The emergence of superoxide anion radicals (O2-) in the guinea pig inner ear following acoustic trauma was investigated by histochemical methods. Five minutes after exposure to sound at 120-125 dB SPL for 3 h, an O2- reaction product was detected in the cochlea along the luminal membrane of the marginal cells of the stria vascularis. This reaction product could not be found at 30 min, but reappeared at 2 h. The first appearance of O2- is not explainable by our studies, but the second appearance may be related to recirculation of strial blood flow after blood flow stasis. The present observations raise the possibility that free radicals are produced in the inner ear after acoustic trauma and lead to inner ear damage.

These results demonstrate distinct expression of VEGF and its receptors (flt-1 and Flk-1) in atherosclerotic lesions in human coronary arteries. Considering the multipotent actions of VEGF documented experimentally in vivo and in vitro, our findings suggest that VEGF may have some role in the progression of human coronary atherosclerosis, as well as in recanalization processes in obstructive coronary diseases.

The strong association of enhanced ACE expression with the histologic characteristics of plaques suggests that ACE in hypercellular lesions, atheromatous plaques, and ruptured plaques contributes greatly to the further progression of atherosclerosis via an increase in vascular angiotensin II formation and inactivation of bradykinin.