Abstract: In previous papers of this series (1—4) it has been shown that a variety of minor epidermal injuries may induce keratotic closure of the pore of the eccrine sweat gland. Such poral occlusion always results in anhidrosis of the affected glands. Although the capacity to form sweat is unchanged, any sweat secreted cannot escape to the skin surface. Actually it can be demonstrated that under these circumstances the entrapped sweat may rupture the sweat duct at various levels producing different clinical signs of sweat retention. It can he shown from physiologic and histologic studies that in the event of rupture, sweat continues to form and be absorbed at the site of vesiculation. However, in the absence of sweat duct rupture, it is not known whether or not the secretory tubules continue to function. One view is that sweating does continue and that the sweat is reabsorbed by the ductal epithelium or that it diffuses through the intraepidermal ductal segment. The other view holds that sweat formation is stopped by the increased intraluminal pressure. The present study, the fiuial in this series, was undertaken to determine the functional status of the eccrine sweat gland in the presence of poral blockage. Keratotic occlusion of the sweat pores was achieved by the application of aluminum chloride solution, the glands were stimulated and tubular glycogen levels were determined histochemically. In the presence of continued active secretion, the glycogen disappears from the gland (5).