Vasomotor Microcirculatory Insufficiency : Observations On Nonfreezing Cold Injury of the Mouse Ear

Abstract

The pathogenetic significance of vasomotor microcirculatory insufficiency was investigated using as an experimental model the focal cold injury which develops in the ears of mice kept individually caged at 3[degree]C. Rapid in situ freezing of the ears served to fix the terminal vascular bed in a life-like state and permitted temporal and spatial correlation of functional vascular changes with histologic manifestations of tissue damage. The following stages of local circulatory impairment were found to precede the development of irreversible tissue damage: (1) generalized vasoconstriction involving all types of blood vessels throughout the ear; (2) venous and venular relaxation with persistence of segmental arteriolar constriction and plasma leakage from isolated venular segments; (3) venular and capillary stasis with im-paction of erythrocytes; (4) arteriolar-venular shunting with bypassing of capillary and venular beds. The temporary persistence of blood flow through arteriolar-venular thoroughfares was associated with focal fibrinoid necrosis involving the walls of the patent vessels and ultimately the surrounding connective tissue. It is suggested that a slowing of venular blood flow leading to stasis may be an important pathogenetic factor not only in cold injury but also in other lesions characterized by fibrinoid necrosis.