SUMMARY Episodes of atrial fibrillation that occurred after meals developed in a 60 year old man with a history of ischaemic heart disease. The attacks were precipitated by precursors and metabolites of tyramine and tyramine containing foods and drinks, in the absence of monoamine oxidase inhibitors. The patient has remained free of atrial fibrillation for the past twelve months on a diet that does not contain tyramine. Case reportIn 1980, at the age of 56 years, our patient was admitted to the hospital with central chest pain radiating to the left arm and in fast atrial fibrillation. Electrocardiography showed Q waves and ST segment elevation in the anterior chest leads V1-V5, and the plasma activity of the cardiac enzymes was increased, confirming the diagnosis of acute anterior myocardial infarction with atrial fibrillation. A few hours later acute left ventricular failure developed. He was treated with digoxin, diuretics, and anticoagulants. He quickly improved and recovered and sinus rhythm returned. He was transferred from the coronary care unit to the medical ward where he convalesced for 10 days and made a good recovery. Investigations-that is full blood count, urea and electrolyte concentration, liver function and thyroid function tests-were normal. He was discharged home in sinus rhythm on the above drugs.He had a history of migraine in his twenties, which had been successfully treated by his general practitioner. There was no history of palpitation or heart disease nor of any psychiatric illness. He was married with three children and was a non-smoker. He drank two pints of beer a night and was not on any drugs. His father had died of heart disease at the age of seventy but there was no other relevant family history.Two months later when he was reviewed in the outpatient clinic his condition was good, he was in sinus rhythm, and he was not in heart failure. he was referred to the hospital after he developed attacks of palpitation and dyspnoea, and clinical examination disclosed atrial fibrillation and left ventricular failure, which were confirmed by electrocardiogram and chest x ray respectively. The dose of digoxin was increased to 250 dg/day and diuretics were started. He improved and was subsequently reviewed in the clinic and found to be in a stable condition and in sinus rhythm with a heart rate of 64 beats/min; the attacks of palpitation had become less frequent.In May 1983 during one of his clinic reviews he mentioned for the first time that some of the attacks of palpitation occurred after meals. When he was questioned more closely about foods he suspected he identified cheese, chocolate, red wine, and bananas. Later after he had been asked to note his food more closely, he mentioned that broad beans and some tinned food with preservatives had also precipitated palpitation. Urinary concentrations of catecholamines and 5-hydroxyindolacetic acid were normal, however.Th-ere was clearly some connection between the foods he mentioned and the palpitation which was not prevented by digoxin. A change...
In the vascular system, synthesis of the potent vasodilator nitric oxide (NO) is tightly regulated by the constitutively expressed endothelial NO synthase (eNOS). Activity of eNOS is controlled by Ca 2z /calmodulin and various seryl/threonyl protein kinases. Less is known about the importance of phosphorylation and dephosphorylation of tyrosyl residues. Therefore the role of tyrosine phosphatase on the modulation of isolated rat pulmonary artery tone has been assessed. Inhibition of tyrosine phosphatase by sodium orthovanadate (SOV, 1610 -6 M) significantly: 1) increased phenylephrine-induced vasoconstriction and 2) decreased endotheliumdependent relaxation to acetylcholine, but had no effect on endothelium-independent relaxation to the NO donor, sodium nitroprusside. In phenylephrine-precontracted pulmonary arterial rings, SOV (1610 -7 -1610 -5 M) had no effect on vascular tone but significantly relaxed rings which were pretreated with the NO-synthase inhibitor, N v -nitro-L-arginine-methyl ester (L-NAME). SOV-induced relaxation in the presence of L-NAME was, however, abolished by glibenclamide.In conclusion, inhibition of tyrosine phosphatase altered pulmonary vascular tone by increasing vasoconstrictor response to phenylephrine and decreasing endotheliumdependent relaxation to acetylcholine. Furthermore, the tyrosine phosphatase inhibitor, sodium orthovanadate, exhibited original vasodilator properties which were only observed when nitric oxide synthesis was inhibited. Thus a new pathway involving the inhibitory effect of nitric oxide on a glibenclamide-sensitive diffusible relaxing factor, that might play an important role in the control of pulmonary vascular tone is described. Pulmonary vascular tone is modulated by a variety of endothelium-derived relaxing factors including prostacyclin, nitric oxide (NO) [1,2], and the endothelium-derived hyperpolarizing factors (EDHF) [2,3]. NO is one of the most potent vasodilators known to date. Its synthesis is tightly regulated by intracellular free Ca 2z and the Ca 2z / calmodulin complex that, in turn, stimulate the constitutive isoform of endothelial NO synthase (eNOS). Alternatively, phosphorylation on seryl and threonyl residues by various seryl/threonyl kinases is also thought to modulate eNOS activity [4,5].Shear stress is the major physiological factor modulating pulmonary vascular tone in health and disease. The underlying mechanism most likely involves synthesis and release of NO from pulmonary endothelial cells. Recent evidence suggests that endothelial production of NO is increased in response to shear stress through tyrosine phosphorylation via a calcium-independent pathway in the systemic circulation [4,6]. Contradictory studies alternatively suggest that tyrosine phosphorylation of eNOS might also reduce its activity [7]. Whether or not alteration of phosphorylation and/or dephosphorylation of tyrosyl residues of eNOS affects its activity in the pulmonary artery has yet to be investigated.In various vascular beds, EDHF causes relaxatio...
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