Kulka, J. Peter
October 1961
Angiology;Oct1961, Vol. 12 Issue 10, p491
Academic Journal
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�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 onset of tissue necrosis followed that of local circulatory insufficiency, which developed in the following four stages: (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 impaction of erythrocytes; (4) arteriolar venular shunting with bypassing of capillary and venular plexi. The venular statis appears to result principally from venular dilation in the presence of arteriolar constriction, which leads to a critical showing of blood flow, and from plasma leakage which leads to hemoconcentration and ultimate cessation of the local circulation due to viscous resistance to flow. It is suggested that a similar type of vasomotor or vasotonic microcirculatory disorder producing stasis in the terminal vascular bed, may also be significant in the pathogenesis of other inflammatory conditions, particularly those typically associated with fibrinoid necrosis of blood vessels and connective tissue.


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