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PubMed1955

Studies on the pathogenesis of acute inflammation. I. The inflammatory reaction to thermal injury as observed in the rabbit ear chamber.

A special adaptation of the rabbit ear chamber has been devised to study in vivo, under high magnification, the acute inflammatory reaction to thermal injury. Systematic observations of the cellular response have led to the following conclusions. 1. Contrary to the commonly accepted view, vasodilatation does not always precede the adherence of leucocytes to vascular endothelium. 2. The fact that leucocytes often adhere to one another as well as to the endothelium indicates that the increased adhesiveness characteristic of the early stages of inflammation is not limited to the surfaces of the endothelial cells. 3. The sharing of erythrocytes and platelets in this increased stickiness suggests that a "plasma factor" is involved. There is indirect but as yet inconclusive evidence that the plasma factor may concern the clotting mechanism of the blood. 4. The adherence of leucocytes to the endothelium is usually first noted on the side of the vessel closest to the site of injury. This previously undescribed phenomenon of "unilateral sticking" is in keeping with the concept that the vascular reaction is caused by products of cellular damage which diffuse to the vessel from the site of injury. 5. Leucocytes always become adherent to the endothelium before penetrating the vessel wall. They often migrate about for some time on the endothelial surface before undergoing diapedesis. 6. Although no definite stomata are at any time visible in the endothelium, penetrating leucocytes may leave behind temporary defects through which other leucocytes and even erythrocytes may pass. 7. The diapedesis of leucocytes appears to depend primarily upon cellular motility. It may occur in static vessels where there is presumably little if any hydrostatic pressure. 8. The diapedesis of erythrocytes, on the other hand, is a passive process depending upon intravascular pressure. Its occurrence is greatly exaggerated in areas in which intravascular pressure becomes elevated. Such elevations occur as the result of proximal arteriolar dilatation and distal occlusion of vessels. 9. Once they have reached the extravascular tissues the leucocytes move about more or less at random, apparently uninfluenced by any compelling chemotactic force. Their resultant migration, however, is toward the site of injury around which they eventually tend to congregate. 10. The histiocytes normally present in the connective tissue appear to play no role in the type of acute inflammatory reaction produced in these experiments.

Animals↗
PubMed1955

Studies on the pathogenesis of acute inflammation. II. The action of cortisone on the inflammatory response to thermal injury.

The anti-inflammatory action of cortisone upon the acute cellular response to thermal injury has been systematically studied in the rabbit ear chamber. The hormone has been shown to suppress the reaction of acute inflammation in its earliest recognizable phase; i.e., that involving vasodilatation and the adherence of leucocytes to the vascular endothelium. Evidence has been presented that the anti-inflammatory effect of the hormone cannot be explained on the basis of its vasoconstrictive properties alone. The experimental observations support the hypothesis that cortisone exerts a direct protective action upon endothelial cells and leucocytes, and that in so doing, it renders them refractory to the tissue products which initiate inflammation.

Animals↗