Ag. Harris et al., MECHANISMS OF CELL INJURY IN RAT MESENTERY AND CREMASTER MUSCLE, American journal of physiology. Heart and circulatory physiology, 43(3), 1998, pp. 1009-1015
The events responsible for cell injury after a tissue stimulation are
only incompletely understood. The purpose of this study was to examine
mechanisms of cell injury in two tissues, rat mesentery and cremaster
muscle, after tissue stimulation with N-formylmethionyl-leucyl-phenyl
alanine (FMLP) and platelet-activating factor (PAF). The response was
studied in the same animal in random order using normal and leukopenic
rats. The tissues were exteriorized after pentobarbital anesthesia. F
ive to six vascularized areas were chosen in each tissue, and cell inj
ury and hydroperoxide production were assessed visually by continuous
superfusion with 1 mu M propidium iodide and 5 mu M dichlorofluorescin
diacetate (DCFH), respectively. FMLP (1 x 10(-8) M) and then PAF (1 x
10(-8) M) were added to the superfusate, and measurements were made a
t several time paints. The second tissue was then examined using the s
ame protocol. In the cremaster, there was Little hydroperoxide product
ion, and the tissue injury was eliminated after leukopenia. Leukopenia
had no effect on tissue injury in the mesentery. Although hydroperoxi
de production was observed, there was no correlation between it and th
e tissue injury. The level of preactivation showed no correlation with
either tissue injury or hydroperoxide production. In light of these r
esults, mast cell degranulation may be an important mechanism of tissu
e injury in the mesentery.