RESUMO
Ischemia-reperfusion (IR) lung injury is a significant cause of morbidity and mortality in certain clinical scenarios that include transplantation, thromboendarterectomy and reexpansion injury of the lung. Edema of the contralateral lung after IR injury of one lung has been reported and this study was aimed to clarify the pathophysiology of this phenomenon. One-lung ischemia/hypoxia followed by reperfusion with either blood or an acellular plasma substitute was achieved in an isolated rabbit lung model by hilum clamping. After reperfusion, we studied the isolated effects of vasoconstriction and inflammation on contralateral lung injury by using papaverine or hydrocortisone as vasodilator and anti-inflammatory, respectively. We observed that IR of one lung induces edema of the contralateral lung. Absence of leukocytes and platelets in the perfusate or use of hydrocortisone completely inhibits IR injury. Moreover, papaverine suppresses edema of the contralateral, but not that of the reperfused lung. We concluded that IR of one lung produces edema in the contralateral lung that requires vasoconstriction of the latter.
Assuntos
Pulmão/irrigação sanguínea , Edema Pulmonar/etiologia , Traumatismo por Reperfusão/complicações , Traumatismo por Reperfusão/fisiopatologia , Vasoconstrição , Animais , Feminino , Técnicas In Vitro , CoelhosRESUMO
El daño pulmonar por isquemia-reperfusión (IR) es una importante causa de morbilidad y mortalidad en ciertas condiciones clínicas que incluyen trasplantes, tromboendarterectomía y daño pulmonar por reexpansión. El edema pulmonar contralateral posterior al daño por IR de un pulmón ha sido reportado y esta investigación tiene como objetivo esclarecer la fisiopatología de dicho fenómeno. En un modelo de pulmones aislados y perfundidos de conejo, fue ocluido el hilio pulmonar de forma unilateral induciendo isquemia/hipoxia de dicho órgano, seguido de reperfusiones con sangre o con un substituto plasmático acelular. Los efectos aislados de vasoconstricción e inflamación en el daño pulmonar contralateral fueron estudiados posterior a la reperfusión, usando papaverina e hidrocortisona como agente vasodilatador y antiinflamatorio, respectivamente. En esta investigación se observó que la IR de un pulmón induce edema en el pulmón contralateral. La ausencia de leucocitos y plaquetas en la perfusión y el uso de hidrocortisona inhibió por completo el daño por IR. La papaverina suprimió el edema en el pulmón contralateral mas no en el reperfundido. Se concluye que la IR de un pulmón produce edema en el pulmón contralateral, para lo cual se requiere la presencia de vasoconstricción.
Ischemia-reperfusion (IR) lung injury is a significant cause of morbidity and mortality in certain clinical scenarios that include transplantation, thromboendarterectomy and reexpansion injury of the lung. Edema of the contralateral lung after IR injury of one lung has been reported and this study was aimed to clarify the pathophysiology of this phenomenon. One-lung ischemia/hypoxia followed by reperfusion with either blood or an acellular plasma substitute was achieved in an isolated rabbit lung model by hilum clamping. After reperfusion, we studied the isolated effects of vasoconstriction and inflammation on contralateral lung injury by using papaverine or hydrocortisone as vasodilator and anti-inflammatory, respectively. We observed that IR of one lung induces edema of the contralateral lung. Absence of leukocytes and platelets in the perfusate or use of hydrocortisone completely inhibits IR injury. Moreover, papaverine suppresses edema of the contralateral, but not that of the reperfused lung. We concluded that IR of one lung produces edema in the contralateral lung that requires vasoconstriction of the latter.
Assuntos
Animais , Coelhos , Edema Pulmonar/patologia , Isquemia/complicações , Traumatismo por Reperfusão , Vasoconstrição , Animais de Laboratório , PneumopatiasRESUMO
Hypocapnia/alkalosis is a consequence of several lung and metabolic pathologies. The aim of this study was to determine whether the increase of fluid filtration rate (FFR) that occurs during Hypocapnia/alkalosis circumstances is determined by hypocapnia, alkalosis or both. 7 groups were formed (N=36) using isolated rabbit lungs. Group 1: Control (PCO2 6%, pH: 7.35-7.45); Group 2 (n=6): Hypocapnia/Alkalosis (CO2 1%, pH: 7.9); Group 3 (n=6): Hypocapnia/Normo-pH (CO2 1% pH 7.35-7.45), Group 4 (n=6) Normocapnia/Alcalosis (CO2 6%, pH: 7.9). Fenoterol, papaverine and hydrocortisone were added to Groups 5, 6 and 7 (n=4) respectively, all under Normocapnia/Alkalosis. FFR and Pulmonary Arterial Pressure (Pap) were considerably higher in group 2 than in control (FFR: 1.92g/min +/- 0.6 vs 0.0 g/min +/- 0.006). A strong influence exerted by pH was observed when Group 3 and group 4 were compared (FFR: 0.02 g/min +/- 0.009 vs 2.3 g/min +/- 0.9) and (Pap: 13.5 cmH2O +/- 1.4 vs 90 cmH2O +/- 15). A reduced effect was observed in groups 5 and 6 (papaverine and hydrocorisone) and a totally abolished effect was observed in group 7 (fenoterol) (FFR: 0.001 +/- 0.0003 mL/min and Pap: 14 +/- 0.8 cmH2O). Pulmonary edema induced by Hypocapnia/alkalosis is a consequence of alkalosis and not of hypocapnia. This effect could be due to inflammatory damage in the lung parenchyma and alkalosis-mediated vasoconstriction.
