Cardiovascular Effects of Histamine Infusion in Man

Vigorito, Carlo; Russo, Paolo; Picotti, G. B.; Chiariello, Massimo; Poto, S; Marone, Gianni

doi:10.1097/00005344-198307000-00004

Cited by 75 publications

(40 citation statements)

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“…Histamine is arrhythmogenic 10,16 and can cause coronary vasoconstriction in a significant percentage of patients with ischemic heart disease and unstable angina. 11,16 In vivo administration of peptide leukotrienes can increase coronary vascular resistance in man.…”

Section: Discussionmentioning

confidence: 99%

Stem Cell Factor in Mast Cells and Increased Mast Cell Density in Idiopathic and Ischemic Cardiomyopathy

et al. 1998

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Background-We compared cardiac mast cell (HHMC) density and the immunological and nonimmunological release of mediators from mast cells isolated from heart tissue of patients with idiopathic dilated (DCM) (nϭ24) and ischemic cardiomyopathy (ICM) (nϭ10) undergoing heart transplantation and from control subjects (nϭ10) without cardiovascular disease. Methods and Results-HHMC density in DCM (18.4Ϯ1.6 cells/mm 2 ) and ICM (18.4Ϯ1.5 cells/mm 2 ) was higher than that in control hearts (5.3Ϯ0.7 cells/mm 2 ; PϽ.01). The histamine and tryptase contents of DCM and ICM hearts were higher than those of control hearts. The histamine content of the hearts was correlated with mast cell density (r s ϭ.91; PϽ.001). Protein A/gold staining of heart tissue revealed stem cell factor (SCF), the principal growth, differentiating, and activating factor of human mast cells, in HHMC secretory granules. Histamine release from cardiac mast cells caused by immunological (anti-IgE and rhSCF) and nonimmunological stimuli (Ca 2ϩ ionophore A23187) was higher in patients with DCM and ICM compared with control subjects. Immunological activation of HHMC induced a significantly greater release of tryptase and LTC 4 in patients with DCM and ICM compared with control subjects. Conclusions-Histamine and tryptase content and mast cell density are higher in failing hearts than in control hearts. SCF, present in secretory granules of HHMC, might represent an autocrine factor sustaining mast cell hyperplasia in heart tissue in these patients. The increased local release of fibrogenic factors (eg, histamine, tryptase, and leukotriene C 4 ) might contribute to collagen accumulation in the hearts of patients with cardiomyopathy. 1 Mast cells are present in human heart tissue 2,3 and in adventia and intima of coronary arteries of patients with coronary artery disease. [4][5][6] Moreover, the in vitro immunological activation of human heart tissue with anti-IgE induces the release of histamine and prostaglandin D 2 . 7,8 The concentration of histamine and the density of mast cells are increased in the arteries of cardiac patients, 4,5,9 and coronary arteries from cardiac patients are hyperresponsive in vitro to histamine. 4 Furthermore, in vivo administration of histamine and other mast cell-derived mediators (peptide LTC 4 ) in humans causes significant cardiovascular effects. 10 -12 Finally, serum IgE levels are increased in patients with coronary artery disease. 13,14 Taken together, these observations raise the possibility that local activation of cardiac mast cells might contribute, through the release of vasoactive mediators, to certain cardiovascular diseases. 15,16 Fibrosis is a hallmark of failing hearts in DCM and ICM. 17 The cells and the mediators responsible for fibroblast proliferation and collagen accumulation in failing hearts in DCM and ICM are largely unknown. Mast cells are involved in many types of inflammation and repair processes and are found in increased numbers in fibrotic tissues. For example, increased mast cell density has be...

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Section: Discussionmentioning

confidence: 99%

Stem Cell Factor in Mast Cells and Increased Mast Cell Density in Idiopathic and Ischemic Cardiomyopathy

et al. 1998

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“…e increases in cardiac mast cell density and release of vasoactive mediators in patients with cardiomyopathy might also have clinical implications given the marked cardiovascular e ects of histamine, cysteinyl leukotrienes, and PGD 2 [31,32,51,52,53].…”

Section: Resultsmentioning

confidence: 99%

“…Pioneering studies have started to shed light on the cardiovascular e ects in humans caused by such mast cell-derived mediators as histamine [51,52,53] and leukotrienes [12]. Interestingly, these studies provided the important information that the hemodynamic e ects of mediators depend on both the underlying cardiovascular conditions and pharmacologic treatment (e. g., H 2 blockade).…”

Section: Resultsmentioning

confidence: 99%

“…Low doses of histamine (0.4 µg/kg/min) infused in patients with normal le ventricular (LV) function undergoing diagnostic catheterisation induced signi cant drops in systolic, diastolic, and mean aortic pressure, systemic vascular resistance, LV end-diastolic pressure, and stroke index [51]. Hemodynamic changes started 1-2 min a er the infusion started and reverted to normal within 5 min a er the infusion.…”

Section: Cardiovascular E Ects Of Histamine In Manmentioning

confidence: 99%

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The Human Heart As a Shock Organ in Anaphylaxis

Marone

Bova

Detoraki

et al. 2004

Novartis Foundation Symposia

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“…56 It further leads to a baroreceptor-mediated tachycardia by decreasing mean aortic pressure. 57 However, in patients with coronary artery disease and vasospastic angina, intravenous histamine causes a decrease in coronary blood flow, and in some cases severe coronary spasm. 56,58 Histamine also induces tissue factor expression in endothelial cells and vascular smooth muscle cells, thus mediating thrombus formation in acute coronary syndromes.…”

Section: Pathophysiologymentioning

confidence: 99%

Kounis syndrome: a narrative review

Fourie

2016

Southern African Journal of Anaesthesia and Analgesia

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Inflammatory mediators released from activated mast cells and basophils during hypersensitivity reactions have direct pathological effects on the myocardium and coronary vasculature. It was traditionally thought that cardiovascular signs and symptoms in anaphylaxis are largely due to peripheral vasodilation and increased vascular permeability. However, there is extensive evidence of primary cardiac involvement during hypersensitivity reactions, most notably coronary vasoconstriction as well as atherosclerotic plaque erosion and rupture, leading to angina pectoris and acute coronary syndromes. Furthermore, mast cells are well established as effector cells in atherosclerosis, through their effects on atherosclerotic plaque progression and destabilisation. It was noted over 30 years ago that cardiac patients have a markedly higher concentration of biologic amines (especially histamine) in their coronary vasculature, and, additionally, are hyper-reactive to the effects thereof. This is borne out by the disproportionate mortality rate of those with cardiac disease that suffer a hypersensitivity reaction. Kounis syndrome refers to angina pectoris or an acute coronary syndrome secondary to a hypersensitivity reaction, with the subtypes dependent on the underlying state of the coronaries and presence of a drug-eluting stent or not. This review will focus mainly on the aetiology, pathophysiology, diagnoses and treatment of this important syndrome.

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Cardiovascular Effects of Histamine Infusion in Man

Cited by 75 publications

References 0 publications

Stem Cell Factor in Mast Cells and Increased Mast Cell Density in Idiopathic and Ischemic Cardiomyopathy

Stem Cell Factor in Mast Cells and Increased Mast Cell Density in Idiopathic and Ischemic Cardiomyopathy

The Human Heart As a Shock Organ in Anaphylaxis

Kounis syndrome: a narrative review

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