Karl M. Bowman

Effect of Metrazol Convulsions on Brain Metabolism.

The wide use of metrazol in the treatment of schizophrenia has made it advisable to study the physiological changes produced by metrazol convulsions. 1 Twelve observations were made on 7 patients with schizophrenia. As seen in Table I, 7 samples of blood were collected from the femoral artery during various stages of the convulsions, 4 pairs of samples were collected simultaneously by 2 observers from the femoral artery and internal jugular vein immediately after the seizure had ceased, as was one additional sample of arterial blood. Breathing was greatly diminished during the convulsions and this was reflected in the analyses of the arterial blood, which disclosed a retention of CO2 as well as a diminished O2 content. Even during the first part of the seizure, as seen in Wi, 9/13, the O2 content was diminished so that the Hb saturation was reduced from a theoretical normal of 95% to 84%. As the convulsions progress, the Hb saturation continues to fall so that towards the end of the seizure the saturation of Hb may be below 50% (M., 9/7). During these convulsions the patients face is at first a dark red color. When the convulsion is completed, the anoxemia is evidenced by a leaden cyanosis, Neyertheless, as soon as unimpeded breathing is reëstablished the Hb saturation, though still reduced, is found rapidly rising towards a normal value (last 5 observations of Table I). The anoxemia, as well as the severe muscular effort, combine to increase blood lactic acid and blood sugar. These convulsions, grand mal in character, cause a temporary but marked depression of cerebral functions as evidenced by amnesia, confusion, disorientation, and the elicitation of various abnormal reflexes, such as the Babinski and ankle clonus.

The Sugar Tolerance of Alcoholic Patients

Summary and Conclusions The sugar tolerance was studied in a group of 18 alcoholic patients. On admission there was a marked diminution of the sugar tolerance, which improved after one week in the hospital on a normal diet. It is suggested that the diminished tolerance was due to an undernourished state previous to admission.

Changes in Cerebral Blood Flow and Arterio-Venous Oxygen Difference During Insulin Hypoglycemia.∗

Previous work has disclosed that the arterio-venous oxygen difference of cerebral blood is diminished during insulin hypogly-cemia. 1 , 2 However, the arterio-venous oxygen difference is determined not only by the metabolic rate of the brain, but also by velocity of blood flow. Therefore, thd possibility exists that the smaller oxygen difference found may be due to a more rapid blood flow during hypoglycemia. Observations by Loman and Myerson 3 on human subjects and Leibel and Hall 4 on rabbits, have failed to demonstrate any marked changes in the rate of cerebral blood flow during insulin hypoglycemia uncomplicated by convulsions. However, for conclusive information regarding changes of brain metabolism, it is necessary to determine, simultaneously, the cerebral blood flow and the arterio-venous oxygen difference. The results of such a study on patients with schizophrenia are presented in this preliminary report. Methods for the collection and analysis of the blood samples have been previously described. 2 The rate of blood flow in the internal jugular vein was estimated by a modification of the Gibbs thermostromuhr. This instrument proved to be at least as sensitive as the original and will be described elsewhere. Observations on the blood flow were made over long periods during which the position of the thermostromuhr in the vein was maintained constant. A special technique was devised which prevented error resulting from the formation of clots on the needle. In 5 cases the blood flow and the arterio-venous differences were determined before injection of insulin as well as throughout the course of the coma and the subsequent administration of glucose. In 3 other instances the observations were begun during coma and continued until after arousal with intravenous glucose.

The Effect of Glucose on the Oxidation of Alcohol in vitro

The metabolism of alcohol has been the subject of numerous recent publications in which it has been suggested that the oxidation of alcohol may be catalyzed by the simultaneous oxidation of carbohydrate. The ingestion of food (Southgate 1 ) or glucose (Bornstein and Loewy 2 ) along with alcohol resulted in a lower blood concentration of alcohol. Carpenter and Lee 3 found that after the ingestion of glucose or fructose with alcohol, the alcohol was present in the expired air for a shorter period. Clark and Morrissey 4 measured the rate of disappearance of alcohol from the blood of dogs given doses of 3 g per kilo. They found that the administration of insulin and glucose accelerated the disappearance of alcohol. More recently Clark, Morrissey and Fazekas 5 have shown that the liver of depancreatized cats could not oxidize alcohol in the Warburg apparatus. In this respect the metabolism of alcohol in the body resembles that of the acetone substances. Shaffer 6 showed that the oxidation of acetoacetic acid in alkaline solution by hydrogen peroxide was accelerated when glucose was simultaneously oxidized. We are here reporting similar experiments on the effect of glucose on the in vitro oxidation of alcohol. The control solution contained 100 mg % of alcohol, 20 milli-equivalents percent of hydrogen peroxide, 1% sodium hydroxide, and 1 mg % ferric ammonium citrate. The experimental solution contained 1% glucose in addition. The reaction was studied at 25°C Alcohol analyses were made at various intervals during the following 24 hours by the macro-method of Abels. 7 The accuracy of the method was estimated from a series of analyses of 39 known solutions ranging from 30 to 110 mg % in which the average error was 5.1 mg %. In 34 instances the error was less than 10 mg %, while in the remaining 5 it was 15 mg %.