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The anatomy of the coronary circulation was correlated with left ventricular segmental contractile motion in 162 patients: 43 with normal coronary arteriograms, 119 with significant (> 75%) obstruction of the right coronary artery and/or left anterior descending coronary artery. Collateral vessels were identified in 69% of the patients with coronary artery disease (82/119). The cases with collaterals were graded poor, fair, or good according to the number of vessels and the quality of opacification. Segmental contractile motion was determined angiographically by the percent shortening of each of the six chords of the left ventricle in the right anterior oblique projection. The range of normal shortening (mean ± one standard deviation) for each chord was established in the 43 normal patients as follows: [See Equation in PDF File] Patients were grouped according to the site of coronary artery obstruction and quality of collateral circulation to the area supplied by the obstructed coronary artery. The percent shortening and number of abnormal segments were determined for each patient; there was no consistent difference in segmental contraction between patients with and without collaterals. The quality of collateral vessels did not correlate with either the number of abnormal segments or the percent of chord shortening. In summary, the development of collateral vessels is not associated with the restoration of normal segmental wall motion in patients with coronary artery disease.

Temporal variation in perfusion to small segments of the myocardium was studied in 19 opened-chest dogs. In six control dogs, three or four differently labeled 7-10 mu microspheres were injected simultaneously into the left atrium to assess the variability in measured myocardial perfusion due to the microsphere technique. In 13 other dogs, microspheres were injected four times at 5 minute intervals while various hemodynamics parameters (mean aortic pressure, peak systolic pressure, heart rate, left ventricular end-diastolic pressure, and Vmax) were stable (less than 10% variation in any one parameter). The left ventricles were divided into 96 segments, the mean weight+/- SD of each segment was 0.95+/-0.17 grams. The flow to each segment was expressed as a percent of the mean flow of the three or four measured flows to that segment, and the difference between the largest and the smallest percent of each segment was taken as a measure of the variability of flow to that segment. The average variability of segmental flow (mean +/-SD) when the three to four differently labeled microspheres were injected was 14.0+/-4.7; and the variability when differently labeled microspheres injected sequentially was 31.0+/-10.8% (P less than 0.001). Furthermore, in the sequentially injected animals the magnitude of temporal variation was similar in various subdivisions of the ventricle (layers, walls, apex to base). The mean and standard deviation of the variability of flow to the endo, mid, and epicardial layers were 28.7+/-10.2, 30.0+/-11.3 and 34.5+/-12.4%, respectively. These changes may reflect either spontaneous or local autoregulatory changes in precapillary sphincters or arterioles.

Measurements were made of water, Na, and K content of the albumin, yolk, subembryonic liquid, and whole blastula of the chick 24 hr after fertilization. The close similarity of cell Na and K concentrations to those of the subembryonic liquid (Na, 22:27; K, 24:31) and the absence of ouabain-inhibitable uptake of 42 K by the blastula suggested that cells and subembryonic liquid were in diffusion equilibrium. The loss of virtually all nonerythrocyte cells upon the transfer of the deembryonated blastula to a culture medium allows investigation for evidence of development of an Na:K pump in the erythrocyte. At 24 hr the cultured cells maintained cation gradients of 40:140 mequiv/liter for Na and 49:5 mequiv/liter for K. At 48 hr the figures were 33:140 mequiv/liter for Na and 58:5 mequiv/liter for K. The cells cultured for 24 hr took up 13.4% of available 42 K without ouabain and 2.8% with 10−5 M ouabain, (P

A group of patients whose dietary potassium was unrestricted and who received 12-18 h of Kiil dialysis twice weekly against a bath containing no potassium, had body potassium concentrations (total body potassium/intracellular volume) of 7.6% lower than normal. Despite marked hypokalemia at the end of dialysis, suprisingly few electrocardiographic changes were seen. Another group of subjects, dialyzed fro 5-6 h thrice weekly against a bath containing 1 mEq/liter of potassium in a Dow dialyzer, showed more marked electrocardiographic abnormalities despite smaller alterations in transmembrane potassium gradients. Rapidity of establishment of potassium gradients is important as well as magnitude. The following changes occur in a single dialysis: 100 mEq of cell potassium and 20 mEq of extracellular potassium leave the body; 100 mEq of extracellular sodium enter the cells and 415 mEq of extracellular sodium leave the body; 3.5 liters of water leave the extracellular fluid, 2.5 liters into the bath and 1 liter into the cells.

We describe a rapid and accurate osmometric method for the measurement of total CO 2 1 which is considerably simpler than techniques previously and currently used [1–7].

SummaryPlatelet aggregation induced by ADP can be inhibited by plasma from uremic patients or by toxins isolated from their plasma, e. g. guanidinosuccinic acid, methylguanidine, phenol and hydroxyphenylacetic acids. Since these chemical substances can interfere with energy metabolism in tissues other than platelets and since ATP production is needed for ADP-induced aggregation, alterations in platelet energy metabolism could underlie excessive bleeding in uremic patients. Platelets incubated with idioacetate and deprived of anaerobic glycolysis produced the same quantity of ATP through respiration in the presence of all the uremic toxins studied as in their absence. Similarly, platelets incubated with cyanide and deprived of the oxidative pathway utilized anaerobic glycolysis to produce normal quantities of ATP in the presence of all the uremic toxins. The utilization of ATP, as indicated by active transmembrane potassium transport, was also unaffected by the above listed guanidines and phenols. It is concluded that the in vitro inhibition of ADP-induced platelet aggregation by the guanidines and phenols studied is not due to inhibition of production or utilization of ATP.

Total corticosteroid concentrations were determined in the plasma and brains of five species: mouse, rat, cat, monkey and man. Corticosteroid concentrations were measured also in the livers of mice, rats and monkeys. Competitive protein binding techniques were validated and used for the tissue corticosteroid assays. In each species the brain corticosteroid value was less than the total plasma corticosteroid level but greater than the presumed unbound fraction of plasma corticosteroids. A clear circadian variation of brain corticosteroid values was found in mice, together with a rapid elevation of the tissue levels in response to stress. Reduction of both plasma and tissue corticosteroid concentrations was observed after adrenalectomy and in response to dexamethasone treatment of mice. Between 24 and 48 h post morten, mouse brain corticosteroid values decreased greatly. In cat, monkey and human brains all regions examined contained approximately equal amounts of corticosteroids. In particular, brain areas which are not involved in pituitary-adrenocortical regulation contained large amounts of corticosteroids.

In this paper, two separate problems are solved by similar techniques. The first involves estimating a density at an unknown point such as a quantile or the mode. The second involves providing a competitor to the interquartile range in selection of that one of k populations with the lightest tail.