Soma Weiss

Electrocardiographic manifestations and the cardiac effect of drugs in vitamin B1 deficiency in rats

Abstract 1. 1. An analysis has been made of the cardiac rate, electrocardiographic complexes, and the response to drugs of rats in the nondeficient state and in repeatedly induced vitamin B 1 deficiency. 2. 2. The heart rate of rats on a diet deficient in vitamin B 1 fell gradually to a level of from 350 to 300 beats per minute, from which it could usually be returned to approximately the normal level (450 to 500) within a few hours by adequate doses of crystalline vitamin B 1 , even if food was withheld. 3. 3. In all but four or five of the 22 vitamin-deficient rats studied, the decrease in heart rate was accompanied by changes in the electrocardiographic complexes, consisting most frequently of an increase in height, flattening, inversion, or high or low take-off of the T-waves and depression of the S-T segment. With the doses of vitamin B 1 used the T-waves usually returned to normal within from several hours to a day, although occasionally several days were required. The changes in the electrocardiographic complexes had no close relation to the level of the heart rate, and were not identical in the same animals on successive deficiencies. 4. 4. With the exception of very low cardiac rates the P-R interval remained essentially unchanged. The ratio of the Q-T interval to the square root of the R-R interval (K) usually did not increase as the cardiac rate decreased. 5. 5. Only one of four rats which were allowed to exercise on running wheels became deficient sooner than other vitamin-deficient animals. In none of the four exercising rats were the cardiac changes more marked or of different character than those found in the control vitamin-deficient rats. 6. 6. The cardiac responses of normal and vitamin-deficient rats to epinephrine were essentially the same. Occasional irregularities were observed in the vitamin-deficient animals. 7. 7. Atropine and section of the vagus nerves did not abolish the cardiac slowing or the electrocardiographic changes produced by vitamin B 1 deficiency. 8. 8. The vitamin-deficient rats were more sensitive to the toxic effects of subcutaneous doses of strophanthin, and depression of the S-T or inversion of the T-wave supervened with doses which caused no change in normal rats.

The age and sex incidence of arterial hypertension

It has often been stated that essential hypertension† is found most frequently among middle-aged and pre-elderly individuals. In only a few instances, however, have the statements been accompanied by statistics. Similarly, although the condition has been said to be more common among men than among women, the basis for establishing this as a fact has not been presented. There are few data available that concern directly either the age or the sex incidence of hypertension. However, a number of contributions appear in the literature, which contain reference to the ages of patients who were presented as illustrations of various aspects of hypertension or sphygmomanometry. Tables I-A-I-E compare the results of some of these investigations calculated and arranged according to the percentage of patients in different age periods. These reports have been separated into four groups as follows: A, hypertension as found in different periods of life; B, age of patients with hypertension at time of death; C, life insurance statistics; D, E, hospital reports. This classification is necessary for a discussion of the age incidence of hypertension because each group possesses characteristics which make it difficult to compare one group with another.

Bisulphite Binding Substances in the Blood in Health and in Disease, Particularly Vitamin B1 Deficiency

Bisulphite binding substances (B.B.S.) in the blood have been reported increased in vitamin B1 deficiencies both in experimental animals 1 and in clinical “wet beriberi”. 2 The present study of the B.B.S. in the blood was undertaken to determine its value in distinguishing vitamin B1 deficiencies from other disease states. Oxalated blood samples were taken fasting and at rest from 30 healthy controls, and from 110 patients. The method of Clift and Cook 3 was modified to adapt its use to trichloracetic acid filtrates of whole blood. Five milliliters of oxalated blood were precipitated with 20 ml. of 10% trichloracetic acid, allowed to stand 30 minutes and centrifuged. Five milliliter aliquots of the supernatant liquid were adjusted to pH 2 by the addition of 1.5 ml. of normal sodium hydroxide and allowed to react with 0.2 ml. of saturated sodium bisulphite solution for 15 minutes. Twenty-five milliliters of distilled water and 2 ml. of fresh starch solution were added and the excess of bisulphite titrated out with normal and N/10 iodine solutions adjusting the end point with N/200 iodine solution and N/100 sodium thiosulphate solution. The bound bisulphite was released by the addition of 2 gm. of solid disodium phosphate (Na2HPO4· 12 H2O) and titrated within 5 minutes with N/200 iodine solution. The values were expressed in milligrams of pyruvic acid per 100 ml. of blood, using the expression: 1 ml. N/200 iodine = 0.22 mg. pyruvic acid. In most cases the non-protein nitrogen, the plasma carbon dioxide capacity and blood sugar were measured on the same samples. In a smaller group the urine was tested for sugar, acetone, acetoacetic acid and pyruvic acid. Results. Thirty normal subjects had values for B.B.S. in the blood ranging between 3.66 and 5.75 mg. with an average of 4.74 mg. per 100 ml. Values for B.B.S. above 6.0 mg. are accepted as elevated. Normal values were found in the following conditions: arteriosclerosis, compensated heart disease, carcinomatosis, glomerulonephritis, hepatitis with jaundice, severe anemia, toxemia of pregnancy, acute alcoholism, chronic alcoholism without vitamin deficiency, chronic alcoholism with vitamin (B1) deficiency after treatment.

