During a two months treatment both drugs showed a good efficacy. Flunarizine tended to more markedly suppress severity of pain and duration of attacks than pizotifen. Daytime drowsiness and weight gain occurred with both drugs; the first side effect was more evident in the group treated with flunarizine, the second one in the group treated with pizotifen.

Adult↗