Cardiac necrosis markers associated with low nitric oxide levels in the plasma of rabbits after treatment with vasopressin: protective effects of nitroglycerin administration

Pinelli, A; Trivulzio, Silvio; Tomasoni, Livio; Bertolini, Boris; Brenna, Sergio; Bonacina, Edgardo

doi:10.1006/phrs.2002.0967

Cited by 9 publications

(13 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Vasopressin induces coronary vasoconstriction, as suggested by the ischemic electrocardiographic signs and increased diastolic pressure observed by us and others [12–18]. The coronary and vessel constriction can be attributed to the observed lowering of vasodilatory NO levels.…”

Section: Discussionmentioning

confidence: 63%

Myocardial infarction non‐invasively induced in rabbits by administering isoproterenol and vasopressin: protective effects exerted by verapamil†

Pinelli¹,

Trivulzio²,

Tomasoni³

et al. 2004

Fundamemntal Clinical Pharma

Self Cite

View full text Add to dashboard Cite

Myocardial infarction is usually induced in small animals by means of invasive procedures: the aim of this study was to cause heart necrosis lesions by non-invasive means. We injected rabbits with isoproterenol (3 mg/kg, i.p.) and vasopressin (0.3 mg/kg/5 min, i.v.) alone and in combination, and studied their effects on myocardial histology, electrocardiographic profiles, the appearance of the plasma cardiac necrosis marker c-troponin I (c-TPN I), hemodynamic parameters (blood pressure, heart rate), the coagulative process partial throboplastine time (PTT), and plasma nitric oxide (NO) levels. In the rabbits treated with vasopressin alone, the ischemic damage was associated with a decrease in NO values, and the appearance of electrocardiographic T-wave inversion and low plasma c-TPN I levels, whereas the animals treated with isoproterenol alone had necrotic bands in the myocardium, plasma c-TPN I, and electrocardiographic modifications (ST-segment changes and T-wave inversion). Combined treatment increased myocardial alterations such as contraction band necrosis, induced the appearance of specific hypoxic lesions such as areas of coagulative necrosis and leukocyte infiltration, and led to higher plasma c-TPN I levels and altered ECG profiles. Both drugs favored a decrease in plasma NO values and further alterations in hemodynamic parameters, such as higher blood pressure and greater procoagulant activity. The myocardial necrosis and modified cardiovascular parameters were attributed to calcium activated processes and the decrease in NO levels. As this model of myocardial damage involves the use of drugs that facilitate the opening of L-calcium channels, we also investigated their effects on cardiovascular parameters and heart histology after pretreatment with the calcium antagonist verapamil; this drug protected against the appearance of histological myocardial lesions, electrocardiographic alterations and high plasma c-TPN I levels, and prevented the hemodynamic and procoagulation changes, but did not affect the decrease in plasma NO values. The protective effects were attributed to the drug's calcium antagonist activity. In conclusion, the injection of isoproterenol and vasopressin induces a myocardial infarction non-invasively and seems to be suitable for studying early myocardial ischemic lesions and the effects of drugs interfering with myocardial damage and its related phenomena.

show abstract

Section: Discussionmentioning

confidence: 63%

Myocardial infarction non‐invasively induced in rabbits by administering isoproterenol and vasopressin: protective effects exerted by verapamil†

Pinelli¹,

Trivulzio²,

Tomasoni³

et al. 2004

Fundamemntal Clinical Pharma

Self Cite

View full text Add to dashboard Cite

show abstract

“…A porcentagem de CK-MB em relação ao valor total de CK fornece um dado confiável quando se avalia uma possível lesão do miocárdio, pois valores aumentados de CK-MB acompanhados de aumento de CK podem ser resultantes de esforço físico, por exemplo. Porém, quando se observa aumento de CK-MB não acompanhado de aumento da CK total, a porcentagem dessa isoenzima fica elevada, comprovando lesão específica do músculo cardíaco (Melo et al, 2008 limite (Horton et al, 1995), com concentrações plasmáticas de até 2ng/mL (Pinelli et al, 2002 (Gava et al, 1998;Vasconcelos et al, 2008), porém sem acompanhamento de urinálise e avaliação de provas bioquímicas da função renal. Portanto, não existe paralelo entre degeneração hidrópico-vacuolar dos túbulos contorcidos distais e da função renal.…”

Section: Methodsunclassified

Perfil bioquímico sanguíneo na intoxicação experimental com extrato de Mascagnia rigida (A. Juss.) Griseb. (Malpighiaceae) em coelhos

Borboleta¹,

Labarrére²,

Ribeiro³

et al. 2011

Arq. Bras. Med. Vet. Zootec.

