The chronology of SEM studies of the embryonic endocardium is followed in this review by discussion of species, stages and localizations studied. In reviewing the methodology of SEM studies of the embryonic endocardium, particular weight is given to standard methods which can be applied to all species of interest. Two main aspects are more deeply analysed: the perfusion fixation and the effects of the osmolarity of the fixative vehicle. Using these standardized techniques, the embryonic endocardium of chick, mouse, dog, human and, to a lesser extent, rat hearts are described in SEM. All species investigated presented microvilli ruffles, filopodia, cytosegresomes, intercellular openings and phagocytes. Marginal folds, lamellipodia, dividing cells and incomplete endocardium could be observed in some species only. Each of these microappendages is discussed in relationship to observations of other authors on four levels - embryonic endocardium, adult endocardium, embryonic endothelium and adult endothelium. The general tendency in differentiation of the embryonic endocardium results in a progressive loss of the majority of the microappendages mentioned. Contrary to a relative absence of interspecific differences in endocardial morphology as seen in SEM, there is a strong variation of this morphology relating to the intracardiac localization of the endocardial cells. The discovery of autolytic postmortem changes in the material from pregnancies terminated by prostaglandins leads to the recommendation that the further use of this source of embryonic and fetal material be discouraged. Finally, the modifications of the morphology of embryonic endocardial cells under the effects of cytochalasin B, altered hemodynamics, and the hereditary congenital heart defects of the Keeshond strain of dogs are discussed, using the above-mentioned principles of four levels.

Cytochalasin B is known to induce quiescence in cells. We present here a comprehensive view dealing with the effects of cytochalasin B on cell division, movements, exchanges and morphology. The controversial mode of action of the drug is also considered.

Sodium butyrate produces reversible changes in morphology, growth rate, and enzyme activities of several mammalian cell types in culture. Some of these changes are similar to those produced by agents which increase the intracellular level of adenosine 3\',5\'-cyclic monophosphate (cAMP) or by analogs of cAMP. Sodium butyrate increases the intracellular level of cAMP by about two fold in neuroblastoma cells; therefore, some of the effects of sodium butyrate on these cells may in part be mediated by cAMP. Sodium butyrate appears to have properties of a good chemotherapeutic agent for neuroblastoma tumors because the treatment of neuroblastoma cells in culture causes cell death and \"differentiation\"; however, it is either innocuous or produces reversible morphological and biochemical alterations in other cell types.