Eduardo Gaio

Stability of the animal model of oleic acid-induced acute lung injury.

OBJECTIVE To evaluate the stability of hemodynamic, respiratory and gas exchange variables in an animal model of oleic acid-induced acute lung injury. METHODS This was an experimental study involving 10 mongrel dogs. The variables were measured at baseline, as well as at 30, 60, 90 and 120 min after the administration of oleic acid. In order to analyze repeated measurements, linear and quadratic effects were tested. Mixed linear models with diversified variance and covariance structures were used, depending on the variable studied. RESULTS We found that mean arterial blood pressure stabilized at 30 min, as did heart rate, pulmonary arterial pressure and pulmonary capillary pressure at 60 min. Respiratory rate, tidal volume, minute volume and respiratory work stabilized at 30 min. Regarding gas exchange variables, PaO2, PaO2/FiO2 ratio and pulmonary shunt fraction stabilized at 30 min. The remaining variables maintained a continuous rise or fall. CONCLUSIONS This oleic acid-induced acute lung injury model is stable for some of the variables tested, although stabilization occurs at different times. The respiratory and gas exchange variables stabilized at 30 min, whereas the hemodynamic variables stabilized at 60 min.

Respiratory mechanics and lung tissue remodeling in a hepatopulmonary syndrome rat model.

Intrapulmonary vasodilation is a hallmark of the hepatopulmonary syndrome (HPS). However, its effects on respiratory mechanical properties and lung morphology are unknown. To determine these effects, 28 rats were randomly divided to control and experimental HPS groups (eHPS). The spontaneous breathing pattern, gas exchange, respiratory system mechanical properties, and lung and liver morphology of the rats were evaluated. Tidal volume, minute ventilation and mean inspiratory flow were significantly reduced in the eHPS group. Chest wall pressure dissipation against the resistive and viscoelastic components and elastic elastance were increased in the eHPS group. The lung resistive pressure dissipation was lower but the viscoelastic pressure was higher in the eHPS group. The airway volume proportion of collagen and elastic fibers was increased in the eHPS animals (16% and 51.7%; P<0.05 and P<0.001, respectively). The proportion of collagen volume in the vasculature increased 29% in the eHPS animals (P<0.01). HPS presents with respiratory system mechanical disarray as well as airway and vascular remodeling.

Pulmonary arterial hypertension and sepsis: prothrombotic profile and inflammation can changes pulmonary mechanics?

Pulmonary arterial hypertension (PAH) is associated to cellular and structural alterations of lung vasculature. Endothelial dysfunction promotes vasoconstriction, smooth muscle hypertrophy, intimal proliferation, angioproliferative plexiform lesions, and in situ thrombosis increasing pulmonary vascular resistance and arterial stiffness. Indeed, an inflammatory component has been defined in PAH on the last years. Sepsis is a systemic complex syndrome, of infectious origin. The presence of inflammation is well established in this condition and it is also considered a risk factor for acute lung injury. Thrombotic events play important role in sepsis pathophysiology. The association between PAH and sepsis potentiate the metabolic oxygen consumption/offer imbalance, with very high mortality risk. Furthermore, it is possible that the association of these two conditions should intensify thrombotic events on pulmonary microcirculation, reducing area of pulmonary vascular bed available for blood flow. For the other side, an inflammation synergism observed on these two conditions should increase the respiratory system impedance.

Neoadjuvant chemotherapy and salvage surgery for an aldosterone-producing adrenal carcinoma with inferior vena cava thrombus: Case report and literature review

Inferior vena cava (IVC) thrombus is a rare presentation of adrenal carcinoma. Hyperladosteronism is rarely associated with it. We report a case of an aldosterone-producing left adrenal carcinoma with IVC thrombus and invasion of multiple organs, treated with neoadjuvant chemotherapy and salvage surgery. The patient is alive and asymptomatic after 46 months. Surgical aspects and therapeutic options are discussed and compared with the current medical literature. This is believed to be the first report of multiple organ resection combined with IVC thrombus removal for a functioning adrenal carcinoma.

