Reactivity of Arterioles Following Denervation of Subcutaneous Areas of the Bat Wing

Abstract

In studies directed toward determining the behavior of minute blood vessels in peripheral vascular beds in innervated and denervated areas, the wing membrane of the living bat was used, and responses of smooth muscle cells to topical applns. and intraven. injns. of epinephrine were observed at high magnification (1200x). Epinephrine was applied topically to an exposed vascular area to determine the weakest concn. needed to elicit complete closure of an arteriole or terminal arteriole by constriction of encircling smooth muscle cells, and this end-point was designated as the apparent threshold response. Apparent thresholds were detd. in normal wings and found to vary over a wide range. Intraven. injns. of epinephrine showed that increased responsiveness of arteriolar vessels developed in a denervated wing 10-14 days following section of the nerve, indicating that the minute vessels of the bat wing conform to the behavior of similar structures in other animals under the same conditions. Comparisons of responsiveness to topical applns. of epinephrine were made between vessels in denervated and innervated areas in the same animal. No increased responsiveness could be demonstrated in minute vessels of denervated areas when the responsiveness was compared to identical areas in the contralateral innervated wing. The finding that there was no difference in responsiveness between denervated and innervated vascular areas when a chemical excitor was applied directly to the reactive cell implies that no alteration, such as increased permeability of the cellular membrane or super-sensitivity of the cell, could account for the increased responsiveness to intraven. epinephrine following denervation. Various other factors that may contribute to change the relationship between the cell and its environment are discussed. It was concluded that no single factor could be responsible for the increased responsiveness of denervated vascular beds to blood-borne effective agents, and that such an increased responsiveness is the result of changes in the cell-environment equilibrium and not an alteration in intra-cellular conditions alone.