The Value of Alkali in Salicylate Therapy

Morris, Noah; Graham, Stanley

doi:10.1136/adc.6.35.273

Cited by 22 publications

(11 citation statements)

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“…Most observers agree that salicylate causes hyperventilation and a reduction in the carbon dioxide content of the blood. There has been great controversy, with many conflicting reports on the interpretatioa of these findings: whether salicylate causes a primary respiratory alkalosis or a metabolic acidosis with secondary hyperventilation (Johnson, 1930;Morris and Graham, 1931 ;Rapoport and Guest, 1945;Reid, Watson, and Sproull, 1950).…”

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Respiratory Effects of Salicylate

Cochran¹

1952

BMJ

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although only 9 of their-40 reported cases would have been included in our group. Of the 14 deaths three were from causes other than asphyxia, and two more-a therapeutic abortion and another with a gross congenital abnormality-would very probably have occurred whatever methods were employed. Of the remaining nine fatal cases, seven responded initially to insufflation, although they died later after periods ranging from five hours to four days with varying degrees of atelectasis and evidence of amniotic aspiration. Of the two who failed to respond, one was a very small premature infant and the other was the only case to show a mild degree of subpleural emphysema.We have in addition tried to obtain information on precisely how insufflation may modify the physical state of the lungs. The rapid oxygenation of the asphyxiated, as shown by skin colour, the movement -of the chest wall, and the showers of fine crepitations on auscultation at each insufflation, suggested that the alveoli themselves were being expanded. Unfortunately, we were not able to obtain any radiographic records in the labour wards; a number of photographs, however, were obtained very shortly after death. Two of these are shown (Figs. 1 and 2 In all these there was a transient recovery, as evinced by a risin pus rat an imroe coou Lieneesee tobe prlne mor tha a fe hor an the maiua tions of inserting the tube and changing it when blocked with mucus were badly tolerated. Extensive atelectasis without emphysema was revealed in all cases at necropsy. This infornmation, together with that from the post-mortem reports of babies dying of asphyxia, suggests that endotracheal insufflation with the pressures we have used does not to any perceptible degree facilitate the permanent expansion of the atelectatic lung in the newborn, although it may do so in some dead or stillborn infants, especially if fullterm. A satisfactory degree of oxygenation of the blood and tissues can, however, be produced almost immediately.Finally, we would stress the desirability of an established routine in the treatment of asphyxiated infants. For convenience this may be primarily but not exclusively the responsibility of the anaesthetist, the obstetrician, or the paediatrician. To ensure prompt action in the unexpected emergency all should be proficient in the' technique employed.ConclusionsThe administration of oxygen under intermittent positive pressure of up to +20 cm. of water by endotracheal tube is, in experienced hands, a safe, quick, simple, and efficient treatment for severe cases of asphyxia neonatorum.This procedure, though momentarily expanding the alveoli, does not appear permanently to modify the physical state of the unexpanded newborn lung.

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Respiratory Effects of Salicylate

Cochran¹

1952

BMJ

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“…However, it had previously been reported that salicylate caused hyperglycaemia in the dog (Barbour and Herrmann, 1921) and in man (Morris and Graham, 1931).…”

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The Glycogenolytic Action of Sodium Salicylate

Sproull¹

1954

British Journal of Pharmacology and Chemotherapy

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Salicylate, in the form of salts of salicylic acid and of its acetyl derivative, has been used in the treatment of rheumatic fever for many years, and in one form or another it is probably the most widely used of household remedies ; yet our knowledge of its pharmacology remains deficient. This is not from lack of interest in the salicylates, for Gross and Greenberg (1948) have recently listed over 4,000 relevant publications. However, the literature does not afford a clear conception of the relation between the numerous established actions of the drug; it is not even certain which actions are of therapeutic importance and which are purely side-effects. It seemed worth while, therefore, to look into some of the less obvious actions of salicylate. Of these perhaps the most striking is that observed by Lutwak-Mann (1942), that the administration of sodium salicylate caused almost complete disappearance of liver glycogen in the rat; she concluded that this was evidence of interference with enzymatic processes by salicylate.Such an action might be of therapeutic importance, but it would be hazardous to draw this inference from Lutwak-Mann's (1942) data, because large doses of salicylate were used, and because the mortality resulting from such doses made it impracticable to employ fasted animals, so that only fed rats with initially high liver glycogen concentrations were studied.The primary aim of the present investigation was to re-examine the effect of salicylate on liver glycogen, to see whether the effect occurred at dosage levels more comparable with those used therapeutically, and to determine if it occurred in fasted as well as in recently fed animals.The blood sugar was also estimated, since hyperglycaemia might accompany the expected glycogenolysis, although no related change in blood sugar concentration was found by Lutwak-Mann (1942). However, it had previously been reported that salicylate caused hyperglycaemia in the dog (Barbour and Herrmann, 1921) and in man (Morris and Graham, 1931). METHODSSwiss albino mice aged 3-to 5 months were used.Glycogen was estimated, after hydrolysis by the method of Good et al. (1933), by ceric sulphate titration (Miller and van Slyke, 1936); blood sugar was determined by the method of Miller and van Slyke (1936).The mice were dealt with in batches of 9-12 of the same sex per day; two days before use they were given white bread in addition to the usual diet of rat cake. Two series of experiments were performed: in the first food was given until the beginning of the experiment; in the second all food was withdrawn 18 hr. previously.The mice were paired off for weight. One of each pair was given an intraperitoneal injection of 10 mg. sodium salicylate in 0.05 ml. water; the other, control, animal received an intraperitoneal injection of 0.05 ml. normal saline. They were killed by a blow on the head at 1, 2, or 4 hr. after injection, and in each series an untreated group was killed at zero hr. 0.2 ml. blood for the estimation of glucose was obtained, after decapitation, fro...

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“…Sodium bicarbonate appeared to hasten the recovery from the intoxication, the dogs appearing normal within 24 hours after the administration of salicylates while untreated control animals appeared ill for 2 additional days. Sodium bicarbonate may exert its beneficial effect on the duration of the intoxication by causing increased urinary elimination of salicylate (8). The occurrence of tetany after the injection of sodium bicarbonate appears hardly surprising in view of the extent of the elevation of the pH produced.…”

Section: Effect Of Sodium Bicarbonate In Salicylismmentioning

confidence: 99%

“…Since sodium bicarbonate has been thought to ameliorate the toxic effects of salicylates (8,12,18), it appeared of interest to study its effect on the ionic structure of the blood in salicylism. In Figure 7 are presented the data on 1 dog who received 0.6 gram per kgm.…”

Section: Effect Of Sodium Bicarbonate In Salicylismmentioning

confidence: 99%

“…The significance of this observation appears uncertain, since the increases varied widely, and the muscular effort involved in hyperventilation may have accounted for them. A renal mechanism for the metabolic acidosis has been suggested (7,8) but the rapidity of the onset of the hyperpnea and the inconstancy and mildness of the renal changes appear difficult to reconcile with such an hypothesis. Another group of observers has favored the 1 A preliminary report was presented before the American Pediatric Society, May 1, 1942 view that the hyperpnea is of central origin and that changes in the blood are secondary.…”

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