title: Evolving changes in lung interstitial fluid content after acute myocardial infarction: mechanisms and pathophysiological correlates.
abstract: In acute myocardial infarction (AMI), alveolar interstitium edema is generally attributed to a hydrostatic imbalance. However, inflammatory burden and/or neural/hormonal/hemodynamic stimulation might injure the microvascular endothelium, eliciting interstitial overflow and altering alveolar-capillary gas diffusion. In 118 patients with AMI (ejection fraction >or=50% and wedge pulmonary pressure <16 mmHg), admission alveolar-capillary gas diffusing membrane conductance (DM) averaged 35.1 ml.min(-1).mmHg(-1) and was 27% lower than in 25 controls (P < 0.01). Infusion of saline in the pulmonary circulation (to test sodium exchange across the pulmonary capillary wall) lowered DM by 7.1% (P < 0.01) and was neutral in controls. At 1 wk, 83 patients that showed DM improvement >5% were assigned to group 1, and 28 patients with DM worsening >5% were assigned to group 2. Saline retained efficacy in group 2 and had no DM effect in group 1 (supporting a link between changes in baseline DM and those in microvascular salt exchange). Ventricular function was unchanged in group 1, whereas group 2 had developed diastolic dysfunction. At 1 yr, 3% of cases in group 1 and 37% of cases in group 2 had alveolar edema. Thus, AMI is frequently associated with abnormal pulmonary microvascular sodium transport/water conductance that, in the case of ventricular dysfunction supervenience, may persist and worsen the outcome. In 37 AMI similar patients and 11 control subjects, nitric oxide overexpression with l-arginine improved baseline DM and in AMI patients prevented DM reduction by saline, suggesting a mechanistic role of an impaired nitric oxide pathway in the microvascular barrier dysfunction.
authors.affiliation: Cardiopulmonary Unit, Cardiology Division, University of Milano, San Paolo Hospital, Via A. di Rudinì 8, Milano 20142, Italy. marco.guazzi@unimi.it
authors.forename: Marco
authors.initials: M
authors.lastname: Guazzi
authors.forename: Ross
authors.initials: R
authors.lastname: Arena
authors.forename: Maurizio D
authors.initials: MD
authors.lastname: Guazzi
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D001120:Arginine / Q000494:pharmacology; D001794:Blood Pressure / Q000502:physiology; D015824:Blood-Air Barrier; D002097:C-Reactive Protein / Q000378:metabolism; D002196:Capillaries / Q000378:metabolism; D004058:Diffusion; D015150:Echocardiography, Doppler; D004562:Electrocardiography; D045604:Extracellular Fluid / Q000502:physiology*; D005260:Female; D006400:Hematocrit; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000473:pathology; D008168:Lung / Q000503:physiopathology*; D008297:Male; D008566:Membranes / Q000502:physiology; D008875:Middle Aged; D009203:Myocardial Infarction / Q000503:physiopathology*; D011650:Pulmonary Alveoli / Q000503:physiopathology; D012129:Respiratory Function Tests; D013318:Stroke Volume / Q000502:physiology; D016896:Treatment Outcome; D016277:Ventricular Function, Left / Q000502:physiology
chemical_list: D002097:C-Reactive Protein; D001120:Arginine