Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cardiac distribution of mast cells was investigated after the induction of acute myocardial infarction in the rat. The left anterior descending coronary artery (LAD) was occluded by ligation in the infarct group, whereas in sham rats only a superficial ligature was placed beside the LAD. Rats of both groups were killed at 4, 7, 14, 21, 35, and 85 days following surgery. Hearts were excised and formalin-fixed. Mast cell densities were monitored in subepicardial and subendocardial layers of the left ventricle (LV) in 6 microns thick toluidine blue-stained cross-sections. In control (non-operated) animals, mast cell densities were comparable in the LV subepicardial and subendocardial layers (1.5-2.0 cells per mm2). Following infarction, the mast cell density at the subepicardial site of the infarction gradually increased, reaching a maximum of 25 cells per mm2 on day 21, while a non-significant increase was observed at the subendocardial site. In the non-infarcted regions, the mast cell density increased transiently to reach a maximum of 7 cells per mm2 on day 35 in the subepicardial layer. Again, changes in mast cell density in the subendocardial layer were non-significant. In the sham group, a gradual increase to 9 cells per mm2 on day 21 and a subsequent decrease to 5 cells per mm2 on day 85 were observed in the subepicardial layers. These findings indicate a massive accumulation of mast cells in the subepicardial layers of the infarcted region and a small but significant effect of the surgical procedure on cardiac mast cell deposition, especially in the outer layers of the left ventricle.
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PMID:Transmural changes in mast cell density in rat heart after infarct induction in vivo. 856 98

The role of inflammation and mast cell activation has been implicated in atherosclerotic plaque destabilization and rupture. To investigate the role of immunoglobulin E (IgE) in acute coronary syndrome, a prospective clinical study was conducted in patients with acute myocardial infarction (AMI), unstable angina pectoris (UAP), stable angina pectoris (SAP), and healthy controls. IgE levels were serially measured and compared in consecutive patients with AMI (n = 16) and UAP (n = 14) on days 1, 3, 7, 21 after admission and 3 months later and only once in stable angina pectoris (n = 15) and healthy controls (n = 14). In addition, blood eosinophil and basophil levels on admission were measured in all groups and compared. Initial IgE levels determined at admission in patients with AMI, UAP, and SAP were significantly higher than levels in the control group (p = 0.002). Initial high IgE level in AMI on day 1 increased to a peak by day 7 (p = 0.024), then gradually decreased by day 21 and at 3 months (p = 0.052). High IgE level in UAP persisted by day 7 and gradually decreased by day 21 and 3 months (p = 0.037 and p = 0.018, respectively). Blood eosinophil count on admission was significantly higher in UAP than in the control group (p = 0.005). Basophil levels of both AMI and UAP groups on admission were found to be elevated as opposed to control group (p = 0.02 and p = 0.012, respectively). This study demonstrates that the level of IgE significantly increased during the acute phase of acute coronary syndromes and gradually decreased, supporting the role of acute inflammatory response and mast cell involvement in plaque rupture.
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PMID:Increased immunoglobulin E response in acute coronary syndromes. 1259 98

Concentrations of the circulating hepatocyte growth factor (HGF) increase in the very early phase of acute myocardial infarction, and are a marker of arterial thrombosis. A recently developed, highly sensitive HGF assay can detect the early stages of arterial thrombosis in patients with unstable angina pectoris, acute aortic dissection and pulmonary thromboembolism. Heparin rapidly induces the release of HGF into the circulation, and HGF is a major factor involved in heparin-induced angiogenesis. Furthermore, the activation of mast cells by thrombus formation releases HGF into the circulation. This new pathway, thrombus formation-mast cell activation- degranulation-heparin-HGF-angiogenesis, may be both diagnostically useful and a therapeutic target.
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PMID:Roles of hepatocyte growth factor and mast cells in thrombosis and angiogenesis. 1536 30

Two cases of allergic angina and allergic myocardial infarction (Kounis syndrome) following penicillin administration are described. The patients suffered from lung and mandible neoplasms and had previously received several courses of antineoplastic therapy without any sequelae. One patient had normal coronary arteries (type I variant of the syndrome) and the other had coronary artery disease with previous myocardial infarction (type II variant of the syndrome). The allergic reaction following penicillin administration seemed to have triggered the development of an acute coronary artery spasm in the first patient and an acute myocardial infarction in the second. This report shows that susceptible individuals expressing a magnified mast cell degranulation effect may be more vulnerable to coronary artery spasm and plaque erosion or rupture.
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PMID:Penicillin allergy in cancer patients manifesting as Kounis syndrome. 1602 65

