Knowledge of the rate of sedimentation of the red blood corpuscles is now generally considered a valuable aid in determining the presence or absence of infection or of tissue damage in the body.2 The test is also of prognostic value and can serve as an index of the relative severity of infection and tissue damage.Obviously the value of the test rests on the assumption that the only factors which affect the rate of settling are directly dependent on the severity of infection or tissue damage. Rourke and Plass (1) have shown that, to obtain a reliable measurement of sedimentation rate, heparin should be used as the anticoagulant, venous stasis should be avoided in collecting the blood, the test should be completed on the day the blood is drawn, and the room temperature during the measurement should remain between 200 and 25°C. These investigators also demonstrated that, all other factors being equal, the rate of settling bears an inverse proportion to the volume percentage of red blood cells; the fewer the red blood cells in a given specimen, the faster the sedimentation rate. If heparinized normal blood is prepared so that the cell volume is only 30 per cent, the sedimentation rate will be as rapid as that of blood from a patient with pronounced infection but with no anemia.
Several observers have directed attention to the fact that insulin hypoglycemia may precipitate symptoms and signs of serious disturbance in the cardiovascular system. Gigon (1), in 1923, reported that a patient with diabetes mellitus had died from myocardial failure after the third dose of insulin. Reinwein (2) observed two patients with diabetes mellitus and circulatory insufficiency in whom the administration of insulin caused a decided increase in the degree of congestive failure. Joslin (3) and Blotner (4) reported cases in which cardiac infarction developed shortly after the administration of insulin, and von Noorden and Isaac (5) observed several patients with coronary artery disease in whom insulin hypoglycemia apparently was the cause of death. Several instances have been recorded in which insulin hypoglycemia precipitated typical attacks of angina pectoris (6,7,8).Further evidence of altered cardiac physiology during insulin hypoglycemia is afforded by the electrocardiographic studies of Middleton and Oatway (9) and others. The changes observed consisted of diminished amplitude or inversion of the T-wave.Although the effect of insulin shock on the pulse rate and arterial blood pressure of man has been studied by several investigators (10,11,12,13), but little attention has been paid to the effect of the hypoglycemic state on the minute volume output of the heart. In the only reported measurements, Lauter and Baumann (13)
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