Hemodynamic effects of experimental acute right ventricular overload

FUNDAMENTO: A sobrecarga ventricular direita aguda esta associada a situacoes clinicas de elevada morbimortalidade, tais como: resseccoes pulmonares extensas, tromboembolismo pulmonar, transplante pulmonar e edema pulmonar das altitudes. Alguns pontos de sua fisiopatologia permanecem obscuros. OBJETIVO: Avaliar os efeitos hemodinâmicos da sobrecarga ventricular direita aguda experimental em suinos. METODOS: A sobrecarga ventricular direita foi induzida pela oclusao das arterias pulmonares atraves de ligaduras. Vinte porcos foram utilizados no estudo, sendo alocados em 04 grupos: um controle, nao submetido a oclusao vascular pulmonar, e tres de sobrecarga ventricular direita submetidos a oclusao das seguintes arterias pulmonares: SVD1 (arteria pulmonar esquerda); SVD2 (arteria pulmonar esquerda e do lobo inferior direito) e SVD3 (arteria pulmonar esquerda, do lobo inferior direito e do lobo mediastinal), obstruindo a vasculatura pulmonar em 42, 76 e 82,0% respectivamente. Variaveis de hemodinâmica foram medidas a cada 15 minutos durante a uma hora do estudo. Na analise estatistica, foram utilizados ajustes de modelos lineares mistos com estrutura de variâncias e covariâncias. RESULTADOS: Nas comparacoes intergrupais, houve aumento significativo da frequencia cardiaca (p = 0,004), pressao arterial pulmonar media (p = 0,001) e pressao capilar pulmonar (p < 0,0001). Houve reducao significativa da pressao arterial media (p = 0,01) e do indice sistolico (p = 0,002). Nao houve diferenca significativa no indice cardiaco (p = 0,94). CONCLUSAO: Apesar da intensa sobrecarga ventricular direita promovida pela obstrucao de 82,0% da vasculatura pulmonar e pelo aumento significativo da pressao arterial pulmonar nao houve disfuncao cardiovascular severa e/ou choque circulatorio no periodo estudado.BACKGROUND Acute right ventricular overload is associated with high morbidity and mortality clinical situations such as: extensive lung resection, pulmonary thromboembolism, lung transplantation and high altitude pulmonary edema. Some points of its pathophysiology remain unclear. OBJECTIVE To assess the hemodynamic effects of experimental acute right ventricular overload in pigs. METHODS Right ventricular overload was induced through the occlusion of the pulmonary arteries using ligationss. Twenty pigs were used in the study, divided into 04 groups: one control group not subject to pulmonary vascular occlusion, and three right ventricular overload groups subject to occlusion of the following pulmonary arteries: SVD1 (left pulmonary artery); SVD2 (left pulmonary artery and right lower lobe) and SVD3 (left pulmonary artery, right lower lobe and mediastinal lobe), obstructing the pulmonary vasculature in 42, 76 and 82.0% respectively. Hemodynamic variables were measured every 15 minutes during one hour of study. The statistical analysis employed mixed linear models with variance and covariance structures. RESULTS Group comparisons revealed significant increases in heart rate (p = 0.004), mean pulmonary artery pressure (p = 0.001) and pulmonary capillary wedge pressure (p < 0.0001). There was no significant difference in cardiac index (p = 0.94). CONCLUSION Despite the severe right ventricular overload promoted by 82.0% obstruction of the pulmonary vasculature and the significant increase in pulmonary arterial pressure, there was no severe cardiovascular dysfunction and/or circulatory shock during the study period.

