RESUMO
Beyond the regulation of cardiovascular function, baroreceptor afferents play polymodal roles in health and disease. Sepsis is a life-threatening condition characterized by systemic inflammation (SI) and hemodynamic dysfunction. We hypothesized that baroreceptor denervation worsens lipopolysaccharide (LPS) induced-hemodynamic collapse and SI in conscious rats. We combined: (a) hemodynamic and thermoregulatory recordings after LPS administration at a septic-like non-lethal dose (b) analysis of the cardiovascular complexity, (c) evaluation of vascular function in mesenteric resistance vessels, and (d) measurements of inflammatory cytokines (plasma and spleen). LPS-induced drop in blood pressure was higher in sino-aortic denervated (SAD) rats. LPS-induced hemodynamic collapse was associated with SAD-dependent autonomic disbalance. LPS-induced vascular dysfunction was not affected by SAD. Surprisingly, SAD blunted LPS-induced surges of plasma and spleen cytokines. These data indicate that baroreceptor afferents are key to alleviate LPS-induced hemodynamic collapse, affecting the autonomic control of cardiovascular function, without affecting resistance blood vessels. Moreover, baroreflex modulation of the LPS-induced SI and hemodynamic collapse are not dependent of each other given that baroreceptor denervation worsened hypotension and reduced SI.
Assuntos
Inflamação/metabolismo , Lipopolissacarídeos/farmacologia , Animais , Barorreflexo/imunologia , Barorreflexo/fisiologia , Pressão Sanguínea/efeitos dos fármacos , Frequência Cardíaca/efeitos dos fármacos , Hemodinâmica/imunologia , Hemodinâmica/fisiologia , Inflamação/imunologia , Masculino , Ratos , Ratos WistarRESUMO
The endocrine heart produces the polypeptide hormones Atrial Natriuretic Factor (ANF or ANP) and Brain Natriuretic Peptide (BNP). Through the peripheral actions of these hormones the heart contributes to the regulation of the cardiac preload and afterload. More recently, new functions for these hormones have been described including the modulation of the immune response. Plasma levels of BNP but not those of ANF, increase following an acute rejection episode of a cardiac allotransplant but return to levels pre-rejection with successful treatment. This observation constitutes the first observation leading to characterizing the interactions of BNP with the immune response. Several other pathologies with an inflammatory component are now known to be associated with an increase in the production of BNP. Such an increase is due to an increase in the transcriptional activity of the BNP gene induced by cytokines and related substances. In vitro investigations have shown that an increase in BNP directly modulates immunological activity. Inflammation and hemodynamic changes co-exist in several cardiovascular diseases and therefore it may be beneficial to measure circulating levels of both ANF and BNP as biomarkers of changes in intravascular volume and of changes in intravascular volume plus inflammation, respectively. Changes in plasma ANF, that are relatively larger than those of BNP, might be an indication of hemodynamic deterioration while important changes in circulating BNP could indicate a worsening of the inflammatory process.
Assuntos
Fator Natriurético Atrial/metabolismo , Inflamação/metabolismo , Miócitos Cardíacos/metabolismo , Peptídeo Natriurético Encefálico/metabolismo , Animais , Fator Natriurético Atrial/imunologia , Pesquisa Biomédica , Hemodinâmica/imunologia , Humanos , Miocardite/imunologia , Miocardite/metabolismo , Peptídeo Natriurético Encefálico/genética , Peptídeo Natriurético Encefálico/imunologia , Sepse/imunologia , Sepse/metabolismoRESUMO
The endocrine heart produces the polypeptide hormones Atrial Natriuretic Factor (ANF or ANP) and Brain Natriuretic Peptide (BNP). Through the peripheral actions of these hormones the heart contributes to the regulation of the cardiac preload and afterload. More recently, new functions for these hormones have been described including the modulation of the immune response. Plasma levels of BNP but not those of ANF, increase following an acute rejection episode of a cardiac allotransplant but return to levels pre-rejection with successful treatment. This observation constitutes the first observation leading to characterizing the interactions of BNP with the immune response. Several other pathologies with an inflammatory component are now known to be associated with an increase in the production of BNP. Such an increase is due to an increase in the transcriptional activity of the BNP gene induced by cytokines and related substances. In vitro investigations have shown that an increase in BNP directly modulates immunological activity. Inflammation and hemodynamic changes co-exist in several cardiovascular diseases and therefore it may be beneficial to measure circulating levels of both ANF and BNP as biomarkers of changes in intravascular volume and of changes in intravascular volume plus inflammation, respectively. Changes in plasma ANF, that are relatively larger than those of BNP, might be an indication of hemodynamic deterioration while important changes in circulating BNP could indicate a worsening of the inflammatory process.
