Increase in PGE<sub>2</sub> and TXA<sub>2</sub> in the Saliva of Common Migraine Patients. Action of Calcium Channel Blockers

Tuca, J. Obach; Planas, Jordi; Parellada, R Puig

doi:10.1111/j.1526-4610.1989.hed2908498.x

Cited by 43 publications

(25 citation statements)

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“…Along with other research, this may indicate that each migraine attack serves to reset the system with regard to the activation, which has been built up during the headache‐free interval, meaning that migraine is subject to cyclicity 29,30 . Thus, in accordance with previous work on inflammatory mediators in the periphery, the present data may indicate that migraine is a process localized to the central nervous system 10‐12 . However, future studies are needed to investigate whether the peripheral level of inflammatory mediators could be an indicator of an impending migraine attack.…”

Section: Commentssupporting

confidence: 88%

“…It has been shown that leukotriene plasma levels are increased during migraine attacks 10 . Tuca and coworkers also found that PGE 2 and thromboxane A 2 (TXA 2 ) levels were increased in saliva during migraine attacks 11 . Comparable to these results, another study showed a significant increase in PGE 2 plasma levels during the attack; in a headache‐free interval, PGE 2 levels were reported to be lower in patients with migraine compared with a control group 12 .…”

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confidence: 93%

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Peripheral Levels of Inflammatory Mediators in Migraineurs During Headache‐free Periods

et al. 2001

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Objectives.-The present study investigated the peripheral inflammatory changes of the trigeminovascular system by measuring the inflammatory mediators leukotriene B 4 (LTB 4 ), prostaglandin E 2 (PGE 2 ), and thromboxane B 2 (TXB 2 ) in the nasal fluid, as well as saliva, of patients with migraine.Background.-Migraine has been hypothesized to be as a result of changes in the peripheral or central nervous system or both. It is still unclear whether peripheral changes in the trigeminovascular system are involved in the pathogenesis of migraine.Methods.-Participants were 18 subjects, 9 patients with migraine and 9 controls, matched for age and sex. Each subject took part in one experimental session during which nasal lavage fluid and saliva samples were collected. These samples were analyzed by competitive enzyme immunoassay using goat anti-rabbit polyclonal antibody.Results.-With the exception of TXB 2 , correlational analyses indicated good correlations between results obtained using nasal lavage or saliva (LTB 4 , r 18 ϭ 0.91; PGE 2 , r 18 ϭ 0.95). When comparing inflammatory mediators measured in controls and migraineurs, the LTB 4 level was significantly lower in migraineurs, while no differences were found for PGE 2 and TXB 2 .Conclusions.-The study demonstrated that nasal lavage, a noninvasive method, can be easily used for investigations of pathophysiological mechanisms of migraine. In addition, the results may indicate that there is no peripheral trigeminal sensitization in the headache-free period of migraineurs compared with controls when PGE 2 , LTB 4 , and TXB 2 in saliva and nasal lavage samples are measured.

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confidence: 88%

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confidence: 93%

Peripheral Levels of Inflammatory Mediators in Migraineurs During Headache‐free Periods

et al. 2001

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“…We recently reported that the combination of increasing dietary n- 3 fatty acids with concurrent reduction in n-6 LA produced statistically significant, clinically relevant improvements in headache frequency, intensity and quality of life in chronic headache patients [24], a condition with reported elevations of AA-derived mediators in blood and saliva [25, 24, 26]. Blood collected from this trial provides a unique opportunity to evaluate the effects of targeted alterations of dietary n-3 and n-6 fatty acids on plasma esterified and unesterified fatty acid concentrations [19, 24], which could be used as biomarkers to relate efficacy in dietary treatment effects.…”

Section: Introductionmentioning

confidence: 99%

Dietary omega-6 fatty acid lowering increases bioavailability of omega-3 polyunsaturated fatty acids in human plasma lipid pools

Taha

Cheon

Faurot

et al. 2014

Prostaglandins, Leukotrienes and Essential Fatty Acids

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Background Dietary linoleic acid (LA, 18:2n-6) lowering in rats reduces n-6 polyunsaturated fatty acid (PUFA) plasma concentrations and increases n-3 PUFA (eicosapentaenoic (EPA) and docosahexaenoic acid (DHA)) concentrations. Objective To evaluate the extent to which 12 weeks of dietary n-6 PUFA lowering, with or without increased dietary n-3 PUFAs, change unesterified and esterified plasma n-6 and n-3 PUFA concentrations in subjects with chronic headache. Design Secondary analysis of a randomized trial. Subjects with chronic headache were randomized for 12 weeks to: (1) average n-3, low n-6 (L6) diet; or (2) high n-3, low n-6 LA (H3-L6) diet. Esterified and unesterified plasma fatty acids were quantified at baseline (0 weeks) and after 12 weeks on a diet. Results Compared to baseline, the L6 diet reduced esterified plasma LA and increased esterified n-3 PUFA concentrations (nmol/ml), but did not significantly change plasma arachidonic acid (AA, 20:4n-6) concentration. In addition, unesterified EPA concentration was increased significantly among unesterified fatty acids. The H3-L6 diet decreased esterified LA and AA concentrations, and produced more marked increases in esterified and unesterified n-3 PUFA concentrations. Conclusion Dietary n-6 PUFA lowering for 12 weeks significantly reduces LA and increases n-3 PUFA concentrations in plasma, without altering plasma AA concentration. A concurrent increase in dietary n-3 PUFA for 12 weeks further increases n-3 PUFA plasma concentrations, but also reduces AA.

