Secretion by the parotid gland of the sheep has been studied in acute preparations and by means of fistulae. The sheep is unusual in having a continuous flow of parotid saliva which increases in amount both with feeding and with cud chewing (Ellenberger & Hofmeister, 1887). As in the ox its parasympathetic nerve supply arrives via the buccal branch of the mandibular nerve as fine branches which go from the anterior border of the masseter muscle with the duct to the gland (Moussu, 1888(Moussu, , 1890, not via the auriculo-temporal nerve. Moussu demonstrated that after section of this nerve the gland continued to secrete and he attributed this continued secretion to a non-nervous mechanism postulated by Colin (1886). Eckhard (1893) who in 1867 (Eckhard, 1867), before Moussu's discovery, had convinced himself that there was no secretomotor nerve to the gland, held the view that it was due to the 'nature' of the gland.Eckhard (1893), after amplifying these observations and confirming Moussu's observation that stimulating the buccal branch of the mandibular nerve (henceforth referred to as Moussu's nerve) increased secretion, nevertheless stated that section of the nerve did not cause any reduction in the rapidity of secretion by the gland. This view has not been refuted, and is often quoted with the reservation that it requires confirmation (Langley, 1898, in Schafer's Physiology text-book; Babkin, 1944). It is associated with statements that salivary secretion in the ruminant is not stopped by atropine. However, the reduction by atropine of normal secretion to a lower rate is recognized by Babichev, Perstnov & Kulesco (1930) as indicating a biphasic secretomotor mechanism. In this paper we have endeavoured to establish with certainty the effect of the parasympathetic nerve on the gland.Another controversial matter is the effect of stimulation of the sympathetic fibre', to the parotid upon its secretory activity. Eckhard (1869) attacked the
A clinical case of linoleic acid deficiency has been investigated because of the unknown effect in an adult man. The patient had had all but 60 cm of his small intestine removed and was maintained solely by intravenous therapy for 100 days, without fat. At this stage there was no clinical evidence of malnutrition, but his serum phospholipids were found to contain 10% 5,8,11 eicosatrienoic acid and he developed a skin rash. A soybean fat emulsion containing 86 g/l of linoleic acid was given intravenously for 12 days, discontinued for 43 days and then resumed. During each period of fat administration (linoleic acid intake 22.8 g/day) the serum phospholipid content of eicosatrienoic acid fell and arachidonic acid rose. Simultaneously the serum triglycerides fell to normal, the proportions of the triglycerides carried by the lipoproteins (d < 1.006) rose to normal and the rash disappeared. A second case of linoleic acid deficiency, in this instance associated with severe malnutrition, was investigated and here also a high level of plasma triglycerides was mostly associated with lipoproteins with d < 1.006. In an attempt to estimate his minimal daily requirements, feeding 7.5 g/day of linoleic acid in this form did not eliminate the eicosatrienoic acid, but instead allowed a small increase. It is concluded that adult man requires at least 7.5 g/day of linoleic acid and that the proportion of the triglycerides carried by the very low density lipoproteins is lowered in the absence of linoleic acid.
Alterations in the concentrations of sodium and potassium in saliva have been extensively studied and related to the external balance of these ions, and to the level of function of the adrenal cortex. Rather less interest has been shown, however, in the relationship between these concentrations and the degree of activity of the salivary glands manifested by altering rates of flow, and in factors influencing the salivary concentration of anions. Heidenhain (1878) showed an increase in the salt content of dogs' submaxillary saliva from 0-19 to 0-50% associated with an increase in flow from 0419 to 1V37
THE management of a patient with acute tetraplegia is beset with many different problems. The problems may be divided into those associated with the injury to the spine and spinal cord, those associated with other common complications such as head, chest and limb injuries, and those associated with the respiratory and metabolic consequences of this type of injury. The term injury includes not only the accidental trauma but also, where necessary, subsequent operative treatment, with or without general anaesthesia. On occasions there may be days or even weeks between these components of the 'injury'. In a previous paper (Cheshire, 1964) a broad plan for respiratory assessment and management was suggested, and while the hypoventilation syndrome, the management of a tracheostomy and the effects of body temperature on the oxygen requirements of the tetraplegic patient will be discussed in this paper, its primary purpose is to present the special metabolic problems of the acute tetraplegic and to propose a regime for the coordinated treatment of respiratory and metabolic states. I Since Volume (Yrs) Lesion Accident Capacity (Months) (ml) (ml) l. (G. B.) 21 Complete below C6 3 310 2200 , 2. (B.R.) 27 Complete below C6 3 460 2000 3. (D. C.) 14 Complete below C6 4 445 2000 4. (A.M.) 19 Complete below C5 23 500 1950 5. (B. P.) 28 Complete below C5 33 530 3000 6. (B. S.) 29 Complete below C5 38 250 1500 7. (A. P) 46 Complete below C6 39 470 1550 8.
In a previous publication (Harris, McDonald, Munro and Williams, 1952) changes were described in the extracellular electrolyte pattern, blood and extracellular fluid volumes, and muscle composition of sheep, following bilateral ureteric ligation.It was noted that the extracellular fluid volume as measured by the diffusion space of inulin fell progressively. A possibility existed that the fall in inulin space did not necessarily reflect a fall in extracellular volume, because inulin may have been concentrated in the renal pelves (i.e., outside the extracellular compartment) when it was injected immediately after ureteric ligation. This would have given a falsely high value for the initial extracellular volume determination. In fact, these initial volumes were in the range of 25-30 p.c. of body weight, whereas the average value for normal sheep is 16-18 p.c. of body weight. Partly for this reason, the investigation was repeated, anuria being produced by bilateral nephrectomy, instead of by ureteric ligation. By this change in technique the possibility of inulin being concentrated outside the extracellular compartment in this way was avoided. Another reason for repeating the investigation with nephrectomizcd animals was because of the claims by IMendoza, Diaz and Linazasoro (1950) and Diaz and Mendoza (1952) that the biocliemical changes and clinical course of nephrectoiiiized dogs differed from those of animals with ligated ureters. Tliese authors claimed that the presence of renal tissue in the body considerably modified the effects of anuria. Thus it was of interest to see whether similar considerations applied to the sheep. EXPERIMENTAL METHODS.Cro99-bred wethera were used, weighinpr between 24 and 40 kg. The animals were anaesthetized with "Nembutftl" administered intravenously (30 mg./kg, body weight), and the kidneys were removed through loin incd.sions. Both kidneys were removed at the one operation in two animnls, and ia the other four the second kidney wns removed one week after the first.Blood for analysis was taken daily, and ioulin, thiocyanate and antipyrine space determinations were made at intervals of 2-3 daya.'This work was carried out witb the asaistance of grants from the Wool Researfh Fund, The Rural Credits Development Fund and the National Health and Medical Research Council.
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