Vitamin B12-binding substances elaborated by the mucous membrane of the stomach]

Accurate electrocardiographic diagnosis of myocardial ischemia or infarction is difficult in patients with the Wolff-Parkinson-White syndrome; however, myocardial ischemia may also have profound effects on the electrophysiologic characteristics of the bypass tract in these patients. Comparison of studies performed during and two months following an episode of significant myocardial ischemia demonstrated substantial prolongation of the refractoriness of the bypass tract during the period of ischemia. Bypass refractoriness was prolonged by 196 msec, yet atrioventricular nodal refractoriness was not significantly different from normal. These studies, therefore, suggest that, on occasion, the presence of acute myocardial ischemia may, in fact, obscure the electrocardiographic diagnosis of the Wolff-Parkinson-White syndrome.     

Myocardial distribution of antegrade cold crystalloid and tepid blood cardioplegia

BACKGROUND: Tepid blood (TB) cardioplegia combines the improved rheologic characteristics and the augmented oxygen and substrate delivery of blood cardioplegia with the advantages of moderate hypothermia. In addition, the intramyocardial distribution of continuous TB cardioplegia may also be better than intermittent cold crystalloid (CC) cardioplegia. We sought to compare the distribution of TB and CC cardioplegia at varying infusion pressures. METHODS: In situ, isolated canine hearts were randomized to antegrade, continuous TB (28 degrees C, n = 8) or intermittent CC (n = 8) cardioplegia infused at 50, 75, and 100 mm Hg. The regional distribution of cardioplegia at each pressure was measured by 15-microm colored microspheres. Cardioplegia distribution was measured from three areas each of the right ventricle (inflow, outflow, and apex) and the left ventricle (anterior, lateral, and posterior). Left ventricular samples were subdivided into subepicardial, midmyocardial, and subendocardial. RESULTS: Delivery of cardioplegia to all areas of the right and left ventricles showed a linear pressure-flow relationship over the range of pressures tested. Right ventricular distribution was two-thirds of that to the left ventricle, and left ventricular subepicardial distribution was approximately one half of subendocardial flow in both groups at all delivery pressures. However, the subendocardial to subepicardial ratio was significantly greater with TB cardioplegia than with CC cardioplegia. Transmural right ventricular cardioplegia flow was comparable in both groups. In contrast, left ventricular distribution of CC cardioplegia was greater than TB cardioplegia at all three pressures tested. CONCLUSIONS: The pressure-flow relationship in both CC and TB cardioplegia is linear in both the right and left ventricular myocardium over clinically applicable delivery pressures. The distribution of cardioplegia to the right ventricle is not altered by increased pressure.     

Isolation of eukaryotic ribosomal proteins. Purification and characterization of the 40 S ribosomal subunit proteins Sa, Sc, S3a, S3b, S5', S9, S10, S11, S12, S14, S15, S15', S16, S17, S18, S19, S20, S21, S26, S27', and S29

The proteins of the small subunit of rat liver ribosomes were separated into five main groups by stepwise elution from carboxymethylcellulose with LiCl at pH 6.5. Twenty-one proteins (Sa, Sc, S3a, S3b, S5', S9, S10, S11, S12, S14, S15, S15', S16, S17, S18, S19, S20, S21, S26, S27', and S29) were isolated from three groups (A40, C40, and D40) by ion exchange chromatography on DEAE-cellulose, carboxymethylcellulose, and phosphocellulose and by filtration through Sephadex. The amount of protein obtained varied from 0.1 to 11 mg. Six of the proteins (S5', S10, S11, S18, S19, and S27') had no detectable contamination; the impurities in the others were no greater than 9%. The molecular weight of the proteins was estimated by polyacrylamide gel electrophoresis in sodium dodecyl sulfate; the amino acid composition was determined.