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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.
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Histopathological evidence for pulmonary emboli in experimental decompression sickness in dogs detected by radioisotopic lung scanning
P wave and P loop changes during transvenous pacing of specific locations in coronary sinus and left atrium in dogs and man
Vertical distribution of pulmonary blood flow /DPBF/ in dogs without thoracotomy prone, supine, head-up, head-down and right and left decubitis positions
Position dependent variations in intrapericardial, pleural and esophageal pressures and cardiac output in thorax of dogs
Hemodynamic response to dopamine before and after myocardial infarction in dogs
Serum calcium-digitalis synergism effect on dogs heart excitability, noting hypoxia role in arrhythmia production
Mongrel dogs pulmonary and systemic circulatory responses to dopamine infusion
Hypoxia affecting circulatory responses in dogs, such as cardiac output, left ventricular dp/dt, and stroke volume
Acceleration effects on aortic, coronary and carotid flows in dogs
Renal hemodynamic factors in whole kidney glomerulotubular balance in anesthetized dogs by manipulating filtration rate through constriction of aorta, thoracic vena cava, etc
Dogs intrapleural and intraesophageal pressures dependence on head positions
Isoproterenol, atrial pacing, ouabain and methoxamine effects on dogs during experimental cardiac tamponade, observing arterial pressure, cardiac output and heart rate changes
Small pressure wave transmission in abdominal venae cavae of dogs in mathematical model development for viscoelastic behavior of large veins
Mitral regurgitant indexes were measured by roentgen videodensitometry in anesthetized dogs without thoracotomy before, during and after extrasystolic potentiation of ventricular contraction while the atria and ventricles were driven in normal temporal sequence simultaneously or in such a way as to induce atrial fibrillation. Small amounts of mitral reflux were observed with simultaneous atrial and ventricular driving and with atrial fibrillation in the control measurements before initiation of extrasystolic potentiation. Reflux became negligible during extrasystolic potentiation and increased beyond control levels after termination of extrasystolic potentiation.
Comparison of previously described theoretical predictions with in vivo data from anesthetized dogs. It is shown that the observed attenuation of the pressure and axial waves cannot be accounted for by fluid viscosity alone. For large values of the frequency parameter alpha, the previous analysis is extended to include the effects of viscoelasticity of the vessel wall. The results indicate that the speeds of both types of waves are essentially unaffected by a realistic viscoelasticity model while the attenuation per wavelength is significantly increased and becomes frequency independent. There is fair agreement between theory and experiment.
Three levels of decreased arterial oxygen saturation elicited a graded circulatory response in dogs, manifested by stepwise increases in cardiac output, left ventricular dp/dt, and stroke volume, and decreases in systemic vascular resistance. Responses to similar hypoxia challenges after experimental myocardial infarction were qualitatively similar but quantitatively less. Although the circulatory compensation for hypoxia was less effective after myocardial infarction, no further deterioration of the haemodynamics was noted.
Artificially ventilated and perfused dog lungs were rapidly frozen under various physiological conditions. In 2-micron-thick sections the number of red blood cells (RBCs) per 10-micron length of alveolar septum was counted. Under conditions in which alveolar pressure exceeded venous pressure, variation in RBC concentration within areas supplied by single arterioles accounted completely for variation between areas supplied by different arterioles. Except at very high perfusion pressures when venous pressure exceeded alveolar pressure, there was no significant correlation between RBC concentrations of pairs of adjacent septa.
This investigation set out to answer two questions: (1) are the distal alveoli in the terminal lung units less well perfused than the proximal alveoli, i.e., is there stratification of blood flow; and (2) if so, does this enhance gas exchange in the presence of stratified inequality of ventilation. Excised dog lungs were ventilated with saline and perfused with blood. Following single inspirations of xenon 133 in saline and various periods of breath holding, the expired xenon concentration against volume was measured and it confirmed marked stratified inequality of ventilation under these conditions. By measuring the rate of depletion of xenon from alveoli during a period of blood flow, we showed that the alveoli which emptied at the end of expiration had 16% less blood flow than those exhaling earlier. However, by measuring the xenon concentration in pulmonary venous blood, we found that about 10% less tracer was transferred from the alveoli into the blood when the inspired xenon was stratified within the respiratory zone. Thus while stratification of blood flow was confirmed, it was shown to impair rather than enhance the efficiency of gas transfer.