Effect of supplementary feeding on infant growth in an aboriginal family.
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Biomedical subjects
Publications and source records attributed to J W Cox.
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The National Library of Medicine's computer system has developed from a second generation computer to the large IBM multiprocessor system that is now used to maintain the MEDLINE file, provide retrieval services, and produce the computer photocomposed products of the NLM. On-line maintenance facilities have been developed for the final steps in the input and file maintenance processes. The retrieval program, ELHILL, and its supporting programs now provide more bibliographic searches than any other system in the world. The photocomposed products, including Index Medicus, are produced through the use of flexible publication programmes which have allowed NIH to use several different photocomposers.
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An image torso may be viewed as a one-to-one transform of a physical volume conductor to a geometric form which defines both the axis and sensitivity of any electrocardiographic connection. In this report, the image surfaces of laminar, spherical, rectangular and humanoid physical torsos are explored theoretically and experimentally. All proved to be rounded or spherical in form despite the marked differences in the configuration of the physical conductor. Moderate degrees of dipole eccentricity induced only small departures from this basic circular pattern. Introduction of phase inhomogeneity, however, resulted in more striking deviations from roundness.
Junctional depression is often observed during physical exercise in overtly normal subjects. To explore its pathogenesis, 15 normal volunteers were studied during supine, bicycle ergometer, submaximal stress tests. Electrocardiograms were simultaneously recorded from 42 electrodes on the left anterior precordium at two minute intervals at rest and during exercise. Data were used to construct isopotential maps throughout the P-QRS-T intervals. At rest, maps throughout the ST segment were dominated by a single maximum along the upper left sternal border. During exercise, all subjects developed junctional depression that was maximal along the lower left sternal border. Exercise maps during the early to mid-ST segment showed an intense minimum along the lower left sternal border that was continuous with terminal QRS forces in both intensity and location. Later in ST, this minimum decreased in strength and was replaced by a maximum located in the same area as that observed at rest. These observations suggest that junctional depression is the result of competition between two effects, one being normal repolarization which is obscured in the early ST segment by the second, possibly representing delayed terminal depolarization forces.
We studied the relative dipolar and nondipolar content of signal energy throughout ventricular excitation and recovery in 34 isolated, perfused rabbit hearts, suspended in an electrolyte-filled spherical chamber. Computer-processed signals were derived from 20 evenly spaced tank-surface electrodes, and a single, moving, equivalent cardiac dipole generator was optimally fitted to the recorded potentials for each 1-msec sampling interval. Superimposed, time-based plots of signal energy for the 34 preparations showed ventricular excitation to be strikingly more nondipolar than was recovery. In terms of the summed square ratio of nondipolar residual energies, overall nondipolarity of QRS exceed that of ST-T by 41%. Furthermore, the maximum instantaneous ratio during QRS was considerably greater than during the ST-T. Evaluation of paired differences, comparing nondipolar behavior throughout QRS with all of ST-T, proved highly significant (P less than .005). We also found that in contrast to the considerable mobility exhibited by the equivalent QRS dipole, the ST-T dipole locus remained nearly stationary during most of ventricular recovery. Presumably because repolarization is temporally and spatially a relatively diffuse process, it may generate electrical fields which are notably more dipolar than those caused by depolarization.
The ability of a numerical procedure to detect and to localize two experimentally induced, epicardial dipolar generators was tested in 24 isolated, perfused rabbit heart preparations, suspended in an electrolyte-filled spherical tank. Electrocardiograms were recorded from 32 electrodes on the surface of the test chamber before and after placement of each of two epicardial burns. The second lesion was located either 180 degrees, 90 degrees, or 45 degrees from the first. Signals were processed by iterative routines that computed the location of one or two independent dipoles that best reconstruced the observed surface potentials. The computed single dipole acounting for 99.68% of root mean sequare (RMS) surface potential recorded after the first burn was located 0.26 +/- 0.10 cm from the centroid of the lesion. Potentials recorded after the second lesions were fit with two dipoles that accounted for 99.36 +/- 1.51% of RMS surface potentials and that were located 0.42 +/- 0.26 cm and 0.57 +/- 0.49 cm from the centers of the corresponding burn. Seventy-one percent of computed dipoles were located within the visible perimeter of the burn. Thus, two simultaneously active dipolar sources can be detected and accurately localized by rigorous study of the generated electrical field.
