Intravenous injection in wound shock : being the Oliver-Sharpey lectures delivered before the Royal College of Physicians of London in May 1918 . hin. Here again we are dealing witha concentration far beyond those possible in theblood. The mechanism of oxidation in cells isobscure, and it is clear that lactic acid is rapidlyoxidised by the muscle cells in an acid medium,provided that oxygen is supplied in due amount. Diabetes.—Hasselbalch showed (1912) that, inthe so-called acidosis of carbohydrate starvation,the hydrogen-ion concentration of the blood remainsunaltered. Any increase of acid ci
Intravenous injection in wound shock : being the Oliver-Sharpey lectures delivered before the Royal College of Physicians of London in May 1918 . hin. Here again we are dealing witha concentration far beyond those possible in theblood. The mechanism of oxidation in cells isobscure, and it is clear that lactic acid is rapidlyoxidised by the muscle cells in an acid medium,provided that oxygen is supplied in due amount. Diabetes.—Hasselbalch showed (1912) that, inthe so-called acidosis of carbohydrate starvation,the hydrogen-ion concentration of the blood remainsunaltered. Any increase of acid circulating in theblood is compensated for by a diminution in thecarbon dioxide content. Although there is frequently a low value ofbicarbonate, there is a normal blood pressure andthe condition has no resemblance to that of (1915) has shown that in diabetic coma,although there is undoubtedly decrease of bicar- IN WOUND SHOCK 59 bonate (Stillman, Van Slyke, Cullen, and Fitz, 1917),there is no increase of hydrogen-ion case may be quoted : the alveolar carbon di-oxide tension was only 12 mm., indicating a very. Fig. 21.—Fall of Blood Pressure produced by Acid Injection. Decerebrate cat. 52 of half-normal hydrochloric acid per kilo hadbeen injected into a vein before the tracing begins. The secondary fall beganat a, half an hour after the acid had been given. The level b was reachedeighteen minutes later. At this time the bulbar centres were capable of reflexstimulation, so that it does not appear that intracranial haemorrhage had takenplace in consequence of the decerebration and affected their functions. Beforec, half an hour after b, a further small dose of acid had been given. 60 INTRAVENOUS INJECTION marked production of fixed acids, but it was lowenough to compensate and the hydrogen-ion con-centration was normal (7*33). Nevertheless, thepatient died in coma eighteen hours later. There-fore, the pathological symptoms must be due to some
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