title: Alloxan diabetes abolishes the increased negativity of interstitial fluid pressure in rat trachea induced by vagal nerve stimulation.
abstract: Increased negativity of interstitial fluid pressure (Pif) occurs concomitantly with oedema formation in acute airway inflammation. This observation is principally important because the loose connective tissues become 'active' and provide the driving force for the rapid oedema formation via Pif. The present study reports Pif in acute airway inflammation in alloxan diabetic rats. The basis for the study was, firstly, that inflammation is important in the pathogenesis of asthma. Secondly, that clinically there is almost a mutual exclusion between diabetes and asthma and, lastly, that the inflammatory response is attenuated in alloxan diabetic rats. Pif was measured on the ventral side of the trachea with sharpened glass capillaries (3-6 microns) connected to a servocontrolled counterpressure system. Measurements and nerve stimulation were performed after circulatory arrest, since oedema formation associated with inflammation will increase Pif, causing an underestimation of a potentially increased negativity of Pif. Control or diabetic rats (alloxan 45 mg kg-1 i.v. 5 days earlier) received either the mast cell degranulating substance compound 48/80 (100 micrograms), dextran 70 (60 mg) i.v. or vagal nerve stimulation. After dextran, Pif was -4.7 +/- 0.9 (SD) mmHg (n = 6) and -1.3 +/- 0.3 mmHg (n = 6) (P < 0.01) in normal and diabetic rats, respectively. Corresponding values after vagal nerve stimulation were -5.3 +/- 1.8 mmHg (n = 5) and -0.7 +/- 0.2 mmHg (P < 0.01). Insulin treatment restored the Pif response to dextran and vagal stimulation. Pif after Compound 48/80 did not differ between control and diabetic rats. Interstitial volume, total tissue water and transcapillary albumin extravasation increased significantly in controls after vagal nerve stimulation, but was attenuated in diabetic rats.
authors.affiliation: Department of Physiology, University of Bergen, Norway.
authors.forename: K
authors.initials: K
authors.lastname: Woie
authors.forename: R K
authors.initials: RK
authors.lastname: Reed
mesh_terms: D000418:Albumins / Q000378:metabolism; D000496:Alloxan; D000818:Animals; D001786:Blood Glucose; D003594:Cytoplasmic Granules / Q000187:drug effects; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy / Q000503:physiopathology*; D004487:Edema / Q000209:etiology / Q000276:immunology; D005110:Extracellular Space / Q000502:physiology*; D005119:Extravasation of Diagnostic and Therapeutic Materials; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007328:Insulin / Q000494:pharmacology; D008407:Mast Cells / Q000187:drug effects / Q000378:metabolism; D010953:Plasma Volume; D011189:Potassium Chloride / Q000494:pharmacology; D011312:Pressure; D051381:Rats; D017208:Rats, Wistar; D013268:Stimulation, Chemical; D014132:Trachea / Q000276:immunology / Q000294:innervation*; D014136:Tracheitis / Q000150:complications / Q000276:immunology*; D014630:Vagus Nerve / Q000187:drug effects / Q000502:physiology*; D014867:Water / Q000378:metabolism
chemical_list: D000418:Albumins; D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin; D014867:Water; D011189:Potassium Chloride; D000496:Alloxan