Assuntos
Alcalose/fisiopatologia , Deslocamentos de Líquidos Corporais/fisiologia , Hipocapnia/fisiopatologia , Pulmão/fisiopatologia , Edema Pulmonar/fisiopatologia , Agonistas Adrenérgicos beta/farmacologia , Alcalose/complicações , Animais , Anti-Inflamatórios/farmacologia , Pressão Sanguínea/efeitos dos fármacos , Fenoterol/farmacologia , Deslocamentos de Líquidos Corporais/efeitos dos fármacos , Hidrocortisona/farmacologia , Concentração de Íons de Hidrogênio , Hipocapnia/complicações , Pulmão/irrigação sanguínea , Pulmão/efeitos dos fármacos , Papaverina/farmacologia , Perfusão , Artéria Pulmonar , Edema Pulmonar/etiologia , Coelhos , Vasoconstrição/efeitos dos fármacos , Vasoconstrição/fisiologia , Vasodilatadores/farmacologiaRESUMO
La hipocapnia/alcalosis es una situación que se presenta como consecuencia de diversas patologías pulmonares o metabólicas. El objetivo de este estudio fue determinar si el aumento de la tasa de filtración de liquido (TFL) que ocurre bajo estas circunstancias, está determinado por la hipocapnia, la alcalosis o la suma de ambas. Se realizaron 7 grupos (n=36), utilizando pulmones aislados de conejos. Grupo 1: Control (PCO2 6 por ciento, pH: 7,35-7,45); Grupo 2 (n=6): Hipocapnia/Alcalosis (CO2 1 por ciento, pH: 7,9); Grupo 3 (n=6): Hipocapnia/Normo-pH (CO2 1 por ciento pH 7,35-7,45), Grupo 4 (n=6) Normocapnia/Alcalosis (CO2 6 por ciento, pH: 7,9). En los grupos 5, 6 y 7 (n=4), todos bajo condición de Normocapnia/Alcalosis se añadió fenoterol, papaverina, e hidrocortisona respectivamente. La TFL y la presión de arteria pulmonar (Pap) fueron considerablemente mayores en el grupo 2 que en el control (TFL:1,92g/min ± 0,6 vs 0,0g/min ± 0,006), observándose una marcada influencia del pH, al comparar el grupo 3 y el grupo 4 (TFL: 0,02g/min ± 0,009 vs 2,3g/min ± 0,9) y (Pap: 13,5 cmH2O ± 1,4 vs 90 cmH2O ± 15). Se observó una disminución del efecto en los grupos 5 y 6 (papaverina e hidrocortisona) y su abolición total con fenoterol (grupo 7) (TFL: 0,001 ± 0,0003 g/min y Pap: 14 ± 0,8 cmH2O). El edema pulmonar inducido por Hipocapnia/Alcalosis es consecuencia principalmente de la alcalosis y no de la hipocapnia. Dicho efecto podría ser debido a un daño inflamatorio a nivel del parénquima y a la vasoconstricción causada por la alcalosis.
Assuntos
Animais , Coelhos , Alcalose , Edema Pulmonar/patologia , Fenoterol , Hidrocortisona , Hipocapnia , PapaverinaRESUMO
BACKGROUND AND OBJECTIVE: Mechanical obstruction has been considered the prime determinant of haemodynamic changes after pulmonary embolism (PE); however, the function of vasoconstrictive and inflammatory mediators in the physiopathology of this disease is unclear. The aim of this investigation was to study the effect of an anti-inflammatory and a vasodilator in a setting of induced PE. METHODS: A prospective, laboratory study was undertaken using 30 New Zealand white rabbits. A model of isolated and perfused rabbit lungs was used; PE was induced using autologous blood clots. Six study groups were established (each n = 5): PE without any drug (PG); PE + papaverine (PpG); PE + hydrocortisone (HG); PE in West's Zone III (ZIIIG); PE using acellular perfusate (AG) and PE using acellular perfusate + papaverine (APpG). The pulmonary artery pressure (PAP) and fluid filtration rate (FFR) were continuously measured during the experiments. RESULTS: Increases in PAP and oedema formation were observed in the PG after embolization. The PpG and the APpG showed neither oedema nor significant PAP increases. The HG group developed less oedema and less increase in PAP compared with the PG. The ZIIIG developed oedema the fastest. The AG developed less oedema and increases in PAP compared with the PG. CONCLUSION: These findings suggest that vasoconstriction and inflammatory mediators play an important role in the physiopathology of PE, as neither PAP increases nor oedema were observed in the PpG and a reduction of oedema and PAP was seen in the HG group. The decrease in oedema and PAP in the acellular group strongly suggests a key role of circulating blood cells.
Assuntos
Anti-Inflamatórios/farmacologia , Hidrocortisona/farmacologia , Papaverina/farmacologia , Embolia Pulmonar/fisiopatologia , Vasoconstrição/fisiologia , Vasodilatadores/farmacologia , Animais , Modelos Animais de Doenças , Hemodinâmica , Técnicas In Vitro , Estudos Prospectivos , Edema Pulmonar/fisiopatologia , Coelhos , Mecânica RespiratóriaRESUMO
Es un estudio prospectivo de ensayo clínico donde se le hizo a las 148 trabajadoras sexuales que acudieron al Centro de transmisión sexual de Puerto Plata pruebas serológicas (VDRL-FTA-ABS), encontrando que 29 casos tenían sífilis actual o pasada y 12 casos tenían sífilis pasada o curada para un total de 41 positivos equivalente 27.7