Paralytic Secretion 1 1 3 



constantly going on as generally assumed, but appears only under 

 certain conditions which involve a sympathetic hyperactivity, and 

 particularly an increased liberation of the hormones of the adrenal 

 medulla (Emmelin and Muren, 1950a and 195 ib\ Emmelin, 1952a 

 and b). Hence, two conditions have to be fulfilled for the paralytic 

 secretion to appear: there must be a pronounced supersensitivity 

 of the gland cells, and a considerable release of adrenaline and 

 noradrenaline. The paralytic secretion would thus have the same 

 mechanism as "paradoxical pupillary dilation" and be related to 

 "pseudomotor contractures". This theory is based on the following 

 facts : 



1. A pronounced supersensitivity is required. There is no para- 

 lytic secretion when removal of the superior cervical ganglion has 

 created its fairly modest degree of supersensitivity. In animals 

 in which section of the chorda causes a moderate sensitization 

 only, the paralytic secretion is slow. No secretion is obtained until 

 the sensitization is discernible, i.e. two or three days after cutting 

 the chorda ; the rate of flow then increases with the level of sensi- 

 tivity, to reach its maximum after two or three weeks. If the 

 chorda supersensitivity is further raised by removal of the superior 

 cervical ganglion or acute injection of cocaine, the paralytic flow 

 increases. In a normally innervated gland, treated for some time 

 with a parasympathicolytic agent, a rapid paralytic secretion can 

 be elicited; it can further be accelerated by the injection of cocaine. 

 If the hypersensitivity of a gland, the chorda of which has been 

 cut in advance, is abolished by treatment for some days with 

 pilocarpine, no paralytic secretion can be evoked. 



2. Adrenaline and noradrenaline from the suprarenals cause the 

 paralytic secretion. No secretion is obtained unless the release of 

 the hormones is greatly increased. Therefore, paralytic secretion 

 is not seen in chloralose anaesthesia. It is found, however, in 

 morphine anaesthesia, which is known to increase the output from 

 the suprarenals. This explains why early investigators, such as 

 Heidenhain, Bidder, and Langley, who used morphine, observed 

 a paralytic secretion whereas later workers, studying the dener- 

 vated submaxillary gland using modern anaesthetics, do not men- 

 tion a paralytic flow. The denervated parotid gland, which is rela- 

 tively insensitive to adrenaline, shows no paralytic secretion; the 

 denervated submaxillary and sublingual glands, highly sensitive to 

 adrenaline, do. Removal of the suprarenals abolishes the paralytic 



P.S.G. — I 



