C Kamei — Page 8 | PubMed Health

PubMedDate not supplied

Participation of mast cells in colitis inflammation induced by dextran sulfate sodium.

We investigated the participation of mast cells in colitis inflammation induced by dextran sulfate sodium (DSS). The damage score and myeloperoxidase (MPO) activity were measured to confirm the occurrence of colitis. Rat mast cell protease (RMPCP) II levels in the serum were estimated as an index of mast cell degranulation. Tissue RMCP I and RMCP II levels in the rectum were also measured as markers of the numbers of connective tissue mast cells (CTMCs) and mucosal mast cells (MMCs), respectively. Administration of 4% DSS resulted in time-related increases in damage score, MPO activity and serum RMCP II levels, which were statistically significant at 7 and 11 days after treatment. Tissue RMCP I and RMCP II levels in the rectum were also increased significantly at 7 and 11 days, and 11 days, respectively after free drinking of 4% DSS. These results suggested that mast cells proliferated or the amount of protease per mast cell increased in the sites of inflammation induced by DSS, and that these mast cells may modulate the disorders observed in DSS-induced colitis.

Animals↗

PubMedDate not supplied

Role of hypothalamic histamine in stimulating the corticosterone release in rats.

Intracerebroventricular injection of alpha-fluoromethylhistidine caused a significant decrease of the histamine content of the hypothalamus as well as of plasma adrenocorticotropic hormone and corticosterone concentrations. A high correlation was observed between the histamine content of the hypothalamus and the plasma corticosterone concentration. When the histamine content of the hypothalamus decreased, the plasma concentration of corticosterone diminished. Almost the same result was obtained when the posterior hypothalamus was lesioned electrically. The increases in plasma adrenocorticotropic hormone and corticosterone concentrations, induced by intracerebroventricular injection of histamine in sham-operated rats, were abolished after hypothalamic lesioning. When electrical stimulations were applied to the posterior hypothalamus, plasma adrenocorticotropic hormone and corticosterone concentrations increased significantly and, at the same time, evoked potentials were recorded on the adrenal nerve. An increase in plasma corticosterone concentration, induced by hypothalamic stimulation, was also observed even after hypophysectomy, suggesting that another corticosterone-secreting pathway exists apart from the hypophysis-adrenocortex system. The increase in plasma adrenocorticotropic hormone and corticosterone concentrations was inhibited not only by pyrilamine and cimetidine, but also by (R)-alpha-methyl-histamine, and H3 agonist. In addition, the effect of this latter product was inhibited by thioperamide, an H3 antagonist. These results indicate that hypothalamic histamine plays an important role in the stimulation of the corticosterone release in rats.

Adrenal Glands↗