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Mechanisms responsible for increased vascular permeability in acute inflammation

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Abstract

The acute inflammatory response consists of three main vascular effects: vasodilatation and increased blood flow, increased vascular permeability, and leucocytosis into the injured tissues. All three events are induced relatively quickly, and, for all three, the pattern of response is complex but consistent. The characteristic increase of vascular permeability may be monophasic, diphasic or even triphasic. These various patterns of response may nevertheless be ‘dissected’ into three main types of responses: viz., (1) immediate, (2) delayed and (3) early, each of which may occur alone or in various combinations. The problem of mediation, therefore, becomes one of defining the mechanisms underlying each type of response. Immediate responses are usually mediated by histamine and/or 5-hydroxytryptamine. Delayed responses seem to result from pharmacological mediation although the corresponding factors remain unidentified. Early responses seem mainly due to disruption of endothelium, to which is added a small contribution by pharmacological mediation. Evidence will be presented to support the role of kinins as mediators of the delayed response. The evidence mainly arises from recent work illustrating that histamine induces refractoriness of susceptible blood vessels and so can evoke only a short-lived response, whereas kinins induce no such refractoriness and could, therefore, mediate the relatively prolonged responses obtained in delayed-type effects.

The paper will conclude by attempting to answer four questions:

  1. (1)

    Why does the pattern of the permeability response often exhibit an intermediate interval of normal low permeability?

  2. (2)

    Why may erythema be so prominent at a stage when the corresponding permeability effects are minimal?

  3. (3)

    What is the relation of local tissue leucocytosis to the delayed permeability effects induced by injury?

  4. (4)

    Nearly all our knowledge of the permeability response in experimental injury is restricted to the events in skin, to less extent in muscle and serous cavities. Are the permeability responses similar in other tissues and organs?

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Authors and Affiliations

  1. School of Pathology, The University of New South Wales, Kensington, Australia

    D. L. Wilhelm

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  1. D. L. Wilhelm
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Supported by research grants from the National Health and Medical Research Council of Australia, and the Asthma Foundation of New South Wales.

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Wilhelm, D.L. Mechanisms responsible for increased vascular permeability in acute inflammation. Agents and Actions 3, 297–306 (1973). https://doi.org/10.1007/BF01986484

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