Levofloxacin decreased chest wall mechanical inhomogeneities and airway and vascular remodeling in rats with induced hepatopulmonary syndrome

The administration of antibiotics decreases bacterial translocation, reduces the activity of nitric oxide synthase and improves the gas exchange of hepatopulmonary syndrome (HPS) in rats. We hypothesized that levofloxacin could reduce HPS-induced respiratory mechanical inhomogeneities and airway and pulmonary vascular remodeling. We assessed the respiratory mechanical properties and lung tissue structure in 24 rats assigned to the control, HPS (eHPS) and HPS+levofloxacin (eHPS+L) groups. The administration of levofloxacin reduced the HPS-induced chest wall but not the lung mechanical inhomogeneities. The eHPS airway proportion of elastic fibers increased 20% but was similar between the control and eHPS+L groups. The eHPS vascular collagen increased 25% in eHPS but was similar between the control and eHPS+L groups. Compared to the control group, the vascular proportion of elastic fibers of the eHPS and eHPS+L groups increased by 60% and 16%, respectively. The administration of levofloxacin decreased the HPS-induced chest wall mechanical inhomogeneities and airway and vascular remodeling.

Efeitos hemodinâmicos da sobrecarga ventricular direita aguda experimental

FUNDAMENTO: A sobrecarga ventricular direita aguda esta associada a situacoes clinicas de elevada morbimortalidade, tais como: resseccoes pulmonares extensas, tromboembolismo pulmonar, transplante pulmonar e edema pulmonar das altitudes. Alguns pontos de sua fisiopatologia permanecem obscuros. OBJETIVO: Avaliar os efeitos hemodinâmicos da sobrecarga ventricular direita aguda experimental em suinos. METODOS: A sobrecarga ventricular direita foi induzida pela oclusao das arterias pulmonares atraves de ligaduras. Vinte porcos foram utilizados no estudo, sendo alocados em 04 grupos: um controle, nao submetido a oclusao vascular pulmonar, e tres de sobrecarga ventricular direita submetidos a oclusao das seguintes arterias pulmonares: SVD1 (arteria pulmonar esquerda); SVD2 (arteria pulmonar esquerda e do lobo inferior direito) e SVD3 (arteria pulmonar esquerda, do lobo inferior direito e do lobo mediastinal), obstruindo a vasculatura pulmonar em 42, 76 e 82,0% respectivamente. Variaveis de hemodinâmica foram medidas a cada 15 minutos durante a uma hora do estudo. Na analise estatistica, foram utilizados ajustes de modelos lineares mistos com estrutura de variâncias e covariâncias. RESULTADOS: Nas comparacoes intergrupais, houve aumento significativo da frequencia cardiaca (p = 0,004), pressao arterial pulmonar media (p = 0,001) e pressao capilar pulmonar (p < 0,0001). Houve reducao significativa da pressao arterial media (p = 0,01) e do indice sistolico (p = 0,002). Nao houve diferenca significativa no indice cardiaco (p = 0,94). CONCLUSAO: Apesar da intensa sobrecarga ventricular direita promovida pela obstrucao de 82,0% da vasculatura pulmonar e pelo aumento significativo da pressao arterial pulmonar nao houve disfuncao cardiovascular severa e/ou choque circulatorio no periodo estudado.BACKGROUND Acute right ventricular overload is associated with high morbidity and mortality clinical situations such as: extensive lung resection, pulmonary thromboembolism, lung transplantation and high altitude pulmonary edema. Some points of its pathophysiology remain unclear. OBJECTIVE To assess the hemodynamic effects of experimental acute right ventricular overload in pigs. METHODS Right ventricular overload was induced through the occlusion of the pulmonary arteries using ligationss. Twenty pigs were used in the study, divided into 04 groups: one control group not subject to pulmonary vascular occlusion, and three right ventricular overload groups subject to occlusion of the following pulmonary arteries: SVD1 (left pulmonary artery); SVD2 (left pulmonary artery and right lower lobe) and SVD3 (left pulmonary artery, right lower lobe and mediastinal lobe), obstructing the pulmonary vasculature in 42, 76 and 82.0% respectively. Hemodynamic variables were measured every 15 minutes during one hour of study. The statistical analysis employed mixed linear models with variance and covariance structures. RESULTS Group comparisons revealed significant increases in heart rate (p = 0.004), mean pulmonary artery pressure (p = 0.001) and pulmonary capillary wedge pressure (p < 0.0001). There was no significant difference in cardiac index (p = 0.94). CONCLUSION Despite the severe right ventricular overload promoted by 82.0% obstruction of the pulmonary vasculature and the significant increase in pulmonary arterial pressure, there was no severe cardiovascular dysfunction and/or circulatory shock during the study period.

