Experimental cardiac anaphylaxis

Feigen, George A.; Prager, Denis J.

doi:10.1016/0002-9149(69)90490-1

Cited by 65 publications

(6 citation statements)

References 60 publications

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“…Cesaris-Demel presented in 1911 the first direct evidence of the involvement of the heart itself as a primary target in anaphylaxis and showed conclusively that isolated hearts of immunized rabbits and guinea pigs reacted specifically to some antigens. 2 During anaphylaxis in guinea pigs, sinus tachycardia, ventricular fibrillation, conduction disturbance, and coronary flow changes have been documented.…”

Section: Discussionmentioning

confidence: 99%

“…2,3 Severe coronary artery spasm may be combined with an anaphylactoid reaction. Wyman et al 1 reviewed 2,801 cases of cardiac angiography and found that only 1 was complicated by anaphylactoid reaction.…”

Section: Introductionmentioning

confidence: 99%

“…Coronary spasm is a well-established feature in experimental anaphylaxis. 2,3 Severe coronary artery spasm may be combined with an anaphylactoid reaction. [3][4][5][6] Both should be considered when a patient presents with persistent shock.…”

Section: Introductionmentioning

confidence: 99%

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Severe Coronary Artery Spasm with Anaphylactoid Shock Caused by Contrast Medium

et al. 2006

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This study reports 2 cases of severe coronary artery spasm with anaphylactoid shock caused by contrast medium. The first patient had anaphylactoid shock in response to contrast medium and severe coronary spasms of both the left anterior descending coronary artery and the left circumflex coronary artery. The patient developed ventricular arrhythmia and complete atrioventricular block following the severe coronary spasm. The second patient had a totally occluded right coronary artery, owing to a spasm after anaphylactoid shock. Anaphylactoid shock should always be considered when persistent shock is noted after the coronary artery spasm has been relieved.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Severe Coronary Artery Spasm with Anaphylactoid Shock Caused by Contrast Medium

et al. 2006

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“…Male Hartley guinea pigs (300 -350 g; Charles River) were passively sensitized by i.p. administration of 0.8 mg/ml rabbit anti-OA IgG (Rockland Immuno) according to established methods whereby these antibodies sensitize mast cells for subsequent anaphylactic challenge (41,42). Twenty-four hours later, the animals were anesthetized with CO 2 and killed by exsanguination.…”

Section: Isometric Force Generationmentioning

confidence: 99%

Mast cell renin and a local renin–angiotensin system in the airway: Role in bronchoconstriction

Veerappan¹,

Reid²,

Estephan³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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We previously reported that mast cells express renin, the ratelimiting enzyme in the renin-angiotensin cascade. We have now assessed whether mast cell renin release triggers angiotensin formation in the airway. In isolated rat bronchial rings, mast cell degranulation released enzyme with angiotensin I-forming activity blocked by the selective renin inhibitor BILA2157. Local generation of angiotensin (ANG II) from mast cell renin elicited bronchial smooth muscle contraction mediated by ANG II type 1 receptors (AT 1R). In a guinea pig model of immediate type hypersensitivity, anaphylactic mast cell degranulation in bronchial rings resulted in ANG II-mediated constriction. As in rat bronchial rings, bronchoconstriction (BC) was inhibited by a renin inhibitor, an AT 1R blocker, and a mast cell stabilizer. Anaphylactic release of renin, histamine, and ␤-hexosaminidase from mast cells was confirmed in the effluent from isolated, perfused guinea pig lung. To relate the significance of this finding to humans, mast cells were isolated from macroscopically normal human lung waste tissue specimens. Sequence analysis of human lung mast cell RNA showed 100% homology between human lung mast cell renin and kidney renin between exons 1 and 10. Furthermore, the renin protein expressed in lung mast cells was enzymatically active. Our results demonstrate the existence of an airway renin-angiotensin system triggered by release of mast-cell renin. The data show that locally produced ANG II is a critical factor governing BC, opening the possibility for novel therapeutic targets in the management of airway disease.angiotensin II ͉ angiotensin II type 1 receptors ͉ asthma ͉ hypersensitivity ͉ lung T he renin-angiotensin system (RAS) has been traditionally viewed as a circulating axis, whereby renin is released into the circulation from the kidneys in response to decreased renal perfusion pressure, decreased delivery of NaCl at the macula densa, and/or increased renal sympathetic nerve activity (1). The proteolytic cleavage of angiotensinogen (aogen) by renin constitutes the rate-limiting step of the RAS cascade.In addition to this classical view, it is believed that many tissues, including the lung, may possess the capacity to generate angiotensin (ANG II) locally (2, 3). This is supported by experiments demonstrating that ANG II persists in lung of nephrectomized rats (4) and findings showing that ANG II can be elevated in the lungs in the absence of an elevated systemic RAS (5). Components of RAS have been identified in lung tissue, including aogen mRNA (6, 7), and angiotensin-converting enzyme (ACE), the pulmonary endothelium being the primary source for ACE in the body (8). ANG II receptors are also expressed in lung tissue, with the ANG II type 1 receptor (AT 1 R) subtype found on bronchial smooth muscle cells (9) and ANG II type 2 receptor (AT 2 R) observed on the bronchial epithelial cell brush border (10). An intrapulmonary source of renin protein has not yet been identified.We previously reported that mast cells synthesize, st...

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“…Male Hartley guinea pigs (300–350 g; Charles River) were passively sensitized by intraperitoneal administration of 0.8 mg/ml rabbit anti-ovalbumin IgG (Rockland Immunochemicals) [5, 7]. Twenty-four hours later, the animals were anesthetized with CO 2 and euthanized by exsanguination (Institutional Animal Care and Use Committee approved).…”

Section: Methodsmentioning

confidence: 99%

Immediate Hypersensitivity Elicits Renin Release from Cardiac Mast Cells

Kano¹,

Tyler²,

Salazar-Rodriguez³

et al. 2007

Int Arch Allergy Immunol

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Background: We recently reported that murine and cavian heart mast cells are a unique extrarenal source of renin. Ischemia/reperfusion releases this renin leading to local angiotensin formation and norepinephrine release. As mast cells are a primary target of hypersensitivity, we assessed whether anaphylactic mast cell degranulation also results in renin and norepinephrine release. Methods: Hearts isolated from presensitized guinea pigs were challenged with antigen. Results: Cardiac anaphylaxis was characterized by mast cell degranulation, evidenced by β-hexosaminidase release and associated with renin and norepinephrine release. Mast cell stabilization with cromolyn or lodoxamide markedly attenuated the release of β-hexosaminidase, renin and norepinephrine. Renin inhibition with BILA2157 did not affect mast cell degranulation, but attenuated norepinephrine release. Conclusions: Our findings disclose that immediate-type hypersensitivity elicits renin release from mast cells, activating a local renin-angiotensin system, thereby promoting norepinephrine release. As renin is stored in human heart mast cells, allergic reactions could initiate renin release, leading to local angiotensin formation and hyperadrenergic dysfunction.

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Experimental cardiac anaphylaxis

Cited by 65 publications

References 60 publications

Severe Coronary Artery Spasm with Anaphylactoid Shock Caused by Contrast Medium

Severe Coronary Artery Spasm with Anaphylactoid Shock Caused by Contrast Medium

Mast cell renin and a local renin–angiotensin system in the airway: Role in bronchoconstriction

Immediate Hypersensitivity Elicits Renin Release from Cardiac Mast Cells

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