Leukocyte and platelet accumulations around apparently empty spaces ("air bubbles") in the blood of the right heart or branches of the pulmonary artery should constitute histomorphological evidence of a venous air embolism prior to death. Such findings have been evaluated as the result of active cellular reactions to air bubbles and as a vital reaction. This interpretation was reviewed by injecting a frothy mixture of blood and air into the pulmonary artery of six human lungs 12-110 h post mortem. The lungs were fixed and (immuno)histologically prepared (haematoxylin-eosin staining, immunohistological visualization of platelets, fibrinogen and fibrin). Leukocyte and platelet accumulations around "air bubbles" in blood were provoked late post mortem by injection of the frothy blood-air mixture and are thus possibly not the result of vital cellular reactions. The case is rather that attachment of particles (cells) to flowing air bubbles in an aqueous medium (blood) could correspond physicochemically to a flotation process such as those used in industry for separation techniques. A flotation process would, however, require an intensive dynamic blood-air bubble contact, which would only be obtainable if cardiac action is maintained for a sufficient length of time after air embolism. Leukocyte and platelet accumulations around "air bubbles" in the blood would then indeed be properly interpreted as a vital reaction (albeit possibly not resulting from vital cellular reactions) and could be used as evidence of an air embolism prior to death.

The short-term effect of intravenous (i.v.) angiotensin converting enzyme (ACE) inhibitor enalaprilat in 10 critically ill patients, being ventilated with positive end-expiratory pressure (PEEP), on sodium and water excretion was investigated. Mean arterial pressure (MAP) decreased. Heart rate and central venous pressure (CVP) did not change. Glomerular filtration rate (GFR), urine volume (V) and sodium excretion (UNaV) decreased in two patients with reduced MAP. GFR, V and UNaV increased in two patients with decreased MAP. No relation between changes in MAP and excretion was observed in six patients. ACE decreased in all patients. Plasma renin activity increased, aldosterone decreased, while atrial natriuretic peptide as well as antidiuretic hormone did not change. Enalaprilat did not facilitate sodium and water excretion during ventilation with PEEP. Decreased MAP indicates that the investigated patients were very dependent on their renin-angiotensin system to maintain systemic perfusion pressure. Base-line MAP and CVP values were no predictors of haemodynamic and excretory changes following acute ACE inhibition.

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