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“…During myocardial infarction and angina, plasma concentrations of thromboxane and histamine are increased (29,31). Thromboxane concentration has also been reported to increase during migraine attacks (32). Thus these endogenous ligands may act in concert to augment vasoconstrictor effects of sumatriptan, especially under conditions of vascular injury.…”

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Amplification of sumatriptan-induced contraction in rabbit saphenous vein but not in basilar artery

Bhattacharya

Schenck

Cohen

2003

American Journal of Physiology-Heart and Circulatory Physiology

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. Amplification of sumatriptan-induced contraction in rabbit saphenous vein but not in basilar artery. Am J Physiol Heart Circ Physiol 284: H719-H726, 2003; 10.1152/ajpheart.00345.2002.-The modulation of serotonin (5-HT1B/1D) receptor-induced vascular contractility by histamine and U-46619 was compared in the rabbit basilar artery and saphenous vein. In the saphenous vein, histamine (5 ϫ 10 Ϫ7 M) significantly increased the potency (from pEC50 of 6.0 to 6.8) and efficacy (from 52.3% to 88.2%) of sumatriptan. Likewise, U-46619 (5 ϫ 10 Ϫ9 M) also increased the potency (from pEC50 of 5.9 to 6.6) and efficacy (from 51.8% to 92.1%) of sumatriptan in the saphenous vein. In contrast, equieffective concentrations of histamine (10 Ϫ7 M) and U-46619 (3 ϫ 10 Ϫ9 M) failed to amplify contraction to sumatriptan in the basilar artery. Contraction to sumatriptan was inhibited by nitrendipine (10 Ϫ7 M) in the basilar artery but not in the saphenous vein, suggesting that different contractile signaling mechanisms are operating in these tissues. Furthermore, U-46619-and thrombin-induced contractility in the basilar artery were also not amplified by histamine, suggesting that lack of amplification of contraction in the basilar artery was not restricted to sumatriptan but was rather a characteristic of this cerebral vessel. These data suggest that in the in vivo plasma milieu sumatriptan will more markedly contract the peripheral saphenous vein than the basilar artery, a cerebral blood vessel. nitrendipine; histamine; U-46619; serotonin receptors SUMATRIPTAN is an antimigraine drug (20) with a high affinity for serotonin 5-HT 1B and 5-HT 1D receptors (27). The antimigraine efficacy of sumatriptan has been attributed, in part, to its ability to activate central vascular 5-HT 1B/1D receptors (8). However, much of the information on the vascular effects of sumatriptan has been derived from studies using peripheral vascular serotonin receptors. For example, sumatriptan-induced peripheral vascular contraction has been widely studied in the rabbit saphenous vein (9), femoral artery (4), mesenteric artery (5), and iliac artery (36). Because the cardiovascular liabilities of sumatriptan may be related to its ability to constrict coronary arteries (23), sumatriptan has also been studied in coronary arteries from dogs (21) and humans (1). In contrast, the cerebral vascular effects of sumatriptan have been less extensively studied (3,16,17).Modest increases in vascular tone with threshold concentrations of vascular contractile agonists such as prostaglandin, angiotensin, histamine, endothelin, or adrenergic agonists are known to increase sumatriptaninduced vascular contractility (35). Whereas this amplifying effect is well established in peripheral blood vessels (7,9,21,22

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Increase in PGE₂ and TXA₂ in the Saliva of Common Migraine Patients. Action of Calcium Channel Blockers

Cited by 43 publications

References 23 publications

Peripheral Levels of Inflammatory Mediators in Migraineurs During Headache‐free Periods

Peripheral Levels of Inflammatory Mediators in Migraineurs During Headache‐free Periods

Dietary omega-6 fatty acid lowering increases bioavailability of omega-3 polyunsaturated fatty acids in human plasma lipid pools

Amplification of sumatriptan-induced contraction in rabbit saphenous vein but not in basilar artery

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Increase in PGE2 and TXA2 in the Saliva of Common Migraine Patients. Action of Calcium Channel Blockers

Cited by 43 publications

References 23 publications

Peripheral Levels of Inflammatory Mediators in Migraineurs During Headache‐free Periods

Peripheral Levels of Inflammatory Mediators in Migraineurs During Headache‐free Periods

Dietary omega-6 fatty acid lowering increases bioavailability of omega-3 polyunsaturated fatty acids in human plasma lipid pools

Amplification of sumatriptan-induced contraction in rabbit saphenous vein but not in basilar artery

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Increase in PGE₂ and TXA₂ in the Saliva of Common Migraine Patients. Action of Calcium Channel Blockers