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The effect of zymosan-induced generalized inflammation on the microcirculation of distant striated skin muscle was studied for a 12 day period in awake Syrian golden hamsters (n = 18) using the dorsal skinfold chamber model and intravital fluorescence microscopy. Intraperitoneal zymosan exposure (125 mg/100 g body weight) induced significant nutritive perfusion failure in the distant striated muscle tissue at Day 1 without complete recovery over the 12 day observation period, as indicated by the marked reduction of functional capillary density when compared with both baseline values and values of sham-treated control animals. Moreover, intraperitoneal zymosan exposure induced endothelial disintegration, as demonstrated by the continuous increase of macromolecular leakage throughout the 12 days of observation. Strikingly, zymosan did not induce significant leukocyte adherence to the endothelial lining of postcapillary and collecting venules of the striated muscle tissue. Thus, we conclude that in this model of generalized inflammation nutritive perfusion failure and loss of endothelial integrity in distant striated muscle is not mediated by activated leukocytes, but must rather be attributed to direct toxic effects of mediators, elicited by the local (intraperitoneal) zymosan challenge and systemically released.
Geeraedts et al. (Sat,) studied this question.