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The effect of perfusion pressure on uteroplacental blood flow was determined in pregnant rabbits utilizing the radioactive microsphere method. Control mean arterial pressure, 93 mm Hg +/- 2.6 SEM, was raised by carotid ligation to 109 +/- 4.1 mm Hg and then reduced with antihypertensive drugs to 74 +/- 1.3 mm Hg. Over this range of pressure there was no significant change in cardiac output, 605 +/- 36, 523 +/- 37, and 540 +/- 39 ml/min; or uteroplacental blood flow, 30 +/- 3.2, 27 +/- 5.2, and 29 +/- 4.5 ml/min, respectively. When prostaglandin synthesis was inhibited with either indomethacin or meclofenamate (2 mg/kg), uterine vascular resistance was higher but maintenance of uteroplacental flow occurred over a perfusion pressure of 89 +/- 6.7-115 +/- 9.3 mm Hg. With more severe hypotension induced with trimethaphan, control arterial pressure fell from 92 +/- 2.4 to 39 +/- 0.9 mm Hg, cardiac output fell from 514 +/- 17 to 407 +/- 22 ml/min (P less than 0.025) and uteroplacental blood flow fell from 6.1 +/- 0.9 to 2.5 +/- 0.9% of cardiac output (P less than 0.05), which represented an absolute fall from 32.4 +/- 5 to 10.6 +/- 3 ml/min (P less than 0.025). There was no significant change in renal blood flow expressed as percentage of cardiac output, 14.9 +/- 2 and 13 +/- 1.5%, or in absolute flow, 75 +/- 7.7 and 54 +/- 7 ml/min with trimethaphan-induced hypotension. These studies indicate that uteroplacental blood flow is maintained relatively constant over a range of perfusion pressure of 60-140 mm Hg in both normal and prostaglandin-inhibited pregnant rabbits. However, with reduction in pressure to 36-42 mm Hg, uteroplacental blood flow falls, expressed as a percentage of cardiac output and in absolute flow.
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Location of the equivalent cardiac dipole has been estimated but not fully verified in several laboratories. To test the accuracy of such a procedure, injury vectors were produced in 14 isolated, perfused rabbit hearts by epicardial searing. Strongly dipolar excitation fronts were produced in 6 additional hearts by left ventricular pacing. Twenty computer-processed signals, derived from surface electrodes on a spherical electrolyte-filled tank containing the test preparation, were optimally fitted with a locatable cardiac dipole that accounted for over 99% of the root-mean-square surface potential. For the 14 burns (mean radius 5.0 mm), the S-T injury dipole was located 3.4 plus or minus 0.7 (SD) mm from the burn center. For the 6 paced hearts, the dipole early in the ectopic beat was located 3.7 mm (range 2.6 to 4.6 mm) from the stimulating electrode. Phase inhomogeneities within the chamber appeared to have a small but predictable effect on dipole site determination. The study demonstrates that equivalent dipole location can be determined with acceptable accuracy from potential measurements of the external cardiac field.
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To further evaluate the mechanism of the oliguria of acute renal failure, a model was utilized in which intense and prolonged vasoconstriction produced the unilateral cessation of urine flow. The radioactive microsphere method was used to measure total and regional blood flow before and after the intrarenal infusion of norepinephrine, 0.75 mug/kg/min, for 2 h in the dog. In the control kidney, renal blood flow increased 32% 48 h after norepinephrine in association with a fall in the fractional distribution of flow to the outer cortex. In the experimental kidney, total renal blood flow fell from 190 ml/min before norepinephrine to 116 ml/min at 48 h (P < 0.025) with a uniform reduction in cortical blood flow. After the administration of 10% body wt Ringer's solution, there was a marked redistribution of flow to inner cortical nephrons in both the control and experimental kidney. In addition, there was a marked increase in total blood flow in both kidneys. On the experimental side, flow rose to 235 ml/min, a value greater than in either the control period (P < 0.05) or at 48 h after norepinephrine (P < 0.001). However, in spite of this marked increase in blood flow, there was essentially no urine flow from the experimental kidney. In separate studies, the animals were prepared for micropuncture. In all studies, the surface tubules were collapsed, and there was no evidence of tubular obstruction or leakage of filtrate. Over 99% of the 15-muM spheres were extracted in one pass through the experimental kidney. An analysis of the forces affecting filtration suggested that an alteration in the ultrafiltration coefficient may be responsible, at least in part, for the anuria in this model. In this regard, transmission and scanning electron microscopy revealed a marked abnormality in the epithelial structure of the glomerulus. It is suggested that a decrease in glomerular capillary permeability may be present in this model of acute renal failure.
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