Following temporary ischemia of the rat lung an atelectasis was observed after resorption of the extravasate. To determine whether changes in osmiophilic lamellated bodies (OLB) precede and perhaps cause the atelectasis the upper lobe of the right lung was in eight white Wistar-rats subjected to temporary ischemia of 10 minutes. The two axial diameters of the intracellular OLB and their precursors were measured on electron micrographs 10 minutes, 60 minutes, 1 day and 2 days after cessation of the ischemia. The mean diameters were compared by statistical methods. Already after 10 minutes the usual elliptic cut surfaces of OLB were found to be more circular presumably because of swelling caused by an osmotic insufficiency of their membranes. After 2 days, the mean diameter of OLB had doubled, while shape and structure stayed normal. At the same time, the small precursor stages were missing. Consequently, we assume that formation of new OLB--represented by small non-lamallated osmiophilic bodies--and the incorporation of lipids into existing lamellar bodies are processes independent of each other. After a short, temporary ischemia only the formation of new osmiophilic bodies seems to be interrupted and this is associated with a quick growth of existing OLB. However, apparently these cannot be excreted in due time. The result could be lack of surfactant, which would account for the postischemic atelectasis.