Pulmonary epithelial permeability is immediately increased after embolisation with oleic acid but not with neutral fat.

Abstract

Pulmonary fat embolism occurs frequently after trauma but its functional significance is often unclear. To obtain direct evidence of lung damage caused by fat embolism we have measured changes in permeability of the alveolar-capillary interface. A permeability index was derived from the half time clearance from lung to blood (T-LB) of 99mTc DTPA introduced into the lung in a 1 ml bolus. Three groups ofrabbits were studied. Baseline Tw LB. did not differ significantly between groups. After intravenous injection of saline placebo in one group and of 300 mg/kg triolein in another group there was no change in permeability index. After intravenous injection of 100 mg/kg oleic acid in the third group there was an immediate change in T' LB from a monoexponential baseline 280 ± 20 min (SEM) to a multiexponential curve which was resolved into two components, one with a T'LB of 3-2 ± 0-6 min (SEM) and the other 39 5 ± 7-6 min (SEM). Statistically significant changes in alveolar-arterial Po2 difference, dynamic compliance, chest radiography, and postmortem lung water accompanied the changes in T'LB in this group. There were no significant changes in these variables in the placebo or triolein group. Histological studies of the lung tissue of these animals using the osmic acid stain for fat showed no fat in the placebo group, extensive fat embolisation which was densely stained in the triolein group and much less densely stained fat in the oleic acid group. Measurement of the permeability of the alveolar-capillary interface provides direct evidence of lung damage after oleic acid embolisation. There were no functional changes in animals with extensive embolisation with triolein.

Alveolar epithelial damage. A critical difference between high pressure and oleic acid-induced low pressure pulmonary edema.

“…After this rapid rise the appearance of FITC-dextran in the blood was similar in OAPE and control. This observation is consistent with the findings of Jones et al (20) and suggests a rapid control ofthe leak after the oleic acid damage. Recent studies by Dvorak et al (21) have shown that extravascular coagulation can be initiated by large microvascular leaks, and the presence of fibrin on the alveolar surface (Fig.…”

“…6 d) suggest that this occurred in OAPE. The observations from these studies and others (20,21) therefore suggest that the fibrin deposition in alveoli that occurs as part of hyaline membrane formation may be a manifestation ofextravascular coagulation that occurs in an attempt to control large microvascular leaks.…”

Fat embolism

“…However, there are difficulties in obtaining satisfactory samples, as shown in one study where only 67 out of 96 samples were adequate for analysis due to low yield of macrophages [24]. Also, the stain used in these investigations is a stain for neutral fat (oil red O) which does not produce lung injury [25]. Despite these reservations, the use of a threshold value (such as 30%) of macrophages staining positive might be useful in trauma patients.…”

“…A flaw in this theory is that neutral fats are the major constituents of bone marrow and they do not display this effect [25]. However, it is highly likely that in vivo there is hydrolysis of neutral fats to FFAs and this may help explain the symptom-free interval before the onset of signs and symptoms during which hydrolysis occurs.…”

Effect of Fat Embolism with Triolein Emulsion on Blood-Retinal Barrier

“…The presence of microemboli was, however, confirmed at least for 12 h by electron microscopy. Triolein can be hydrolyzed to free fatty acid or oleic acid [19] , which was reported to have more potent effects for vascular permeability and toxicity [7,26] . Diffuse leakage of fluorescein at 4 h would represent the diffuse alteration of the BRB caused by the hydrolyzed fatty acid.…”