A 60-year-old male was bitten by a venomous snake (Vipera ammodytes) and gradually developed signs of an allergic reaction including generalized itching, generalized rash, and chest discomfort. This was followed by severe retrosternal pain with electrocardiographic evidence of an inferior myocardial ischemia progressing to acute myocardial infarction. Cardiac enzymes and troponin, serum tryptase, and histamine were elevated. Coronary arteriography showed normal coronary arteries. This is a characteristic type I variant of Kounis syndrome, which is the concurrence of acute coronary syndromes with conditions associated with mast cell activation including allergic or hypersensitivity reactions as well as anaphylactic or anaphylactoid reactions. This is the first report to show that viper bites can induce allergic angina and/or allergic myocardial infarction.
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PMID:Hypersersensitivity and Kounis syndrome due to a viper bite. 1661 60

The study of inflammatory reaction and morphofunctional characteristics of mast cells in aortic intima and pulmonary artery at initial stages of atherosclerosis was performed in 62 persons who had died of accidental causes at the ages of 4-49 years and 44 males who had died of myocardial infarction at the age of 42-73 years. Histological, histochemical and immunocytochemical tests showed permanent presence of lymphocyte-monocytic cell reaction in combination with mast cell infiltration in arterial intima that progressed with age and development of atherosclerosis. Lipoidosis was associated with an increase of T lymphocytes with (CD4+) domination, monocytes/macrophages (CD11+) and mast cells in different functional activity. Marked hyperplasia and high secretory activity of mast cells (expressed in their massive degranulation) were observed in acute myocardial infarction in aortic intima and pulmonary artery.
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PMID:[Inflammatory cell reaction and mast cells in aortic intima and pulmonary artery of humans at early stages of atherosclerosis]. 1675 4

Myocardial injury and acute coronary syndrome have been rarely associated with amoxicillin/clavulanic acid intake. The responsible pathogenetic mechanism is described by an amplified mast cell degranulation inducing coronary artery spasm and/or acute myocardial infarction in susceptible individuals which is called Kounis syndrome. We report here a case of Kounis syndrome presented with acute coronary syndrome due to amoxicillin/clavulanic acid use. All other etiologies, including ischemic reinfarction were appropriately ruled out.
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PMID:Kounis syndrome secondary to amoxicillin/clavulanic acid use. 1770 99

Resident cardiac mast cells, located mainly around coronary vessels and in the right atrium close to the sinoatrial node, are the main repository of cardiac histamine. Inflammatory activation of cardiac mast cells, as occurs upon acute myocardial infarction, causes the release of histamine and prostanoids. These substances lead to severe tachyarrhythmias, cardiodepressive effects and coronary spasm, thus contributing to myocardial damage and early, lethal outcome. Relaxin, known to inhibit mast cell activation, has been recently validated as a cardiotropic hormone, being produced by the heart and acting on specific heart receptors. In this study, we report on a swine model of heart ischemia/reperfusion, currently used to test cardiotropic drugs, in which human recombinant relaxin (2.5 and 5 microg/kg b.w.), given at reperfusion upon a 30-min ischemia, markedly reduced cardiac injury as compared with the vehicle-treated animals. Evidence is provided that relaxin, at both the assayed doses, causes a clear-cut, significant reduction of plasma histamine, increase in cardiac histamine content and decrease in cardiac mast cell degranulation. This is accompanied by a reduction of oxidative cardiac tissue injury (assessed as tissue malondialdehyde) and of the occurrence of severe ventricular arrhythmias. In conclusion, this study provides further insight into the cardioprotective effects of relaxin, which also involve mast cell inhibition, and confirms the relevance of histamine in the pathophysiology of ischemia-reperfusion-induced cardiac injury and dysfunction. It also offers additional evidence for the potential therapeutic effects of relaxin in animal models of disease involving mast cell activation.
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PMID:Relaxin induces mast cell inhibition and reduces ventricular arrhythmias in a swine model of acute myocardial infarction. 1806 99

Kounis syndrome is the concurrence of acute coronary syndromes with conditions associated with mast cell activation including allergic or hypersensitivity and anaphylactic or anaphylactoid insults. We present a case of acute myocardial infarction associated with an allergic reaction in a 73-year-old Italian woman with recent implantation of stents.
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PMID:Acute myocardial infarction and Kounis syndrome. 1837 25

Stent components acting as potential antigens and promoting intracoronary mast cell activation can lead to catastrophic intrastent thrombosis. Patients with drug-eluting stent (DES) implantation are prone to hypersensitivity reactions from five potential antigens namely, nickel strut, polymer coating, eluted drug, as well as, concomitant drugs clopidogrel and aspirin. These events may be more common than suspected because it is hard to document them, unless they become systemic, in which case they manifest themselves as the Kounis syndrome characterized by the concurrence of acute coronary events with hypersensitivity reactions. This report concerns of a patient with implanted DES who developed an acute myocardial infarction in the stent area following an allergic reaction to contrast material.
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PMID:Kounis syndrome: a manifestation of drug-eluting stent thrombosis associated with allergic reaction to contrast material. 2054 82


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