Distribution of actin and myosin in the cochlear microvascular bed

Objective-Previous studies of the microvascular bed of the rat inner ear showed vascular constriction after i.v. application of endothelin-1 (ET-1). Luminal narrowing together with multiple circumscribed constrictions were observed on vascular corrosion casts of initial and small calibre veins. These constrictions were interpreted as being caused by contractile cytoplasmic fibrils, most probably of pericytes; pericytes reportedly respond to ET-1 and the frequency, distribution and dimension of pericytes and their cytoplasmic processes closely corresponded to the constrictions observed. In the present study we analysed the distribution of actin and myosin in order to directly show the presence of contractile cytoplasmic fibrils. Material and Methods-We performed standard immunostaining for actin, smooth muscle actin, smooth muscle myosin and tropomyosin in the cochlea. We used different fixation protocols (methacarn, neutral formalin, Bouin's fluid) and compared observations in two species (rat and guinea pig). Results-Imnumohistohemistry confirmed the presence of contractile cytoplasmic fibrils in cochlear pericytes and vascular smooth muscle cells. Microvessels in the cochlea were much better provided with contractile fibrils in rats compared to guinea pigs. The distribution of contractile fibrils in rats corresponded well to the luminal constrictions observed on vascular corrosion casts. Conclusions-Our results support the assumption that active myofibrillar contraction (in response to ET-I stimulation of pericytes) causes lumin A constriction in cochlear microvessels. Contraction of myofibrils can be influenced by intrinsic or extrinsic agents, which offers new therapeutic regimens to govern cochlear blood flow. As the frequency of contractile cells on cochlear microvessels varied with the species studied, evaluation of human material will be the next step.