PubMed · 5673209
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1968-09-14. Venous ulcers.. https://pubmed.ncbi.nlm.nih.gov/5673209/
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OBJECTIVE: To test whether assessing pulmonary permeability by transpulmonary thermodilution enables to differentiate increased permeability pulmonary edema (ALI/ARDS) from hydrostatic pulmonary edema. DESIGN: Retrospective review of cases. SETTING: A 24-bed medical intensive care unit of a university hospital. PATIENTS: Forty-eight critically ill patients ventilated for acute respiratory failure with bilateral infiltrates on chest radiograph, a PaO(2)/FiO(2) ratio < 300 mmHg and extravascular lung water indexed for body weight >/= 12 ml/kg. INTERVENTION: We assessed pulmonary permeability by two indexes obtained from transpulmonary thermodilution: extravascular lung water/pulmonary blood volume (PVPI) and the ratio of extravascular lung water index over global end-diastolic volume index. The cause of pulmonary edema was determined a posteriori by three experts, taking into account medical history, clinical features, echocardiographic left ventricular function, chest radiography findings, B-type natriuretic peptide serum concentration and the time-course of these findings with therapy. Experts were blind for pulmonary permeability indexes and for global end-diastolic volume. MEASUREMENTS AND RESULTS: ALI/ARDS was diagnosed in 36 cases. The PVPI was 4.7+/-1.8 and 2.1+/-0.5 in patients with ALI/ARDS and hydrostatic pulmonary edema, respectively (p<0.05). The extravascular lung water index/global end-diastolic volume index ratio was 3.0 x 10(-2)+/-1.2 x 10(-2) and 1.4 x 10(-2)+/-0.4 x 10(-2) in patients with ALI/ARDS and with hydrostatic pulmonary edema, respectively (p<0.05). A PVPI >/= 3 and an extravascular lung water index/global end-diastolic index ratio >/= 1.8 x 10(-2) allowed the diagnosis of ALI/ARDS with a sensitivity of 85% and specificity of 100%. CONCLUSION: These results suggest that indexes of pulmonary permeability provided by transpulmonary thermodilution may be useful for determining the mechanism of pulmonary edema in the critically ill.
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Impaired endothelial barrier function resulting in increased vascular permeability is a characteristic vascular response in preeclampsia, a hypertensive and multiple systemic disorder of human pregnancy. During the last two decades, endothelial function in preeclampsia has been intensively studied and significant progress has been made in understanding the cellular and molecular bases of the altered endothelial cell response. In this review, we address the nature and mechanisms that are proposed to underlie the disturbed endothelial barrier function in preeclampsia and discuss the potential relevance of the endothelial cell responses to the initiation and/or progression of this vascular syndrome. Insights gained from the characterization of the endothelial cell phenotype assumed by the preeclamptic microvasculature may lead to novel therapeutic strategies for the management of this syndrome.