Rat atrial responses to Bothrops jararacussu (jararacuçu) snake venom

Rodrigues, Mariana Acedo Pitocco; Dias, Lourdes; Rennó, André L.; Sousa, Norma C.; Smaal, Adriana; Silva, Delano A. da; Hyslop, Stephen

doi:10.1016/j.tox.2014.06.010

Cited by 11 publications

(9 citation statements)

References 66 publications

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“…Snake venom PLA2s can lower blood pressure through the production of arachidonic acid, a precursor of cyclooxygenase metabolites (prostaglandins or prostacyclins). It should be noted that systemic administration of high PLA2 doses can cause disruptions in the structure of myocardial tissue [ 21 , 94 ] and its functioning, such as bradycardia and atrioventricular block [ 95 , 96 ]. Interestingly, some of the cardiotoxic effects observed in in vivo animal studies are due to disruptions in the composition of the internal medium of the organism [ 97 , 98 ].…”

Section: Snake Venoms: Composition and Propertiesmentioning

confidence: 99%

“…PLA2s derived from the venoms of different snakes can differ significantly in their cardiotoxicity; e.g., PLA2s from O. hannah and N. nigricollis cause intracellular structural changes and contracture [ 94 , 96 , 99 ], in contrast to the PLA2 from the venom of N. naja atra that lacks cardiotoxicity [ 99 ]. The inotropic effect can be multidirectional; usually, contractility decreases after short growth, accompanied by an increase in the resting tension that can be transformed into contracture [ 20 , 21 , 99 ]. Acting on blood vessels, PLA2s usually exert a vasorelaxant effect that is independent of the endothelium and is partially mediated by an increase in cGMP in smooth muscle cells [ 18 , 19 ].…”

Section: Snake Venoms: Composition and Propertiesmentioning

confidence: 99%

“…Acting on blood vessels, PLA2s usually exert a vasorelaxant effect that is independent of the endothelium and is partially mediated by an increase in cGMP in smooth muscle cells [ 18 , 19 ]. The PLA2 effects can be significantly weakened by suramin [ 100 ] and a phospholipase A2 inhibitor: p -bromophenacyl bromide [ 21 , 97 ]. As in the case of CTs, the PLA2 effects can be blocked by a high concentration of calcium ions, while calcium channel blockers are ineffective [ 19 , 96 ].…”

Section: Snake Venoms: Composition and Propertiesmentioning

confidence: 99%

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Cardiovascular Effects of Snake Toxins: Cardiotoxicity and Cardioprotection

Аверин

Utkin

2021

Acta Naturae

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Snake venoms, as complex mixtures of peptides and proteins, affect various vital systems of the organism. One of the main targets of the toxic components from snake venoms is the cardiovascular system. Venom proteins and peptides can act in different ways, exhibiting either cardiotoxic or cardioprotective effects. The principal classes of these compounds are cobra cardiotoxins, phospholipases A2, and natriuretic, as well as bradykinin-potentiating peptides. There is another group of proteins capable of enhancing angiogenesis, which include, e.g., vascular endothelial growth factors possessing hypotensive and cardioprotective activities. Venom proteins and peptides exhibiting cardiotropic and vasoactive effects are promising candidates for the design of new drugs capable of preventing or constricting the development of pathological processes in cardiovascular diseases, which are currently the leading cause of death worldwide. For example, a bradykinin-potentiating peptide from Bothrops jararaca snake venom was the first snake venom compound used to create the widely used antihypertensive drugs captopril and enalapril. In this paper, we review the current state of research on snake venom components affecting the cardiovascular system and analyse the mechanisms of physiological action of these toxins and the prospects for their medical application.

