A study of the pharmacologic control of blood flow to delayed skin flaps using xenon washout. Part II.

ABSTRACT

These experiments indicate that there are two components to the delay phenomenon. The first component is passive vasodilation owing to loss in the acute flaps originating from the sympathetic nerve terminals. The second component is active vasodilation not involving loss of a second vasoconstrictor mechanism or sensitization of the beta-receptors. Overall, the increase in blood flow associated with the delay phenomenon was seen to begin near the base of the flap and proceed distally. While the second component could not be identified, its characteristics suggest that its site of action is directly at the smooth-muscle or vascular-architecture level without involving the beta-receptors for vasodilation.