Dexamethasone preventing contractile and cytoskeletal protein changes in the rabbit basilar artery after subarachnoid hemorrhage

Abstract

Object. The aim of this project was to study the perturbations of four smooth-muscle proteins and an extracellular protein, type I collagen, after subarachnoid hemorrhage (SAH) and to examine the possible preventive effects of dexamethasone. Methods. Using a one-hemorrhage rabbit model, the authors first examined the effects of SAH on the expression of α-actin, h-caldesmon, vimentin, smoothelin-B, and type I collagen; second, they studied whether post-SAH systemic administration of dexamethasone (three daily injections) corrected the induced alterations. Measurements were obtained at Day 7 post-SAH. The proteins were studied by performing immunohistochemical staining and using a laserscanning confocal microscope. Compared with control (sham-injured) arteries, the density of the media of arteries subjected to SAH was reduced for α-actin (−11%, p = 0.01) and h-caldesmon (−15%, p = 0.06) but increased for vimentin (+15%, p = 0.04) and smoothelin-B (+53%, p = 0.04). Among animals in which SAH was induced, arteries in those treated with dexamethasone demonstrated higher values of density for α-actin (+13%, p = 0.05) and h-caldesmon (+20%, p = 0.01), lower values for vimentin (−55%, p = 0.05), and nonsignificantly different values for smoothelin-B. The density of type I collagen in the adventitia decreased significantly after SAH (−45%, p = 0.01), but dexamethasone treatment had no effect on this decrease. Conclusions. The SAH-induced alterations in the density of three of four smooth-muscle proteins were prevented by dexamethasone treatment; two of these proteins—α-actin and h-caldesmon—are directly related to contraction. This drug may potentially be useful to prevent certain morphological and functional changes in cerebral arteries after SAH.