Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Afferent discharges of 64 single units were recorded from the left cardiac sympathetic nerve of anesthetized cats. Mechano-sensitive terminals of the afferent fibers were localized in the extrapulmonary part of the pulmonary artery, left atrium, left ventricle and left pericardium, as determined by direct mechanical probing of the heart after death of the animals. Conduction velocity of the fibers ranged from 2.5 to 14.6 m/s. Excitation of these Adelta-fibers with mechanically excitable endings was produced by intravenous injections of acetylcholine, 5-hydroxytryptamine, bradykinin, histamine and veratridine, and/or by topical application of these agents to the receptor region. Noxious heat to the mechanically excitable field in the wall of the pulmonary artery and the left ventricle also activated their afferent fibers. These observations provide evidence for a certain number of afferent units in the cardiac sympathetic nerve with polymodal sensitivity. These afferent fibers can provide the spinal cord with information not only on mechanical changes in cardiac events, but also changes in the chemical environment of the cardiac nerve ending, possibly produced by myocardial ischemia.
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PMID:Activation of afferent cardiac sympathetic nerve fibers of the cat by pain producing substances and by noxious heat. 56 84

Developed for the treatment of migraine, sumatriptan is an agonist of 5-hydroxytryptamine-1-receptors. Though a pressure sensation is a common complaint, significant ECG changes have not been reported after subcutaneous administration of sumatriptan. A case history is given where angina pectoris after sumatriptan self-administration was experienced on two occasions by a 61-year old man with a history of minor myocardial infarction--without post-infarction angina--two years previously. The angina after sumatriptan was accompanied on both occasions by significant ST-segment depression on ECG-monitoring. An extracranial vasoconstrictor action of sumatriptan in patients with ischaemic heart disease is suggested.
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PMID:[Angina pectoris after sumatriptan (Imigran)]. 133 86

Platelet-derived 5-hydroxytryptamine and thromboxane A2 activate vascular smooth muscle cells, blood platelets and myocardial cells, both directly and through mutual amplification. Such an activation triggers: (1) vascular smooth muscle cell mitogenic activity, connective tissue synthetic activity and contractile activity; (2) platelet aggregation, secretion and procoagulant activity; (3) myocardial rhythm disturbances and necrosis. By such mechanisms, these autocoids contribute to arterial vessel wall proliferation, vasospasms and arterial thrombus formation in response to interactions of platelets with a damaged vessel wall, reduce the efficacy of thrombolytic agents and modulate myocardial reperfusion injury. Compounds directed specifically against these autocoids thus may offer possibilities for treating human ischaemic heart disease.
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PMID:5-Hydroxytryptamine and thromboxane A2 in ischaemic heart disease. 213 Sep 32

Adaptation to intermittent hypoxia had a pronounced antiarrhythmic effect in acute myocardial ischemia in conscious animals. This effect was less pronounced in anesthesia and was absent in isolated heart. In reperfusion, the prophylactic effect of adaptation was equally pronounced in all cases. Adaptation prevented stress-induced exhaustion of brain beta-endorphine presumably by its accumulation in adrenal glands and resulted in the accumulation of dopamine, 5-hydroxytryptamine and 5-hydroxyindolacetic acid in brain structures. These data naturally lead to the assumption that central mechanisms play the main role in the antiarrhythmic effect of adaptation to intermittent hypoxia on ischemic arrhythmias, while mechanisms occurring at the level of heart play the main role in the protective effect of the same adaptation against reperfusion arrhythmias.
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PMID:Prevention of cardiac arrhythmias by adaptation to hypoxia: regulatory mechanisms and cardiotropic effect. 256 60

Ketanserin, a recently developed 5-HT2 receptor antagonist, competitively and selectively blocks the vasoconstrictor activity of 5-hydroxytryptamine (serotonin). We explored a possible contribution of serotonin to augmented vascular tone in patients with severe heart failure, using intravenous and oral formulations of ketanserin. When administered intravenously (10 mg bolus, 4 mg/hr infusion for +/- 40 min) to 10 patients with congestive heart failure (NYHA III or IV) secondary to congestive cardiomyopathy (n = 8) or ischemic heart disease (n = 2), the drug produced a significant increase in cardiac output (rest 24%, p less than 0.001; exercise 19%, p less than 0.01) which was accompanied by a fall in systemic arterial pressure (rest 7%, p less than 0.001; exercise 10%, p less than 0.05) and pulmonary wedge (rest 17%, p less than 0.05; exercise 23%, p less than 0.001) pressure. Calculated systemic vascular resistance (SVR, rest 27%, p less than 0.001; exercise 23%, p less than 0.05) decreased significantly. No significant hemodynamic changes were observed when 40 mg of ketanserin was administered orally to the same group of patients. Plasma catecholamines (norepinephrine, NEP:epinephrine, EP:dopamine) were measured before and after ketanserin at rest and during exercise. Baseline NEP levels were markedly elevated at rest and during exercise in all patients (rest: 878 +/- 381 ng/mL, exercise: 1453 +/- 697 ng/mL). Baseline EP levels were within normal limits. Ketanserin did not produce any change in catecholamine concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic and neurohumoral effects of ketanserin, a 5-HT2 receptor antagonist in patients with congestive heart failure. 356 10

