RESUMO
The calcium paradox was first mentioned in 1966 by Zimmerman et al. Thereafter gained great interest from the scientific community due to the fact of the absence of calcium ions in heart muscle cells produce damage similar to ischemia-reperfusion. Although not all known mechanisms involved in cellular injury in the calcium paradox intercellular connection maintained only by nexus seems to have a key role in cellular fragmentation. The addition of small concentrations of calcium, calcium channel blockers, and hyponatraemia hypothermia are important to prevent any cellular damage during reperfusion solutions with physiological concentration of calcium.
Assuntos
Cálcio/metabolismo , Traumatismos Cardíacos/metabolismo , Miócitos Cardíacos/metabolismo , Trifosfato de Adenosina/metabolismo , Animais , Cafeína/efeitos adversos , Cálcio/administração & dosagem , Bloqueadores dos Canais de Cálcio/farmacologia , Permeabilidade da Membrana Celular , Dinitrofenóis/metabolismo , Glicocálix/metabolismo , Insuficiência Cardíaca/etiologia , Traumatismos Cardíacos/etiologia , Traumatismos Cardíacos/patologia , Humanos , Traumatismo por Reperfusão Miocárdica/metabolismo , Miocárdio/metabolismo , Ratos , Sódio/fisiologia , Fatores de TempoRESUMO
O paradoxo do cálcio foi pela primeira vez citado em 1966 por Zimmerman et al. A partir daí, ganhou grande interesse por parte da comunidade científica internacional devido ao fato da ausência do íon cálcio produzir na célula muscular cardíaca dano semelhante à lesão de isquemia-reperfusão. Apesar de não serem conhecidos todos os mecanismos envolvidos no processo da lesão celular no paradoxo do cálcio, a conexão intercelular mantida somente pelo nexus parece ter papel chave na fragmentação celular. A adição de pequenas concentrações de cálcio, bloqueadores de canal de cálcio, hiponatremia ou hipotermia são importantes para evitar que haja lesão celular no momento da reperfusão com soluções com concentração fisiológica de cálcio.
The calcium paradox was first mentioned in 1966 by Zimmerman et al. Thereafter gained great interest from the scientific community due to the fact of the absence of calcium ions in heart muscle cells produce damage similar to ischemia-reperfusion. Although not all known mechanisms involved in cellular injury in the calcium paradox intercellular connection maintained only by nexus seems to have a key role in cellular fragmentation. The addition of small concentrations of calcium, calcium channel blockers, and hyponatraemia hypothermia are important to prevent any cellular damage during reperfusion solutions with physiological concentration of calcium.
Assuntos
Animais , Humanos , Ratos , Cálcio/metabolismo , Traumatismos Cardíacos/metabolismo , Miócitos Cardíacos/metabolismo , Trifosfato de Adenosina/metabolismo , Permeabilidade da Membrana Celular , Cafeína/efeitos adversos , Bloqueadores dos Canais de Cálcio/farmacologia , Cálcio/administração & dosagem , Dinitrofenóis/metabolismo , Glicocálix/metabolismo , Insuficiência Cardíaca/etiologia , Traumatismos Cardíacos/etiologia , Traumatismos Cardíacos/patologia , Traumatismo por Reperfusão Miocárdica/metabolismo , Miocárdio/metabolismo , Sódio/fisiologia , Fatores de TempoRESUMO
The ability of allergens to induce hyperalgesia in immunoglobulin E (IgE)-sensitized rats was investigated. The left hind paws of Wistar rats were sensitized with intraplantar injections of IgE anti-dinitrophenylated bovine serum albumin monoclonal antibody, and challenged with dinitrophenylated bovine serum albumin 24 h later. Allergen challenge yielded rapid thermal hyperalgesia and oedema formation in the ipsilateral paws, both reaching a plateau from 15 min to 3 h, and both diminishing thereafter. Allergen-evoked hyperalgesia was inhibited by intraperitoneal treatment with meclizine or methysergide, histamine and 5-hydroxytryptamine receptor antagonists. There was also sensitivity to local treatment with either bradykinin B(1) or B(2) receptor antagonists, des-Arg(9)-[Leu(8)]-bradykinin or D-arginyl-[Hyp3, Thi5, D-Tic7, Oic8]-bradykinin (Hoe 140). Anaphylactic hyperalgesia was mimicked by the combined administration of histamine, 5-hydroxytryptamine and bradykinin at doses which were ineffective when injected alone. This synergistic effect was abolished by treatment with either meclizine, methysergide, Hoe 140 or des-Arg(9)-[Leu(8)]-bradykinin. Our findings show that local thermal hyperalgesia is a feature of allergen-evoked inflammation, and that a synergistic interaction among bradykinin, 5-hydroxytryptamine and histamine plays a critical role in this phenomenon.