MECHANISMS OF CELL INJURY IN RAT MESENTERY AND CREMASTER MUSCLE

Citation
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
Citations number
23
Categorie Soggetti
Physiology
ISSN journal
03636135
Volume
43
Issue
3
Year of publication
1998
Pages
1009 - 1015
Database
ISI
SICI code
0363-6135(1998)43:3<1009:MOCIIR>2.0.ZU;2-5
Abstract
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.