Efectos hemodinámicos de la sobrecarga ventricular derecha aguda experimental

FUNDAMENTO: A sobrecarga ventricular direita aguda esta associada a situacoes clinicas de elevada morbimortalidade, tais como: resseccoes pulmonares extensas, tromboembolismo pulmonar, transplante pulmonar e edema pulmonar das altitudes. Alguns pontos de sua fisiopatologia permanecem obscuros. OBJETIVO: Avaliar os efeitos hemodinâmicos da sobrecarga ventricular direita aguda experimental em suinos. METODOS: A sobrecarga ventricular direita foi induzida pela oclusao das arterias pulmonares atraves de ligaduras. Vinte porcos foram utilizados no estudo, sendo alocados em 04 grupos: um controle, nao submetido a oclusao vascular pulmonar, e tres de sobrecarga ventricular direita submetidos a oclusao das seguintes arterias pulmonares: SVD1 (arteria pulmonar esquerda); SVD2 (arteria pulmonar esquerda e do lobo inferior direito) e SVD3 (arteria pulmonar esquerda, do lobo inferior direito e do lobo mediastinal), obstruindo a vasculatura pulmonar em 42, 76 e 82,0% respectivamente. Variaveis de hemodinâmica foram medidas a cada 15 minutos durante a uma hora do estudo. Na analise estatistica, foram utilizados ajustes de modelos lineares mistos com estrutura de variâncias e covariâncias. RESULTADOS: Nas comparacoes intergrupais, houve aumento significativo da frequencia cardiaca (p = 0,004), pressao arterial pulmonar media (p = 0,001) e pressao capilar pulmonar (p < 0,0001). Houve reducao significativa da pressao arterial media (p = 0,01) e do indice sistolico (p = 0,002). Nao houve diferenca significativa no indice cardiaco (p = 0,94). CONCLUSAO: Apesar da intensa sobrecarga ventricular direita promovida pela obstrucao de 82,0% da vasculatura pulmonar e pelo aumento significativo da pressao arterial pulmonar nao houve disfuncao cardiovascular severa e/ou choque circulatorio no periodo estudado.BACKGROUND Acute right ventricular overload is associated with high morbidity and mortality clinical situations such as: extensive lung resection, pulmonary thromboembolism, lung transplantation and high altitude pulmonary edema. Some points of its pathophysiology remain unclear. OBJECTIVE To assess the hemodynamic effects of experimental acute right ventricular overload in pigs. METHODS Right ventricular overload was induced through the occlusion of the pulmonary arteries using ligationss. Twenty pigs were used in the study, divided into 04 groups: one control group not subject to pulmonary vascular occlusion, and three right ventricular overload groups subject to occlusion of the following pulmonary arteries: SVD1 (left pulmonary artery); SVD2 (left pulmonary artery and right lower lobe) and SVD3 (left pulmonary artery, right lower lobe and mediastinal lobe), obstructing the pulmonary vasculature in 42, 76 and 82.0% respectively. Hemodynamic variables were measured every 15 minutes during one hour of study. The statistical analysis employed mixed linear models with variance and covariance structures. RESULTS Group comparisons revealed significant increases in heart rate (p = 0.004), mean pulmonary artery pressure (p = 0.001) and pulmonary capillary wedge pressure (p < 0.0001). There was no significant difference in cardiac index (p = 0.94). CONCLUSION Despite the severe right ventricular overload promoted by 82.0% obstruction of the pulmonary vasculature and the significant increase in pulmonary arterial pressure, there was no severe cardiovascular dysfunction and/or circulatory shock during the study period.