RESUMO
This review addresses the pathophysiology of hemorrhagic shock, a condition produced by rapid and significant loss of intravascular volume, which may lead to hemodynamic instability, decreases in oxygen delivery, decreased tissue perfusion, cellular hypoxia, organ damage, and death. The initial neuroendocrine response is mainly a sympathetic activation. Haemorrhagic shock is associated altered microcirculatory permeability and visceral injury. It is also responsible for a complex inflammatory response associated with hemostasis alteration.
Assuntos
Choque Hemorrágico/fisiopatologia , Adaptação Fisiológica , Animais , Volume Sanguíneo , Células Quimiorreceptoras/fisiologia , Coagulação Intravascular Disseminada/etiologia , Coagulação Intravascular Disseminada/fisiopatologia , Hemodinâmica , Humanos , Hipotensão/etiologia , Hipotensão/fisiopatologia , Hipóxia/etiologia , Inflamação/etiologia , Inflamação/fisiopatologia , Microcirculação , Modelos Animais , Oxigênio/sangue , Pressorreceptores/fisiologia , Sistema Nervoso Simpático/fisiopatologia , Vasoconstrição/fisiologiaRESUMO
AIM: Vascular endothelial growth factor (VEGF) is a potent angiogenic and endothelial factor, which is abundantly found in the normal lung tissue. The objective of the study was to assess the VEGF levels in lung tissue and plasma in acute respiratory distress syndrome (ARDS) patients compared with controls who died from non-ARDS causes. METHODS: Plasma and tissue samples were prospectively collected from 20 patients with ARDS within 6 hours after intubation (VEGF in plasma and tissue samples) and on the day of extubation (plasma VEGF) or postmortem (lung tissue). We used an ELISA to measure the VEGF level in plasma. Lung specimens were obtained by bronchoscopic biopsy or by open biopsy during autopsy. All lung samples were stained for standard histopathological analysis and for immunohistochemical methods. Biomarker levels were compared between survivors (N=12), non-survivors (N=8) and controls (N=10). RESULTS: Compared with the levels in controls, in the early stages of ARDS, plasma VEGF levels rose and intrapulmonary levels fell, but during recovery, these levels went back to normal levels. CONCLUSION: The initial phase of ARDS is associated with a decrease in VEGF in the lung and an increase in the plasma. This down-regulation may represent a protective mechanism aimed at limiting endothelial permeability and may participate in the decrease in the capillary number that is observed during early ARDS. A persistent elevation of plasma VEGF over time predicts poor outcome.
