» Articles » PMID: 24895609

Glucagon Effects on 3H-histamine Uptake by the Isolated Guinea-pig Heart During Anaphylaxis

Overview
Journal Biomed Res Int
Publisher Wiley
Date 2014 Jun 5
PMID 24895609
Citations 3
Authors
Affiliations
Soon will be listed here.
Abstract

We estimated the influence of acute glucagon applications on (3)H-histamine uptake by the isolated guinea-pig heart, during a single (3)H-histamine passage through the coronary circulation, before and during anaphylaxis, and the influence of glucagon on level of histamine, NO, O2 (-), and H2O2 in the venous effluent during anaphylaxis. Before anaphylaxis, glucagon pretreatment does not change (3)H-histamine Umax and the level of endogenous histamine. At the same time, in the presence of glucagon, (3)H-histamine Unet is increased and backflux is decreased when compared to the corresponding values in the absence of glucagon. During anaphylaxis, in the presence of glucagon, the values of (3)H-histamine Umax and Unet are significantly higher and backflux is significantly lower in the presence of glucagon when compared to the corresponding values in the absence of glucagon. The level of endogenous histamine during anaphylaxis in the presence of glucagon (6.9-7.38 × 10(-8) μM) is significantly lower than the histamine level in the absence of glucagon (10.35-10.45 × 10(-8) μM). Glucagon pretreatment leads to a significant increase in NO release (5.69 nmol/mL) in comparison with the period before glucagon administration (2.49 nmol/mL). Then, in the presence of glucagon, O2 (-) level fails to increase during anaphylaxis. Also, our results show no significant differences in H2O2 levels before, during, and after anaphylaxis in the presence of glucagon, but these values are significantly lower than the corresponding values in the absence of glucagon. In conclusion, our results show that glucagon increases NO release and prevents the increased release of free radicals during anaphylaxis, and decreases histamine level in the venous effluent during cardiac anaphylaxis, which may be a consequence of decreased histamine release and/or intensified histamine capturing by the heart during anaphylaxis.

Citing Articles

Oxidative Stress and Mitochondria Are Involved in Anaphylaxis and Mast Cell Degranulation: A Systematic Review.

Piotin A, Oulehri W, Charles A, Tacquard C, Collange O, Mertes P Antioxidants (Basel). 2024; 13(8).

PMID: 39199166 PMC: 11352116. DOI: 10.3390/antiox13080920.


Effects of NO/cGMP inhibitors in a rat model of anaphylactoid shock.

Albuquerque A, Ferreira L, Carvalho M, Capellini V, Evora P, Celotto A Braz J Med Biol Res. 2020; 53(3):e8853.

PMID: 32130289 PMC: 7057939. DOI: 10.1590/1414-431X20198853.


Coronary flow and oxidative stress during local anaphylactic reaction in isolated mice heart: the role of nitric oxide (NO).

Milicic V, Zivkovic V, Jeremic N, Arsenijevic N, Djuric D, Jakovljevic V Mol Cell Biochem. 2015; 412(1-2):221-7.

PMID: 26708221 DOI: 10.1007/s11010-015-2628-3.

References
1.
Kaplan Y, Hocaoglu N, Oransay K, Kalkan S, Tuncok Y . Effect of glucagon on amitriptyline-induced cardiovascular toxicity in rats. Hum Exp Toxicol. 2008; 27(4):321-5. DOI: 10.1177/0960327108092289. View

2.
Masini E, Gambassi F, Di Bello M, Mugnai L, Raspanti S, Mannaioni P . Nitric oxide modulates cardiac and mast cell anaphylaxis. Agents Actions. 1994; 41 Spec No:C89-90. DOI: 10.1007/BF02007780. View

3.
Mery P, Brechler V, Pavoine C, Pecker F, Fischmeister R . Glucagon stimulates the cardiac Ca2+ current by activation of adenylyl cyclase and inhibition of phosphodiesterase. Nature. 1990; 345(6271):158-61. DOI: 10.1038/345158a0. View

4.
Calhoun W, REED H, Moest D, Stevens C . Enhanced superoxide production by alveolar macrophages and air-space cells, airway inflammation, and alveolar macrophage density changes after segmental antigen bronchoprovocation in allergic subjects. Am Rev Respir Dis. 1992; 145(2 Pt 1):317-25. DOI: 10.1164/ajrccm/145.2_Pt_1.317. View

5.
Prinz C, Zanner R, Gerhard M, Mahr S, Neumayer N, Gratzl M . The mechanism of histamine secretion from gastric enterochromaffin-like cells. Am J Physiol. 1999; 277(5):C845-55. DOI: 10.1152/ajpcell.1999.277.5.C845. View