Serotonin (5-hydroxytryptamine) has multiple cardiovascular actions. The presence of serotonin in the heart suggests it may be an endogenous source of inotropic support during physiologic or pathologic stress. Serotonin may increase cardiac contractility by augmenting release of norepinephrine at sympathetic nerve endings. Norepinephrine release is markedly elevated in patients with heart failure. To explore the role of serotonin in enhancing norepinephrine release in patients with heart failure, ketanserin, a specific serotonin antagonist, was used as a physiologic tool to examine the effect on transmyocardial norepinephrine flux. Ketanserin (10 mg bolus, 4 mg/hr infusion for +/- 40 min) was administered intravenously to nine patients with congestive heart failure (NYHA III or IV) secondary to congestive cardiomyopathy (N = 7), or ischemic heart disease (N = 2). Plasma catecholamines (norepinephrine, epinephrine, dopamine) were measured in the aorta (Ao) and the coronary sinus (CS) of patients at rest and during supine leg exercise before and after administration of ketanserin. Baseline norepinephrine levels were markedly elevated at rest and during exercise in all patients. Norepinephrine levels were significantly higher in the CS than in the Ao (rest, CS 1185 +/- 235, Ao 878 +/- 381 pg/mL, P less than .05; exercise, CS 2239 +/- 697, Ao 1453 +/- 697 pg/mL, P less than .05). Baseline epinephrine levels were within normal limits. In contrast to norepinephrine levels, epinephrine levels were consistently higher in the Ao than in the CS, indicating unimpaired extraction or uptake across the heart. The relationship between norepinephrine and epinephrine concentration in the Ao and CS suggested a net overflow of norepinephrine in the CS.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of 5-hydroxytryptamine blockade with ketanserin on myocardial uptake of epinephrine and norepinephrine in patients with congestive heart failure. 368 May 95

The post-mortem brain concentrations of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were determined in 16 parts of the brain from patients with no history of neurologic, psychiatric or metabolic illness. The causes of death were either ischemic heart disease, infections disease, cancer or accidents. Forty-two men with a mean age of 57 years (range 18-95 years) and 19 women with a mean age of 62 years (range 23-79 years) were included. The influence of several factors were studied: brain weight, time between death and autopsy, storage time before chemical analysis, age, sex, agonal status, cerebral arteriosclerosis, cancer, opiate treatment and time of death during the day. Most correlations between the 5-HT concentrations in different brain parts were positive, the strongest correlations in the basal ganglia and the limbic system. No consistent pattern of age-related 5-HT changes were found. The females had significantly higher 5-HIAA concentrations in the cortex of the gyrus hippocampus. Final hypoxia seemed to decrease 5-HT concentrations. Opiate treatment reduced 5-HT and increased 5-HIAA concentrations. A marked circadian variation of 5-HT was found, most pronounced in the hypothalamus, the limbic system and some neocortical areas.
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PMID:Distribution of 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in human brain in relation to age, drug influence, agonal status and circadian variation. 616

1 The hypothesis that magnesium deficiency, linked to the magnesium content of drinking water, induces major tone increases in coronary arteries and enhances their responses to vasoactive agents to an extent sufficient to explain sudden death associated with ischaemic heart disease was examined in an in vitro preparation. 2 The spontaneous tone of cattle coronary arteries was not increased during a 30 min exposure to Mg2+-deficient Krebs until the mineral was omitted entirely from the bathing medium, and even then the observed increase was small. Only in strips maintained under extremely deficient conditions for a prolonged period, namely Mg2+ concentration of 0.2 mM and 0.0 mM for 3 h, was tone substantially greater than in controls in standard (1.2 mM) Mg2+-Krebs. 3 Responses to acetylcholine and to noradrenaline were not increased in Mg2+-free Krebs but those to potassium and to 5-hydroxytryptamine were enlarged over the lower parts of their concentration-response curves. Responses to potassium and to 5-hydroxytryptamine were also examined in Krebs containing very low concentration of Mg2+ (0.4 and 0.2 mM) and only modest increases in contraction size were detected. Increases in the Mg2+ concentration of the Krebs (to 4.8 mM) depressed responses to potassium and 5-hydroxytryptamine. 4 It is concluded that Mg2+ deficiency must be nearly complete (0.4-0.0 mM) to induce even moderate tone increases in coronary vessels, or to sensitize them to agonist responses, and that there is no reason to link marginally subnormal Mg2+ levels, occasionally reported in humans with heart disease, to marked changes in coronary dynamics.
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PMID:The effect of magnesium deficiency and excess on bovine coronary artery tone and responses to agonists. 685 Jan 65

