Methylene Blue to Treat Protamine-induced Anaphylaxis Reactions. An Experimental Study in Pigs

Albuquerque, Agnes Afrodite Sumarelli; Margarido, Edson Alves; Menardi, Antônio Carlos; Filho, Adilson Scorzoni; Celotto, Andréa Carla; Rodrigues, Alfredo José; Vicente, Walter Villela de Andrade; Évora, Paulo Roberto Barbosa

doi:10.5935/1678-9741.20160054

Cited by 3 publications

(8 citation statements)

References 20 publications

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“…It is known that nitric oxide (NO), an endogenous vasodilator, is associated with anaphylaxis. Moreover, experimental studies have shown that the inhibition of nitric oxide synthase (NOS) by L-arginine analogues reverses the hypotension caused by anaphylactic shock (8,9).…”

Section: Introductionmentioning

confidence: 99%

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

Albuquerque

Ferreira

Carvalho

et al. 2020

Braz J Med Biol Res

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Anaphylactic shock can be defined as an acute syndrome, and it is the most severe clinical manifestation of allergic diseases. Anaphylactoid reactions are similar to anaphylactic events but differ in the pathophysiological mechanism. Nitric oxide (NO) inhibitors during anaphylaxis suggest that NO might decrease the signs and symptoms of anaphylaxis but exacerbate associated vasodilation. Therefore, blocking the effects of NO on vascular smooth muscle by inhibiting the guanylate cyclase (GC) would be a reasonable strategy. This study aimed to investigate the effects of NO/cGMP pathway inhibitors methylene blue (MB), N o-nitro-L-arginine methyl ester hydrochloride (L-NAME), and indigo carmine (IC) in shock induced by compound 48/80 (C48/80) in rats. The effect was assessed by invasive blood pressure measurement. Shock was initiated by C48/80 intravenous bolus injection 5 min before (prophylactic) or after (treatment) the administration of the inhibitors MB (3 mg/kg), L-NAME (1 mg/kg), and IC (3 mg/kg). Of the groups that received drugs as prophylaxis for shock, only the IC group did not present the final systolic blood pressure (SBP) better than the C48/80 group. Regarding shock treatment with the drugs tested, all groups had the final SBP similar to the C48/80group. Altogether, our results suggested that inhibition of GC and NO synthase in NO production pathway was not sufficient to revert hypotension or significantly improve survival.

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Section: Introductionmentioning

confidence: 99%

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

Albuquerque

Ferreira

Carvalho

et al. 2020

Braz J Med Biol Res

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“…Nine hundred ninety unique studies were found in the literature search and screened for eligibility based on title/abstract screening against the pre-set inclusion and exclusion criteria. Of the 135 studies identified as eligible for full-text screening, 17 studies were finally selected for inclusion in the review [10,14,[23][24][25][26][27][28][29][30][31][32][33][34][35][36][37]. A detailed PRISMA flow diagram regarding the screening and selection process is available in Figure 3.…”

Section: Overviewmentioning

confidence: 99%

“…First, we grouped the studies based on their status as pre-treatment or post-treatment studies. Five studies had experimental models for both [25][26][27][28]35]. We next organized the studies according to animal species.…”

Section: Characteristics Of Included Studiesmentioning

confidence: 99%

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Effect of Nitric Oxide Pathway Inhibition on the Evolution of Anaphylactic Shock in Animal Models: A Systematic Review

Alfalasi

Alzaabi

Östlundh

et al. 2022

Biology

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Nitric oxide (NO) induces vasodilation in various types of shock. The effect of pharmacological modulation of the NO pathway in anaphylactic shock (AS) remains poorly understood. Our objective was to assess, through a systematic review, whether inhibition of NO pathways (INOP) was beneficial for the prevention and/or treatment of AS. A predesigned protocol for this systematic review was published in PROSPERO (CRD42019132273). A systematic literature search was conducted till March 2022 in the electronic databases PubMed, EMBASE, Scopus, Cochrane and Web of Science. Heterogeneity of the studies did not allow meta-analysis. Nine hundred ninety unique studies were identified. Of 135 studies screened in full text, 17 were included in the review. Among six inhibitors of NO pathways identified, four blocked NO synthase activity and two blocked guanylate cyclase downstream activity. Pre-treatment was used in nine studies and post-treatment in three studies. Five studies included both pre-treatment and post-treatment models. Overall, seven pre-treatment studies from fourteen showed improvement of survival and/or arterial blood pressure. Four post-treatment studies from eight showed positive outcomes. Overall, there was no strong evidence to conclude that isolated blockade of the NO/cGMP pathway is sufficient to prevent or restore anaphylactic hypotension. Further studies are needed to analyze the effect of drug combinations in the treatment of AS.

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“…Por el contrario, en el caso de anafilaxia en que se sospeche de la protamina, el antagonismo directo (a través de interacciones químicas) con heparina, se ha demostrado que puede crear complejos con protamina y aliviar el cuadro. También en experiencia animal se ha demostrado que el azul de metileno previene y trata de manera segura las complicaciones hemodinámicas de la protamina, desde el punto de vista de la función endotelial [117].…”

Section: Otros Agentes Es Caso De Refractariedad a La Adrenalinaunclassified

Anafilaxia y anafiláctico

Bozzo¹

2021

Rev. chil. anest.

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Anaphylaxis is a life-threatening clinical condition that results from the activation of mast cells/basophils, inflammatory pathways, or both. It can be specific (allergic), or non-specific (non-allergic). Most anaphylaxis are mediated by IgE, but there are also some mediated by IgM and complement activation. Incidence is about 1:10,000 anesthesia. Recent studies show that the drugs or substances mostly implicated in producing perioperative anaphylaxis are: neuromuscular blockers (60.6%), antibiotics (18.2%), patent blue dye (5.4%) and latex (5.2%). However, all drugs and substances used during anesthesia and surgery, perhaps with the sole exception of inhalation agents and crystalloids, have been reported as potentially causes of anaphylaxis. The clinical presentation is multisystemic, producing signs and symptoms mainly on skin, respiratory, cardiovascular, gastrointestinal and central nervous systems. In its advanced phase, it may evolve to anaphylactic shock, causing tissue hypoperfusion and leading to altered cell integrity and multiple organ failure, associated with high mortality. Diagnosis is based on clinical presentation (history and clinical manifestations), biological evidence (serum tryptase levels, serum histamine levels and search for specific IgE) and allergological evidence (skin tests, provocation test, mediator release tests and tests of activation of basophils). Treatment include 3 stages: general measures, first-line or primary treatment and second-line or secondary treatment. General measures consist of: Trendelenburg position, invasive monitoring (according to the severity of the clinical presentation), 100% oxygen administration, discontinuation of drugs and/or suspected agents and asking for help. The primary treatment is epinephrine in doses proportional to the clinical manifestations, airway support, 100% oxygen and aggressive resuscitation with intravenous fluids. Secondary treatment includesadministration of bronchialodilators, corticosteroids, and antihistamines.

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Methylene Blue to Treat Protamine-induced Anaphylaxis Reactions. An Experimental Study in Pigs

Cited by 3 publications

References 20 publications

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

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

Effect of Nitric Oxide Pathway Inhibition on the Evolution of Anaphylactic Shock in Animal Models: A Systematic Review

Anafilaxia y anafiláctico

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