Relationship of Pyruvic Acid to the Bisulphite Binding Substances of the Blood

Increases in the bisulphite binding substances (B.B.S.) of the blood have been related to increases in pyruvic acid, both in beriberi 1 and following exhaustive exercise. 2 The B.B.S. has been shown to be elevated in beriberi 1 and other disease states, 3 and also following the injection of sodium pyruvate. 4 The present communication gives a brief résumé of the relationship of the B.B.S. to the blood pyruvic acid. Pyruvic acid was estimated in blood by Peters and Thompsons modification of the Neuberg-Case method, 5 B.B.S. by a modification 3 of the Clift and Cook procedure. 6 The methods used for selection of clinical material 3 and for administering sodium pyruvate 4 are given elsewhere. From pure aqueous solutions of lithium pyruvate an average of 85.7% of the theoretical amount of pyruvic acid as B.B.S. and 85.6% as pyruvic acid by the hydrazone method were recovered. The recovery of lithium pyruvate from blood, when added in amounts ranging between 10 and 20 mg. per 100 ml. of blood, averaged 90.4% of theoretical by the B.B.S. method and 79.9% by the hydrazone method. These values were obtained when the blood proteins were precipitated immediately after the addition of the pyruvate. Thirteen subjects having a B.R.S. in the range previously accepted as normal 3 had blood pyruvic acid values between 0.19 and 0.79 mg. per 100 ml. Three patients with nutritional deficiency and with B.B.S. values of 6.6, 9.6, and 13.8, calculated as pyruvic acid in milligrams of pyruvic acid per 100 ml. of Mood, had pyruvic acid values by the hydrazone method of 0.73, 10.46, and 0.72 mg. per 100 ml., respectively. In both normal subjects and those with elevated B.B.S. there was a much greater increase in B.B.S. than could be accounted for on the basis of the amount of pyruvic acid present.

The velocity of venous blood to the right heart in man.

Our previous studies have shown the feasibility of measuring the velocity of blood flow in health and disease by injecting the active deposit of radium into one of the antecubital veins, and determining the time of arrival of the active deposit in the arterial vessels about the elbow of the other arm. The path of the active deposit coursing through the body necessarily included the veins of the arm, the pulmonary circulation, and the artery of the other arm. The velocity measured was a somewhat complex expression, therefore, of the peripheral as well as of the central blood flow. This report deals with an attempt to determine the separate velocities along these paths. A detecting device was placed in a lead block. This block had a hole 5 cm. in diameter bored through its center. The radiations of radium C as it was injected into the veins and as it flowed towards the right heart could not penetrate the lead block and could therefore set up no disturbance in the detecting device. The hole of the lead block with the detector set into it, was placed over the right heart. When the active deposit reached the right heart, the emergent radiations easily traversed the air and tissues between the right heart and the detector, and set up characteristic disturbances in the detecting device. These disturbances were amplified by three electrode vacuum tubes, and were finally registered automatically by a recording pen galvanometer. Knowing the time of injection of the active deposit and knowing the time of its arrival into the right heart, we have a measure of the velocity of the venous blood flow. Figure I is the record of a typical determination.