In‐vivo effects of anti‐inflammatory and other drugs on granulocyte emigration in the rabbit skin collection chamber

Abstract

A method for measuring localised leukocyte mobilisation under in-vivo conditions with a plastic skin collection-chamber adapted to the rabbit ear was used for assessing the effects of anti-inflammatory and other agents on granulocyte emigration. Studies on the effect of oral drug administration to rabbits indicated that most anti-inflammatory drugs, two cystostatic agents (cyclophosphamide and colchicine), but none of the other compounds exhibiting antihistaminc, beta-adrenolytic or neuroleptic properties, significantly inhibited granulocyte mobilisation. The results after topical application of some of these agents into the chamber correlated well with those obtained after oral treatment. This technique may thus prove useful in selecting new compounds inhibiting granulocyte mobilisation in acute inflammatory reactions.

The effect ofin vitro andin vivo dexamethasone on human neutrophil function

“…Furthermore the average chemotactic response on the treatment days was significantly lower than those of the 2 day 'run in' period and were reversed 7 days after taking the last dose of dexamethasone. These findings are in keeping with previous animal studies [13][14][15] although again this result is at variance with others. Sheng et al [29] failed to show an effect on PMN chemotaxis or superoxide anion production in peripheral blood PMN taken from rabbits which had been exposed to dexamethasone 10 days prior to their developing surgical peritonitis.…”

“…In vitro studies have demonstrated that corticosteroids are able to inhibit both PMN chemotaxis [6,7] and superoxide anion generation [8] although other workers have failed to confirm these observations [9][10][11][12]. Despite this controversy, however, there is good evidence from animal studies that corticosteroids inhibit both PMN and monocyte migration [13][14][15], as well as suppressing superoxide anion generation in vivo [4,5,16]. In addition recent studies have shown that high dose methyl prednisolone reduces the chemotactic response, superoxide production and degranulation of PMN in patients with resolving allogenic hepatic graft rejection [17].…”

An analysis of piroxicam in rodent models of arthritis

“…Piroxicam inhibited the formation of pleural exudate Inhibition of leukocyte migration into the pleural cavity after carrageenan administration. Several NSAID's have been reported to decrease total leukocyte migration into inflammatory exudates [13][14][15], as well as PMN's ] [16][17][18] and monocytes [19][20][21][22][23][24]. When the effects of prioxicam on cell infiltration were evaluated in the rat pleural cavity, piroxicam inhibited the influx of leukocytes into the pleural cavity with an EDs0 of 10 mg/kg, p.o., approximately the same EDs0 found for inhibition of exudate formation.…”

Induction of zymosan‐air‐pouch inflammation in rats and its characterization with reference to the effects of anticomplementary and anti‐inflammatory agents

“…Complement-derived chemotactic factor(s), especially C5a and/or C5a des Arg (Borel & Feurer, 1978;Webster, Hong, Johnston & Henson, 1980), seem to play an important role in the accumulation of PMN in the pouch, since K-76COONa, a specific inhibitor of the activation of C5 (Hong et al, 1979), reduced the number of leukocytes in the zymosanair-pouch inflammation ( Figure 5), whereas this drug failed to affect leukocyte accumulation in the caseinair-pouch inflammation (data not shown), in which alkali-solubilized casein, known as a potent chemoattractant (Wilkinson, 1972), was used instead of zymosan. This result also suggests that anticomplementary agents might be effective therapeutic agents in some inflammatory and allergic diseases.…”