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Section: Snake Venoms: Composition and Propertiesmentioning

confidence: 99%

Section: Snake Venoms: Composition and Propertiesmentioning

confidence: 99%

Section: Snake Venoms: Composition and Propertiesmentioning

confidence: 99%

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Cardiovascular Effects of Snake Toxins: Cardiotoxicity and Cardioprotection

Аверин

Utkin

2021

Acta Naturae

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“…Male rats were euthanized with isoflurane (saturated atmosphere) and exsanguinated subsequently; the heart was removed and maintained in modified Krebs-Henseleit (KH) solution (composition in mM: NaCl 118, KCl 4.7, CaCl2 2.5, MgSO4 0.45, NaHCO3 25, KH2PO4 1.03, D-glucose 11.1 and ascorbic acid 0.14, pH 7.4), as essentially described elsewhere (Rodrigues et al, 2014). The right and left atria were dissected and mounted under a tension of 1 g in an organ bath (Panlab, Barcelona, Spain) containing 5 ml of KH solution at 8 37 °C and aerated with carbogen (95% O2-5% CO2).…”

Section: Rat Isolated Atrial Preparationsmentioning

confidence: 99%

Cardiovascular activity of Micrurus lemniscatus lemniscatus (South American coralsnake) venom

Floriano

Torres-Bonilla

Rojas-Moscoso

et al. 2020

Toxicon

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Envenomation by coralsnakes (Micrurus spp.) is characterized by blockade of peripheral neurotransmission mediated by the presence of and -neurotoxins. However, little is known about their cardiovascular activity. Micrurus lemniscatus lemniscatus is a coralsnake found in the Amazon basin and occasionally causes envenomation in humans. In this study, we examined the hemodynamic, vascular and atrial responses to M. l. lemniscatus venom.Anesthetized rats were used for hemodynamic and electrocardiogram (ECG) recordings; in vitro experiments were carried out in rat isolated thoracic aorta and atria preparations. In vivo, venom (0.1 and 0.3 mg/kg) caused immediate and persistent hypotension that was maximal within the first minute with both doses being lethal after ~40 and ~20 min, respectively. ECG, heart and respiratory rates were not altered during the transient hypotension phase induced by venom but all altered prior to death. There was no evidence of myonecrosis in cardiac muscle tissue, pulmonary hemorrhage nor thrombosis in anesthetized rats exposed to venom. In vitro, venom (10 g/ml) did not contract aortic strips nor affected the maximal responses to precontraction with phenylephrine (PE, 0.0001-30 M) in strips with and without endothelium.However, venom (10 g/ml) relaxed aortic strips with endothelium pre-contracted with PE. In aortic strips pre-contracted with PE, venom prevented acetylcholine (0.0001-30 M)-induced relaxation in strips with endothelium without affecting relaxation induced by sodium nitroprusside (0.1-100 nM) in strips without endothelium. Venom (30 g/ml) produced a transient increase of atrial contractile force without affecting atrial rate. Taken together these findings indicate a predominantly vascular action of the venom, most likely involving toxins interacting with muscarinic receptors.

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“…A ação das svPLA 2 sobre os tecidos do organismo gera distúrbios fisiopatológicos após o envenenamento ofídico, como efeitos miotóxicos, cardiotóxicos, neurotóxicos e alterações inflamatórias e hemostáticas (MAMEDE et al 2016;BERNARDES et al, 2015;MOREIRA et al, 2014;RODRIGUES et al 2014;TONELLO et al, 2012;RIGONI et al, 2008;MONTECUCCO et al, 2008;.…”

Section: Fosfolipases a 2 Da Peçonha De Serpentesunclassified

Rastreamento em células in vitro de uma fosfolipase A2 da peçonha de Bothrops alternatus por meio de pontos quânticos de tamanhos mágicos

Dias¹

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Rat atrial responses to Bothrops jararacussu (jararacuçu) snake venom

Cited by 11 publications

References 66 publications

Cardiovascular Effects of Snake Toxins: Cardiotoxicity and Cardioprotection

Cardiovascular Effects of Snake Toxins: Cardiotoxicity and Cardioprotection

Cardiovascular activity of Micrurus lemniscatus lemniscatus (South American coralsnake) venom

Rastreamento em células in vitro de uma fosfolipase A2 da peçonha de Bothrops alternatus por meio de pontos quânticos de tamanhos mágicos

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