Multi-organ damage resulting from experimental faecal peritonitis

Abstract

1. Using specific-pathogen-free New Zealand White rabbits, we have compared the effects of faecal peritonitis over a period of 5 h in eight test animals with eight controls in which a sham operation was performed. 2. There was morphological damage to lungs, liver and spleen of test animals. Lung capillaries and sinusoids of the liver showed occlusion by cell debris and leucocytes, with endothelial damage. The lungs also showed alveolar epithelial disruption, basement membrane exposure and type II pneumocytes lacking lamellar bodies. In the liver there was fibrin deposition and swollen Kupffer cells. The spleen showed degranulating neutrophils, fibrin deposits, platelet aggregates and activated macrophages, with no damage to the endothelium. 3. There was no morphological damage to the kidney or heart of test animals or to any organs of sham-operated animals. 4. There were mixed anaerobes and aerobes in faecal material used to induce peritonitis. Cultures of liver, spleen and kidney isolated four different types of micro-organisms. Blood cultures showed two types of micro-organisms. Cultures of lung and heart showed one type of micro-organism. 5. The presence of micro-organisms in an organ could not be correlated with the degree of histological damage to that organ. 6. In test animals an early significant reduction in circulating leucocytes and platelets was sustained for the duration of the experiment with significant diffuse intravascular coagulation. 7. There was no change in test animal neutrophil adhesiveness until 120 min, when significant reduction was observed. 8. Serum phospholipase A2 (EC 3.1.1.4) activity in the test group showed a threefold increase at 300 min.

Translocation of indigenous microflora in an experimental model of sepsis

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The effect of hydroxyethyl starch and other plasma volume substitutes on endothelial cell activation; an in vitro study

“…In the early phase of the syndrome the histological findCorrespondence to: A.R. Webb ings are of severe alveolar oedema with numerous inflammatory cells, predominately neutrophils, in the airspaces, capillaries and interstitium of the lung [3]. Endothelial activation and its interaction with, and damage by, neutrophils is central in the development of ARDS [1].…”

Faecal peritonitis causes oedema and neuronal injury in pig cerebral cortex

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“…There is panendothelial injury from persistent, uncontrolled inflammation which causes the deposition of fibrin and the formation of thrombi in microvessels [10]. As a result, these organs become underperfused [8] and accumulate activated leucocytes [3], especially degranulating neutrophils [5] which release lysosomal enzymes and superoxide radicals.…”