Oxygen consumption and vital organ masses in young growing quail (Coturnix coturnix japonica)

Increased negativity of interstitial fluid pressure (P_if) 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 P_if. The present study reports P_if 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. P_if was measured on the ventral side of the trachea with sharpened glass capillaries (3–6 μm) connected to a servocontrolled counterpressure system. Measurements and nerve stimulation were performed after circulatory arrest, since oedema formation associated with inflammation will increase P_if, causing an underestimation of a potentially increased negativity of P_if. 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 μg), dextran 70 (60 mg) i.v. or vagal nerve stimulation. After dextran, P_if 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 P_if response to dextran and vagal stimulation. P_if 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.