Assuntos
Fator Natriurético Atrial/metabolismo , Inflamação/metabolismo , Miócitos Cardíacos/metabolismo , Peptídeo Natriurético Encefálico/metabolismo , Animais , Fator Natriurético Atrial/imunologia , Hemodinâmica/imunologia , Humanos , Miocardite/imunologia , Miocardite/metabolismo , Peptídeo Natriurético Encefálico/genética , Peptídeo Natriurético Encefálico/imunologia , Pesquisa Biomédica , Sepse/imunologia , Sepse/metabolismoRESUMO
The endocrine heart produces the polypeptide hormones Atrial Natriuretic Factor (ANF or ANP) and Brain Natriuretic Peptide (BNP). Through the peripheral actions of these hormones the heart contributes to the regulation of the cardiac preload and afterload. More recently, new functions for these hormones have been described including the modulation of the immune response. Plasma levels of BNP but not those of ANF, increase following an acute rejection episode of a cardiac allotransplant but return to levels pre-rejection with successful treatment. This observation constitutes the first observation leading to characterizing the interactions of BNP with the immune response. Several other pathologies with an inflammatory component are now known to be associated with an increase in the production of BNP. Such an increase is due to an increase in the transcriptional activity of the BNP gene induced by cytokines and related substances. In vitro investigations have shown that an increase in BNP directly modulates immunological activity. Inflammation and hemodynamic changes co-exist in several cardiovascular diseases and therefore it may be beneficial to measure circulating levels of both ANF and BNP as biomarkers of changes in intravascular volume and of changes in intravascular volume plus inflammation, respectively. Changes in plasma ANF, that are relatively larger than those of BNP, might be an indication of hemodynamic deterioration while important changes in circulating BNP could indicate a worsening of the inflammatory process.
Assuntos
Fator Natriurético Atrial/metabolismo , Inflamação/metabolismo , Miócitos Cardíacos/metabolismo , Peptídeo Natriurético Encefálico/metabolismo , Animais , Fator Natriurético Atrial/imunologia , Pesquisa Biomédica , Hemodinâmica/imunologia , Humanos , Miocardite/imunologia , Miocardite/metabolismo , Peptídeo Natriurético Encefálico/genética , Peptídeo Natriurético Encefálico/imunologia , Sepse/imunologia , Sepse/metabolismoRESUMO
A insuficiência cardíaca aguda pode ocorrer em pacientes com insuficiência cardíaca congestiva (ICC) crônica descompensada ou em pacientes sem antecedentes de ICC, precipitada por um evento como, por exemplo, o infarto agudo do miocárdio. Nos pacientes crônicos deve-se pesquisar a presença de fatores precipitantes reversíveis. O tratamento vai depender do perfil hemodinâmico, o qual pode, na maioria das vezes, ser determinado clinicamente. Em pacientes com congestão pulmonar sem hipoperfusão tecidual, a utilização de diuréticos por via intravenosa e/ou vasodilatadores geralmente é suficiente. Em pacientes com hipoperfusão sistêmica e congestão, a utilização de agentes simpatomiméticos, inodilatadores e/ou vasodilatadores está indicada. Em indivíduos com hipoperfusão sem sinais de congestão, deve-se suspeitar de hipovolemia ou de infarto de ventrículo direito e o tratamento consiste na administração do volume. Medidas não-farmacológicas incluem os dispositivos mecânicos de assistência circulatória e o suporte ventilatório com pressão positiva