Treatment with a platelet-activating factor receptor antagonist improves hemodynamics and reduces epinephrine requirements, in a lethal rodent model of anaphylactic shock.
anaphylaxis
epinephrine
ovalbumin
platelet-activating factor
shock
Journal
Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
ISSN: 1365-2222
Titre abrégé: Clin Exp Allergy
Pays: England
ID NLM: 8906443
Informations de publication
Date de publication:
03 2020
03 2020
Historique:
received:
02
08
2019
revised:
28
10
2019
accepted:
10
11
2019
pubmed:
23
11
2019
medline:
10
6
2021
entrez:
23
11
2019
Statut:
ppublish
Résumé
In some cases, anaphylactic shock (AS) is still lethal, despite rapid use of epinephrine. High doses of epinephrine are associated with severe complications. Platelet-activating factor (PAF) is secreted in massive amounts during AS, and a high plasma level is correlated with increased AS severity. To assess the effect of ABT-491, a PAF-receptor antagonist and possible adjunct treatment, alone or in combination with epinephrine during AS. AS was induced by intravenous injection of 1 mg ovalbumin into ovalbumin-sensitized rats. Rats were then randomly assigned to 5 groups (n = 10 per group): SHAM (vehicle only), SHOCK (no treatment), ABT (ABT-491 1 mg/kg), EPI (epinephrine 5 µg as a bolus then 10 µg kg Ovalbumin injection resulted in a severe decrease in mean arterial pressure, left ventricular inotropy (max dP/dt) and left ventricular shortening fraction (LVSF). All rats from the ABT group survived until the end of the experiment. ABT-491 prevented the LVSF decrease observed in the SHOCK group (at T15: ABT 50% ± 11% vs SHOCK 36% ± 9%, P = .01), significantly reduced the dose of epinephrine needed to treat anaphylactic shock (EPI-ABT 314 ± 67 µg/kg vs EPI 475 ± 69 µg/kg, P < .001) and reduced the time to restore basal MAP (ABT 23 ± 7 minutes vs EPI-ABT 13 ± 5 minutes, P < .01). AS was characterized by early cardiac dysfunction in our model. Treatment with ABT-491 allowed survival until the end of the experiment and reduced cardiac dysfunction. Use of the PAF-R antagonist had a synergistic effect with epinephrine and allowed a significant reduction in epinephrine consumption. Use of PAF-R antagonists during AS could reduce epinephrine-related complications and improve the treatment of epinephrine refractory cases.
Sections du résumé
BACKGROUND
In some cases, anaphylactic shock (AS) is still lethal, despite rapid use of epinephrine. High doses of epinephrine are associated with severe complications. Platelet-activating factor (PAF) is secreted in massive amounts during AS, and a high plasma level is correlated with increased AS severity.
OBJECTIVE
To assess the effect of ABT-491, a PAF-receptor antagonist and possible adjunct treatment, alone or in combination with epinephrine during AS.
METHODS
AS was induced by intravenous injection of 1 mg ovalbumin into ovalbumin-sensitized rats. Rats were then randomly assigned to 5 groups (n = 10 per group): SHAM (vehicle only), SHOCK (no treatment), ABT (ABT-491 1 mg/kg), EPI (epinephrine 5 µg as a bolus then 10 µg kg
RESULTS
Ovalbumin injection resulted in a severe decrease in mean arterial pressure, left ventricular inotropy (max dP/dt) and left ventricular shortening fraction (LVSF). All rats from the ABT group survived until the end of the experiment. ABT-491 prevented the LVSF decrease observed in the SHOCK group (at T15: ABT 50% ± 11% vs SHOCK 36% ± 9%, P = .01), significantly reduced the dose of epinephrine needed to treat anaphylactic shock (EPI-ABT 314 ± 67 µg/kg vs EPI 475 ± 69 µg/kg, P < .001) and reduced the time to restore basal MAP (ABT 23 ± 7 minutes vs EPI-ABT 13 ± 5 minutes, P < .01).
CONCLUSIONS AND CLINICAL RELEVANCE
AS was characterized by early cardiac dysfunction in our model. Treatment with ABT-491 allowed survival until the end of the experiment and reduced cardiac dysfunction. Use of the PAF-R antagonist had a synergistic effect with epinephrine and allowed a significant reduction in epinephrine consumption. Use of PAF-R antagonists during AS could reduce epinephrine-related complications and improve the treatment of epinephrine refractory cases.
Substances chimiques
Imidazoles
0
Indoles
0
Platelet Membrane Glycoproteins
0
Receptors, G-Protein-Coupled
0
platelet activating factor receptor
0
ABT 491
N7IG7Z867J
Epinephrine
YKH834O4BH
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
383-390Informations de copyright
© 2019 John Wiley & Sons Ltd.
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