Pulmonary mechanic and lung histology induced by Crotalus durissus cascavella snake venom

Neto, Joselito de Oliveira; Silveira, João Alison de Moraes; Serra, Daniel Silveira; Viana, Daniel de Araújo; Borges-Nojosa, Diva Maria; Sampaio, Célia Maria Souza; Monteiro, Helena Serra Azul; Cavalcante, Francisco Sales Ávila; Evangelista, Janaína Serra Azul Monteiro

doi:10.1016/j.toxicon.2017.07.023

Cited by 8 publications

(10 citation statements)

References 24 publications

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“…These results agree with previous findings on lung morphological changes after C.d.t. and C. durissus cascavella whole venom administration, especially the presence of perivascular edema, diffuse hemorrhage, and leukocyte infiltration up to 24 h after venom administration [42,43].…”

Section: Discussionmentioning

confidence: 99%

Crotoxin-Induced Mice Lung Impairment: Role of Nicotinic Acetylcholine Receptors and COX-Derived Prostanoids

et al. 2020

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Respiratory compromise in Crotalus durissus terrificus (C.d.t.) snakebite is an important pathological condition. Considering that crotoxin (CTX), a phospholipase A2 from C.d.t. venom, is the main component of the venom, the present work investigated the toxin effects on respiratory failure. Lung mechanics, morphology and soluble markers were evaluated from Swiss male mice, and mechanism determined using drugs/inhibitors of eicosanoids biosynthesis pathway and autonomic nervous system. Acute respiratory failure was observed, with an early phase (within 2 h) characterized by enhanced presence of eicosanoids, including prostaglandin E2, that accounted for the increased vascular permeability in the lung. The alterations of early phase were inhibited by indomethacin. The late phase (peaked 12 h) was marked by neutrophil infiltration, presence of pro-inflammatory cytokines/chemokines, and morphological alterations characterized by alveolar septal thickening and bronchoconstriction. In addition, lung mechanical function was impaired, with decreased lung compliance and inspiratory capacity. Hexamethonium, a nicotinic acetylcholine receptor antagonist, hampered late phase damages indicating that CTX-induced lung impairment could be associated with cholinergic transmission. The findings reported herein highlight the impact of CTX on respiratory compromise, and introduce the use of nicotinic blockers and prostanoids biosynthesis inhibitors as possible symptomatic therapy to Crotalus durissus terrificus snakebite.

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Section: Discussionmentioning

confidence: 99%

Crotoxin-Induced Mice Lung Impairment: Role of Nicotinic Acetylcholine Receptors and COX-Derived Prostanoids

et al. 2020

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“…Although diffuse bilateral pulmonary infiltration is more common, asymmetrical, or unilateral pulmonary injuries have also been reported [160,161]. Lung damage occurs nearly immediately at the cellular level [19], but clinical signs may be immediate (within minutes to hours) or delayed (days) depending on the mechanisms. Although anaphylaxis occurs acutely (a few minutes), significant sequelae such as pulmonary edema and, less frequently, bleeding, can take longer (a few hours) [131][132][133][134].…”

Section: Overall Clinical Presentation and Therapymentioning

confidence: 99%

“…These causes of pulmonary injuries are mentioned elsewhere. Several toxins directly damage the lungs by increasing airway resistance, which leads to atelectasis or emphysema [ 19 ]. On a microscopic level, many toxins cause pulmonary edema (transudate or exudates), hemorrhage, or embolism through numerous cellular mechanisms, most of which are followed by lung inflammation whose pathophysiologic derangements resemble those of acute lung injury or acute respiratory distress syndrome (ARDS) [ 20 , 21 ].…”

Section: Backgroundsmentioning

confidence: 99%

“…In vivo studies administering PLA 2 from the Javan spitting cobra ( Naja sputatrix ) intravenously and intratracheally in rats resulted in marked pulmonary inflammation and edema, supported by an increase in inflammatory markers and decreased protein expression of Na + /K + ATPase and AQP [ 31 ]. Crotamine and crotoxin's high PLA 2 activity also suggested evident pulmonary inflammation, edema, hemorrhage, and atelectasis in mice injected with the whole venom of the South American rattlesnake ( Crotalus durissus ) intraperitoneally and intramuscularly [ 19 , 32 ].…”

Section: Impaired Normal Cell Functions and Integritymentioning

confidence: 99%

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Pulmonary involvement from animal toxins: the cellular mechanisms

Thumtecho,

Suteparuk,

Sitprija

2023

J. Venom. Anim. Toxins incl. Trop. Dis

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Venomous animals and their venom have always been of human interest because, despite species differences, coevolution has made them capable of targeting key physiological components of our bodies. Respiratory failure from lung injury is one of the serious consequences of envenomation, and the underlying mechanisms are rarely discussed. This review aims to demonstrate how toxins affect the pulmonary system through various biological pathways. Herein, we propose the common underlying cellular mechanisms of toxin-induced lung injury: interference with normal cell function and integrity, disruption of normal vascular function, and provocation of excessive inflammation. Viperid snakebites are the leading cause of envenomation-induced lung injury, followed by other terrestrial venomous animals such as scorpions, spiders, and centipedes. Marine species, particularly jellyfish, can also inflict such injury. Common pulmonary manifestations include pulmonary edema, pulmonary hemorrhage, and exudative infiltration. Severe envenomation can result in acute respiratory distress syndrome. Pulmonary involvement suggests severe envenomation, thus recognizing these mechanisms and manifestations can aid physicians in providing appropriate treatment.

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“…During a study conducted by Jorge et al [34], 3 patients developed respiratory failure (of 249 cases analyzed). Oliveira Neto et al [56] analyzed the pulmonary function in an experimental model of acute lung injury (in mice) induced by the C. durissus cascavella venom and the venom caused mechanical and histopathological changes in the lung tissue.…”

Section: Clinical and Laboratory Aspectsmentioning

confidence: 99%

Clinical, Laboratory, and Therapeutic Aspects of Crotalus durissus (South American Rattlesnake) Victims: A Literature Review

Frare

Resende

Dornelas

et al. 2019

BioMed Research International

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Snakebite envenoming is a neglected public health issue in many tropical and subtropical countries. To diagnosis and treat snakebites may be challenging to health care personnel since sufficient information has not been yet provided. This review presents the clinical, therapeutic, and laboratory aspects of Crotalus durissus (South American rattlesnakes) victims. The clinical setting may show local effects such as little or no pain, mild edema, and recurrent erythema. In contrast, the systemic effects may be quite remarkable, such as changes due to neurological damage, intense rhabdomyolysis, incoagulability of the blood, and variations in the peripheral blood elements. The main complication is acute kidney injury. The appropriate treatment depends mainly on the correct recognition of the aggressor snake and the symptoms expressed by the victim. Rattlesnake venom can cause irreparable damage and lead to death. Therefore, a prompt diagnosis allows the immediate onset of proper serotherapy.

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Pulmonary mechanic and lung histology induced by Crotalus durissus cascavella snake venom

Cited by 8 publications

References 24 publications

Crotoxin-Induced Mice Lung Impairment: Role of Nicotinic Acetylcholine Receptors and COX-Derived Prostanoids

Crotoxin-Induced Mice Lung Impairment: Role of Nicotinic Acetylcholine Receptors and COX-Derived Prostanoids

Pulmonary involvement from animal toxins: the cellular mechanisms

Clinical, Laboratory, and Therapeutic Aspects of Crotalus durissus (South American Rattlesnake) Victims: A Literature Review

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