ABSTRACT
In order to understand the microcirculatory changes and regulatory mechanisms governing passage of neutrophils from the vascular bed to the interstitial tissue during ischemia/reperfusion (I/R) injury, a key component of this injury, tumor necrosis factor-alpha (TNF-α)-induced inflammation was analyzed. Twenty-four Sprague-Dawley rats were divided into four groups, containing six animals in each. The effect of TNF-α-induced inflammation was studied at two different time points, early sequential and late. In the early-effect Groups 1 and 2, animals were given TNF-α and vehicle, respectively. Microcirculatory changes were recorded for 6 hr continuously. In the late-effect Groups 3 and 4, following TNF-α injection and vehicle, microcirculatory changes were measured 16 hr later. In the early-effect groups, the number of rolling and adhering leukocytes was increased immediately following TNF-α injection and remained elevated for the first 3 hr (p<0.05). The number of transmigrated leukocytes remained significantly increased throughout the first 6 hr (p<0.05) and returned to normal at 16 hr. In delayed-effect groups, a second peak in the number of rolling leukocytes was noted at 16 hr (p<0.05). The numbers of rolling and adhering lymphocytes, although remained at the baseline for the first 6 hr, was increased 2- and 1.5-fold at 16 hr, respectively (p<0.05). The number of perfused capillaries gradually decreased over time in the TNF-α-induced inflammation groups. A vasodilatory response was noted at the third and fourth order arterioles within the first 3 hr of measurement (p<0.05), but returned to normal afterward.
The detrimental effects of TNF-α-induced inflammation during I/R injury could be prolonged up to 16 hr at the microcirculatory level of the muscle flaps.
KEYWORD
Tumor necrosis factor-alpha - ischemia-reperfusion injury - chronic effects - cremaster muscle flap
