Effect of Intracoronary Serotonin on Coronary Vessels in Patients with Stable Angina and Patients with Variant Angina

McFadden, Eugène; Clarke, John; Davies, Graham; Kaski, Juan Carlos; Haider, Ahmed; Maseri, Attilio

doi:10.1056/nejm199103073241002

Cited by 342 publications

(124 citation statements)

References 27 publications

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“…Similar findings have also been reported in the rabbit isolated femoral artery (MacLennan & Martin, 1992) and dog coronary artery (Mullane et al, 1982). Whilst this potentiation effect of U46619 is not specific for 5-HT agonists (Cocks et al, 1993), such findings may have important clinical implications as both thromboxane A2 and 5-HT are released locally from aggregating platelets and amplification of the constrictor response to 5-HT receptor agonists, could lead to coronary vasospasm in arteries hyperreactive to 5-HT (Golino et al, 1989;Zeiher et al, 1991;McFadden et al, 1991;Willett et al, 1992).…”

Section: Introductionsupporting

confidence: 63%

Effects of U46619 on contractions to 5‐HT, sumatriptan and methysergide in canine coronary artery and saphenous vein in vitro

Kemp

Cocks

1995

British J Pharmacology

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1 The aim of this study was to investigate the mechanism of enhanced reactivity to 5-hydroxytryptamine (5-HT) and sumatriptan previously observed in human isolated coronary arteries when active force was raised with the thromboxane A2-mimetic, U46619. 2 Ring segments of dog isolated coronary artery and saphenous vein were suspended in organ baths and cumulative concentration-contraction curves to 5-HT, sumatriptan and methysergide were constructed in the absence and presence of low concentrations of U46619. 3 In both endothelium-intact and endothelium-denuded rings of coronary artery, precontraction with U46619 to low (< 10% F..; the contraction to a maximum depolarizing 125 mM KCl Krebs solution; KPSS) levels of active force had no effect on either the maximum contraction or sensitivity (pECmo) to 5-HT, sumatriptan and methysergide. 4 Ketanserin (1 pM) had no effect on contractions to sumatriptan and methysergide in endotheliumdenuded coronary artery rings, but reduced the maximum contraction to 5-HT by z 90% to a value (5% F) similar to that for sumatriptan and methysergide. Under these conditions, U46619 precontraction had no effect on either pECm or maximum for 5-HT, sumatriptan or methysergide.5 In rings of saphenous vein with endothelium and treated with ketanserin (1 pM), 5-HT and sumatriptan caused equal maximum responses of 65% F.. which were approximately double that of methysergide (32% F..). The maximum responses and sensitivity to 5-HT, sumatriptan, methysergide and noradrenaline were unaffected by precontraction with U46619. 6 Pretreatment of the saphenous vein with sodium nitroprusside (SNP; 10 kiM) caused a small sustained relaxation and significantly depressed the maximal contraction to 5-HT without affecting sensitivity and abolished the contraction curve to sumatriptan and methysergide. When the relaxation response to SNP was reversed with U46619 (1-4 nM), the contraction curves to 5-HT, sumatriptan and methysergide were similar to those obtained prior to relaxation with SNP. In contrast, the same treatment with SNP had little affect on the contraction curve to noradrenaline. 7 In conclusion, the pattern of U46619-enhanced reactivity of 5-HT, sumatriptan and methysergide in SNP-treated dog saphenous vein, highlights the importance of functional antagonism when assessing reactivity to contractile agonists in isolated blood vessels.

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Section: Introductionsupporting

confidence: 63%

Effects of U46619 on contractions to 5‐HT, sumatriptan and methysergide in canine coronary artery and saphenous vein in vitro

Kemp

Cocks

1995

British J Pharmacology

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“…Persistent thrombus might predispose to recurrent ischemia.10"' Abnormal vasoconstriction is also implicated in the pathogenesis of the acute coronary syndromes.13-'8 The risk of recurrence in these patients could be related to abnormal vasoreactivity of the culprit lesion due to powerful platelet/thrombin-mediated stimuli.12 "19-22 Substances such as serotonin, thromboxane A2, and endothelin released from an unstable coronary lesion might also influence the tonus and reactivity of the vasculature further downstream. 23 (Fig 1). The luminal diameters of the culprit lesion and of the stable angina control lesion for each of the patients with each of the interventions appear in (Fig 2).…”

mentioning

confidence: 99%

Vasoreactivity of the culprit lesion in unstable angina.

et al. 1994

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BACKGROUND Although abnormal vasoconstriction may be involved in the pathogenesis of the acute coronary syndromes, the vasoreactivity of the lesion responsible for unstable angina (culprit lesion) has not been directly investigated. It is also unknown if enhanced vasoreactivity is found downstream to this lesion or extends to uninvolved coronary arteries. METHODS AND RESULTS We studied seven unstable angina patients whose condition had sufficiently stabilized to allow ergometric bicycle exercise and a cold pressor test to be performed as provocative stimuli during coronary arteriography. We measured the luminal diameter of the culprit lesion, a normal-appearing distal segment, and the segment of an uninvolved coronary artery using quantitative coronary angiography. Seven stable angina patients served as controls. Antianginal medications were tapered and interrupted. The culprit lesion constricted significantly with exercise and the cold pressor test compared with a stable angina control lesion. The culprit lesion measured 1.41 +/- 0.07 mm at baseline and diminished to 1.09 +/- 0.07 mm with exercise (P = .001). It measured 1.26 +/- 0.07 mm before the cold pressor test and diminished to 1.09 +/- 0.03 mm with this test (P = .015). In contrast, the profile of the stable lesion in the stable angina control group differed significantly (P = .006). Its luminal diameter measured 1.42 +/- 0.17 mm at baseline and 1.48 +/- 0.21 mm with exercise (P = NS). It measured 1.57 +/- 0.18 mm before and 1.55 +/- 0.18 mm with the cold pressor test (P = NS). There were no significant changes to these stimuli in the uninvolved coronary artery segments in unstable angina and in the distal segments in both unstable and stable angina patients. CONCLUSIONS This study demonstrates increased vasoreactivity of the culprit lesion in unstable angina compared with a control lesion in stable angina. The lack of an effect either in the uninvolved coronary artery or downstream to the culprit lesion suggests that systemic neurohumoral or seeding mechanisms are not operative. This abnormal vasoreactivity might predispose to, or be a marker for, the recurrence of acute ischemia at this site.

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“…The coronary smooth muscle of patients with vasospastic angina is hypercontractile to various stimuli such as histamine, 20 ergonovine, 7 serotonin, 8 etc. In addition to an altered contractile response of coronary smooth muscle, impaired endothelial function, especially NO function, is associated with coronary vasospasm.…”

Section: Discussionmentioning

confidence: 99%

Differential Effects of Calcium-Channel Blockers on Vascular Endothelial Function in Patients With Coronary Spastic Angina

Miwa

Masai

Shimizu

2009

Circ J

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Effect of Intracoronary Serotonin on Coronary Vessels in Patients with Stable Angina and Patients with Variant Angina

Cited by 342 publications

References 27 publications

Effects of U46619 on contractions to 5‐HT, sumatriptan and methysergide in canine coronary artery and saphenous vein in vitro

Effects of U46619 on contractions to 5‐HT, sumatriptan and methysergide in canine coronary artery and saphenous vein in vitro

Vasoreactivity of the culprit lesion in unstable angina.

Differential Effects of Calcium-Channel Blockers on Vascular Endothelial Function in Patients With Coronary Spastic Angina

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