1. The interaction between the thromboxane A2 receptor agonist, U46619 and two 5-hydroxytryptamine (5-HT) receptor agonists, the non-selective, naturally occurring agonist, 5-HT and the selective 5-HT1-like agonist, sumatriptan were studied in human epicardial coronary arteries in vitro. 2. Coronary artery rings (2-4 mm in diameter) were prepared from epicardial arteries from explant hearts of patients undergoing heart transplant (cardiomyopathy, n = 13; ischaemic heart disease, n = 10) and unused donor hearts (n = 5). Each ring of artery was set at optimal resting conditions to record changes in isometric force. 3. The majority of artery rings developed phasic, rhythmic contractions either spontaneously or in response to all vasoconstrictor agonists tested. Both the spontaneous and agonist-induced phasic contractions were abolished by nifedipine (0.1 microM). 4. Concentration-contraction curves to 5-HT-receptor agonists and noradrenaline (NA), were first constructed in artery rings that did not develop phasic activity. 5-HT and ergometrine were the most potent agonists with EC50 values of 6.8 +/- 0.2 and 7.7 +/- 0.2 (-log M) respectively. Potencies (EC50's) to sumatriptan, methysergide and noradrenaline could not be determined due to their poor ability to contract the coronary artery. Maximum contractions (Emax; normalized as a percentage of the contraction to a maximum-depolarizing concentration of K+ in physiological salt solution (KPSS)) for 5-HT, ergometrine, sumatriptan, methysergide and noradrenaline were 40 +/- 10, 9 +/- 3, < 5, < 5 and < 5% respectively. 5. In arteries without phasic activity, U46619 (1 nM) caused an increase in force of 3.8 +/- 1% KPSS. With U46619 present, the Emax values for 5-HT, ergometrine, sumatriptan and methysergide were all markedly increased. For 5-HT and sumatriptan, E., values were 92+/- 4% and 49 +/- 14% KPSSrespectively. The presence of U46619 did not significantly change the sensitivity (EC50) to 5-HT.6. In a separate series of arteries, nifedipine (0.1 microM) was used to block phasic, contractile activity. The synergy observed between U46619 and 5-HT or sumatriptan still occurred although the Emax values for each agonist were depressed but the EC50 values were again unaffected.7. In conclusion, these in vitro studies indicate that the normally poor contractions to sumatriptan, inhuman coronary arteries are significantly enhanced when active force is induced with a thromboxane A2-receptor agonist, U46619. The enhanced response is not specific for either sumatriptan or 5-HT,-like receptors since contractions to 5-HT, ergometrine and methysergide were also potentiated by U46619.
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PMID:Comparison of contractile responses to 5-hydroxytryptamine and sumatriptan in human isolated coronary artery: synergy with the thromboxane A2-receptor agonist, U46619. 822 Aug 98

Using ELISA we studied the levels and clinical correlation of serum antibodies against gangliosides and 5-hydroxytryptamine (5-HT) in patients with atherosclerosis and clinical manifestations of cardiovascular disease. A range of 70-80% of the patients showed higher titers of anti-GM3(L) and anti-5HT as compared to normal serum. The anti-GM3(L) antibodies appeared to be directed mainly against GM3 present in platelets and were much less reactive against GM3 isolated from the aorta. We concluded that the antigens responsible for the elevated anti-GM3(L) and anti 5-HT levels in atherosclerotic sera are released by vessel-wall activated platelets. These results provide further evidence of on-going autoimmune processes in atherosclerosis. The content of total sialic (TS) and lipid-bound sialic acid (LBS) was measured in sera of patients with IHD and of similar numbers of healthy donors. In the patient groups the average TS and LBS concentration was about 25% higher than in the control group. These changes appeared to be associated with higher degrees of protein sialylation and larger amounts of LDL in the patient sera than in those of healthy controls.
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PMID:Autoantibodies to gangliosides in sera of atherosclerotic patients. 964 60


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