View full text Add to dashboard Cite

Avaliou-se o perfil bioquímico sanguíneo na intoxicação por Mascagnia rigida, uma planta tóxica que gera problema econômico para a pecuária, por causar morte súbita. Nove coelhos Nova Zelândia, machos, com massa corporal média de 3,54kg, foram distribuídos em três grupos (G) (n=3). Os animais receberam, durante oito dias consecutivos, o equivalente a 30g/kg de matéria seca da planta em dois tipos de extratos: solúvel em água (GS) e insolúvel em água (GI), e formou-se também o grupo-controle (GC). Os exames bioquímicos foram realizados previamente ao início do experimento até o nono dia. A administração dos extratos da Mascagnia rigida causou alterações eletrolíticas que podem justificar alguns sinais clínicos observados e atuar de forma significativa na causa mortis.

show abstract

“…As the reagent concentrations in the immunochromatographic test exceeded 0.5 ng/mL, it is possible to infer the occurrence of myocardial injury with low-level cTnI release. However, the use of this marker to detect experimental cardiac lesions in rabbits revealed values of cTnI much higher than that threshold (17), with plasma concentrations of up to 2 ng/mL (18). Therefore, all data obtained here demonstrated that there was no damage of cardiac muscle fibers after the administration of aqueous extracts of A. rigida.…”

Section: Nonementioning

confidence: 49%

Cardiac evaluation after experimental intoxication by Amorimia rigida (Malpighiaceae) extracts in rabbits

Borboleta¹,

Ef²,

Oliveira³

et al. 2012

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

View full text Add to dashboard Cite

Clinical and laboratory changes were evaluated in rabbits after intoxication by Amorimia rigida, a plant that causes sudden death. Nine New Zealand male rabbits, averaging 3.54 kg, were categorized into three groups (n = 3) and received, for eight consecutive days, the equivalent of 30 g/kg dry matter of A. rigida water-soluble (SG) and water-insoluble (IG) extracts via nasoesophageal route. The control group received water. There were no alterations in creatine kinase enzyme (CK), CK myocardial fraction (CKMB) or troponine I (cTnI). None of the animals had clinical or electrocardiographic (conventional and Holter) alterations. There were progressive decreases in the left ventricular ejection fraction and systolic fractional shortening. Doppler echocardiography alterations suggested a systolic dysfunction in the SG and IG groups and diastolic dysfunction in IG group. It was concluded that the soluble and insoluble extracts of A. rigida cause deficit of cardiac function.Key words: toxic plant, Amorimia rigida, cardiac muscle profile, electrocardiography, echocardiography, rabbit. Original PaPer The Journal of Venomous Animals and Toxins including Tropical Diseases ISSN 1678-9199 | 2012 | volume 18 | issue 3 | pages 295-305 INTRODUCTIONThe genus Amorimia (Malpighiaceae) contains one of the 10 most important toxic plants in South America (1), best known of which is Amorimia rigida (Mascagnia rigida), well distributed in Minas Gerais state (Brazil), mainly in the northern and northeastern regions, where it is popularly known as "salsa-rosa" or "suma-roxa". It belongs to a group that causes acute intoxication that may provoke death preceded or not by a short period of clinical signs (2).After A. rigida intake, animals may show apathy, anorexia, rigid walking, prolonged recumbence, muscle tremors and death, among other clinical signs. Significant alterations have not been found at necropsy of animals intoxicated by A. rigida. Multifocal infiltrate of lymphocytes in the myocardium associated with edema and congestion of myocytes was found in the histological exams (3).Studies are necessary to elucidate which physiopathological mechanisms are involved in A. rigida intoxication that leads to sudden death. In spite of the existence of some reports of mortality in the absence of cardiac lesions, it is suggested that the main action of this plant in the heart may be due to its phytochemical characteristics that might affect cardiac function within a period insufficient to produce alterations detectable by optical microscopy (4).To the best of our knowledge, no previous study has concurrently evaluated continuous electrocardiography (Holter), Doppler echocardiography and the cardiac muscle biochemical profile in animals after the intake of A. rigida. Thus, the present work aimed to ascertain the influence of this plant on the cardiac system using the rabbit as the experimental model. MATERIALS AND METHODS Animal AssaysNine six-month-old white New Zealand male rabbits weighing an average of 3.54 kg were used. Firstl...

show abstract

Cardiac necrosis markers associated with low nitric oxide levels in the plasma of rabbits after treatment with vasopressin: protective effects of nitroglycerin administration

Cited by 9 publications

References 53 publications

Myocardial infarction non‐invasively induced in rabbits by administering isoproterenol and vasopressin: protective effects exerted by verapamil†

Myocardial infarction non‐invasively induced in rabbits by administering isoproterenol and vasopressin: protective effects exerted by verapamil†

Perfil bioquímico sanguíneo na intoxicação experimental com extrato de Mascagnia rigida (A. Juss.) Griseb. (Malpighiaceae) em coelhos

Cardiac evaluation after experimental intoxication by Amorimia rigida (Malpighiaceae) extracts in rabbits

Contact Info

Product

Resources

About