Abstract
Interstitial fluid pressure (Pif) has been studied in rat nasal mucosa during early inflammatory reactions induced by dextran anaphylaxis and local application of histamine. Pif was measured by using sharpened micropipettes connected to a servo-controlled counterpressure system. Access to the nasal mucosa was obtained from the facial side of the head through a small cavity drilled in the nasal bone. During dextran anaphylaxis, Pif increased significantly from control values of 2.2 +/- 0.4 to 3.8 +/- 0.21 mmHg (P < 0.05) within 1 h. Corresponding Pif values for histamine were 1.6 +/- 0.9 and 2.9 +/- 0.9 mmHg (P < 0.05), respectively. These measurements support the hypothesis that a major driving force for the rapid exudation across inflamed respiratory mucosa is a hydrostatic pressure gradient created by increased mucosa Pif. When the transvascular fluid shifts accompanying the inflammatory reactions are prevented by circulatory arrest, Pif decreased significantly to subatmospheric values, -0.8 +/- 0.8 and -3.3 +/- 1.2 mmHg in the dextran and histamine group, respectively (P < 0.05). The decrease in Pif in the nasal mucosa after inflammatory stimuli, during circulatory arrest, provides further evidence for "active" modulation of Pif through changes in mechanical properties of the interstitial matrix. The decrease in Pif seen under these circumstances reveals a possible mechanism participating in the rapid and initial edema formation after inflammatory provocations.
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More From: Journal of applied physiology (Bethesda, Md. : 1985)
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