The alkali tolerance of the dog heart

The alkali tolerance of the dog heart

SELECTED Batt, R. C.: Radiology A Roentgenkymographic 46:374, 1947. 461 ABSTRACTS Study of the Heart in Myasthenia Gravis. Early kymograp...

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SELECTED

Batt,

R. C.: Radiology

A Roentgenkymographic 46:374, 1947.

461

ABSTRACTS

Study

of

the

Heart

in

Myasthenia

Gravis.

Early kymographic studies of myasthenic patients showed a slight slowing of the pulse with minor but definite changes in the wave form along the left ventricular border after a test dose of prostigmine. Similar kymographic changes could be obtained in normal subjects used as a conThere trol; thus indicating that the changes were due to the pharmacologic effects of prostigmine. were, however, wave form changes which at first could not be accounted for. It is well known that any change in the ratio between the grid speed and the heart rate will affect the appearance Patients with myasthenia gravis, as well as normal patients, were of the kymographic wave form, The results in all cases studied before and after prostigmine test doses with various grid speeds. were identical. This indicated that the major changes in shape of the kymographic wave produced by prostigmine represents artefacts due to the changing ratio between heart rate and grid speed. These studies showed that there are no characteristic findings in the cardiac roentgenkymoThe prostigmine test produces no characteristic grams of patients with myasthenia gravis. The test cardiac kymographic wave changes in either normal or myasthenia gravis patients. doses may slow the cardiac rate and thereby produce deceptive changes in wave form. ZION. l’erroux, K. Godwin, Gertler, M. M., and Hoff, Heart. Am. J. Physiol. 148:l (Jan.), 1947.

H. E.:

The

Alkali

Tolerance

of the

Dog

In determining the alkali tolerance of the dog heart in situ, twenty-four dogs were used by the authors, and these were infused with 0.3 normal sodium hydroxide in most cases. Blood samples were drawn from a femoral artery, as were the samples for lactate determinations. Electrocardiograms were taken from Lead II at intervals corresponding to 50 C.C. increments of infusion fluid. The results of the experiments fall into three groups. In Group I the dogs died in the initial stages of the experiment, either because of a high initial rate of alkali infusion or because of some Severe anoxia occurred in all these cases. In Group II the inindividual sensitivity to alkali. fusion rates were low and blood lactate did not rise above 100 mg. per cent. These hearts failed at pH values between 7.7 and 7.93. In Group III the overall injection rates were higher than in Group II. These animals showed rigor of the respiratory muscles, as well as of some other muscle groups, accompanied by an increase in the blood lactate level with values up to 200 mg. per cent. The blood pH rose as high as 8.12 to 8.40 before heart failure. Blood pressure was well maintained until the final failure of the heart. In the electrocardio&am, the most interesting changes were in the T wave which became lower in amplitude as the pH rose, with complete reversal of polarity either before or at the time of the first maximum pH. RS-T segment depressions were observed just before heart failure occurred, indicating that this was significant of impending trouble. The R wave changed only in the final stages. Heart rate was essentially unchanged. Intraventricular conduction time was unchanged. Auriculoventricular conduction time was increased in four experiments, decreased in six, and unchanged in five. The value of K in Bazett’s formula was unchanged in three experiments, decreased in five, and increased in eight. There was no change in respiratory movements until the pH rose above 7.8. The mode of death was ventricular fibrillation or failure of myocardial contractility. The phenomenon of cardiac action currents stimulating somatic nerves was found in three cases. BERNSTEIN.

Wilens, S. L.: Med. 79:129

Bearing (Feb.),

of 1947.

General

Nutritional

State

on

Atherosclerosis.

Arch.

Int.

The author points out that in spite of various reports, such as those of French and Dock that overweight and atherosclerosis are definitely connected, other equally definite statements, such as that of Weiss and Minot in 1933, and of Wright in 1943, lead one to believe that “there is no proof that overnutrition leads to atherosclerosis in man.”