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TYPE AND COURSE OF THE INFLAMMATORY CELLULAR REACTION IN ACUTE ANGIOTENSIN‐HYPERTENSIVE VASCULAR DISEASE IN RATS
Author(s) -
Olsen Finn
Publication year - 1970
Publication title -
acta pathologica microbiologica scandinavica section a pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0365-4184
DOI - 10.1111/j.1699-0463.1970.tb00249.x
Subject(s) - cellular infiltration , angiotensin ii , arteriole , infiltration (hvac) , peripheral blood mononuclear cell , medicine , chemistry , inflammation , pathology , endocrinology , microcirculation , immunology , blood pressure , in vitro , biochemistry , physics , thermodynamics
The inflammatory cellular reaction in arterioles damaged by acute experimental angiotensin‐hypertension in rats has been examined 1, 3, 6, 12, 24 and 48 hours after the termination of the hypertensive period. The cellular reaction was predominantly composed of mononuclear cells derived from the blood. The majority of these cells, which were able to phagocytize, looked like lymphocytes, and the rest like typical monocytes. The cellular reaction began as a sticking phenomenon corresponding to the damaged endothelium followed by a penetration of mononuclear cells into the arteriolar walls. The cells left the walls of the arterioles after having carried out the macrophage function, returning directly to the circulation or penetrating through the arteriolar wall to the connective tissue surrounding the arteriole. A marked periarteriolar cellular infiltration like that seen in cases of chronic hypertensive vascular disease in different experimental animals was produced by prolonging the number of days (from one to four) in which experimental angiotensin‐hypertension was induced. Rats treated with cortisone showed absence of or decreased inflammatory cellular reaction and a 2–3 times slower elimination of fluorescent proteins deposited in the arterioles as compared with that found in controls. The delayed elimination is thought to be caused by the decrease in or lack of cellular reaction.