The failure of wound healing in scurvy has long been recognized. Recently, many researchers have observed the influence of ascorbic acid upon the mucopolysaccharide formation in healing wounds. Penney and Balfour (1) found on the basis of metachromatic staining reaction that acid mucopolysaccharides did not appear in muscle wounds of scorbutic guinea pigs, whereas Bunting and White (2), using similar technique, concluded that mucopolysaccharides in skin wounds of scorbutic guinea pigs were more abundant than normal. Ludwig (3) found no difference in hexosamine content of the new connective tissue formed in exophthalmic guinea pigs induced experimentally in normal and scorbutic condition. Similarly, Kodicek and Loewi (4) found similar hexosamine content of repair tissues from tendons of normal and scorbutic guinea pigs, although the vitamin deficiency lowered the uptake of isotopically labelled inorganic sulfate by the tissues. On the other hand, higher content of hexosamine and more intensive polysaccharide staining than normal were reported by Persson (5) for scorbutic tissue preparations. Dunphy and Udupa (6) also reported an increased mucopolysaccharide content in granulation tissue from scorbutic animals. Gersh and Catchpole (7) examined the state of the f ibroblasts and ground substances from interscapular skin of scorbutic guinea pigs by the histochemical method. They observed an increased amount of water soluble glycoprotein and an increased number of enlarged fibroblasts containing greater numbers of glycoproteingranules. They attributed this alteration of ground substances to their depolymerization. Robertson and Hinds (8) similarly found that, in a granulomatous repair tissue induced in guinea pigs by the subcutaneous injection of a carrageenin suspension, the collagen-poor repair tissue under the ascorbic acid deficiency contained a little larger amount of hexosamine than normal. And then they separated mucopolysaccharides from the bulk of tissue protein and assayed them. The extracts from scorbutic tissue contained about 5 times as much mucopolysaccharide as normal. And they yielded fibrous precipitates, upon precipitation with ethanol, in contrast to the flocculent or finely amorphous precipitates obtained from normal repair tissue and showed higher viscosity than normal. The relative high viscosity of the polysaccharide solutions from ascorbic acid deficient animals and the fibrous nature of the precipitates were considered of a more highly polymerized compound, in disagreement with Gersh and Catchpole's view that ascorbic acid deficiency produces the depolymerization of connective tissue matrix. In their report, however, the concentration dependency of mucopolysaccharides upon the measured viscosity was not accounted. As shown above, in spite of many reports concerning the formation of mucopolysaccharides in connective tissue during ascorbic acid deficiency, a clear conclusion was not yet obtained. The present authors reexamined the Robertson and Hind's findings about the alginic acid-grranuloma.

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Since 1956, the mechanism of the reflex apnea caused by nicotine has been studied in our laboratory (Takasaki 1956., Takasaki et al., 1957., Nakano et al., 1957., Takasaki et a1., 1959 a, b, c), and it is likely that the receptors for the reflex may be in the lungs. On the other hand, for the purpose of confirming the site of receptors for the pulmonary reflexes, Bagoury et al. (1941) used the method of the section of the vagus trunk just above or below the hila of the lungs, and Dawes (1947), Aviado et al. (1950), Dawes et al. (1950) injected the drugs in the pulmonal artery. This experiment is attempted to confirm more obviously the site of the receptor of the nicotine apnea by using these methods.

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It has been reported that the apnea caused by nicotine may be due to the reflex from the receptors in the lungs and the afferent fiber pass through the vagus nerves (Takasaki, 1956., Takasaki et al. 1959 a, b). On the other hand, it has been well known that nicotine has a marked effect on the respiratory center and there is no evidence that the nicotine apnea is not connected with its effect on it also. This experiment was attempted to confirm the following two points : 1) This nicotine apnea has no connection with the respiratory center directly using the perfused isolated head technique. 2) The receptors responsible for the nicotine apnea are in the lungs using the lung perfusion's method.

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