Biomedical subjects
Publications and source records attributed to L D Pengelly.
Presented in this short communication are design principles for the construction of a positioning apparatus for biological specimens in magnetically sensitive environments. An apparatus with 3 degrees of freedom was built and found to provide position accuracy to within +/- 0.25 mm throughout a cubic volume measuring 9 cm on each side.
In man, there is wide interindividual range in the tidal volume response to CO2. To determine which (rib cage or abdomen-diaphragm) compartment had a greater influence on this range, ventilatory response to CO2 was measured, using Read's method, in eight men and two women seated in a constant-pressure body plethysmograph. Rib cage and abdominal tidal volume was simultaneously measured using magnetometers. Correcting for body size, the tidal volume response of the abdominal compartment was similar in all subjects, whereas that of the rib cage was larger in subjects with high tidal volume response to CO2; a significant correlation was found (P less than 0.01). Rib cage volume displacement lagged behind abdominal in all subjects; phase lag was greatest in the subject with the lowest ventilatory response to CO2. These results suggest that, at high levels of ventilation, a larger volume displacement of the rib cage may reflect a more effective coupling of the diaphragm pressure generator to it or alternatively a reduction in its impedance relative to the abdominal compartment.
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The relationship between transnasal pressure and nasal flow is markedly curvilinear during tidal breathing in man, and there is poor agreement among the results of various methods used to define this characteristic with a single number. We used Rohrer's equation (P = K1 V + K2 V2), where P = pressure and V = flow, and calculated values for K1 and K2 from 474 nasal inspiratory pressure/flow curves obtained from 34 human subjects by a standard method of posterior rhinometry. Nasal airway inspiratory resistance at an air flow of 0.4 liter per sec (NAIR0.4) was also calculated. Rohrer's equation was found by regression analysis to fit each curve well (0.86 less than r less than 0.9999; mean, 0.983). There was a strong correlation between NAIR0.4 and K2: NAIR 0.4 = 0.91 K2 + 0.39 (r = 0.97). Nasal congestion induced in 7 normal subjects with histamine resulted in larger changes in K2 and NAIR0.4 than K1. Patients given an intranasal corticosteroid aerosol (beclomethasone dipropionate) in a double blind crossover trial showed symptomatic improvement in nasal congestion (P less than 0.01) and significant decreases in K2 (P less than 0.02) and NAIR 0.4 (P less than 0.05), but no change in K1 (P greater than 0.2).
Nasal inspiratory resistance and maximal inspiratory nasal flow were measured in 10 normal subjects while they breathed air and while they breathed a mixture of 80% helium and 20% O2. After the less dense helium-O2 mixture, there was a nonsignificant increase in K1 (15 +/- 93%), a 56 +/- 20% decrease in K2 (P less than 0.001), and a 48 +/- 20% increase in maximal inspiratory nasal flow (P less than 0.001). This is consistent with the accepted concept that K1 represents resistance to laminar flow and K2, resistance to nonlaminar flow (turbulent flow and/or flow due to convective acceleration), and that nonlaminar air flow predominates in the nose.
The effect of respiratory muscle weakness on the maximum static pressure-volume (PV) characteristics of the respiratory system was studied in four healthy males infused slowly with d-tubocurarine (dtc). Inspiratory capacity (IC), expiratory reserve volume (ERV), maximum static inspiratory and expiratory mouth pressures at four lung volumes, and handgrip were measured during induction of, and recovery from muscle weakness. The maximum effect of dtc varied among the muscle groups tested; peripheral muscles were most severely affected, expiratory muscles moderately, and inspiratory muscles least affected. At each level of weakness studied, decreases of IC and ERV were proportional to decreases of maximum static mouth pressures. Vital capacity, measured at each level of weakness was much less than values predicted from the static mechanical properties of the respiratory system. Our findings suggest that the marked change in the extremes of lung volume during submaximal neuromuscular blockade (SMNB) is due, in part, to unequal distribution of muscle weakness, reflected by decreased ability to change ribcage dimensions even at modest levels of SMNB.
Epidemiological information about the health consequences of ambient air pollution is adequate at present to set upper limits so that acute deterioration due to pollution can be prevented in patients with chronic lung disease. However, our knowledge is incomplete with respect to what is a safe chronic background level, particularly with regard to reducing and preventing the amount of chronic respiratory disease presently occurring. This review concentrates exclusively on sulphur dioxide and particulate pollution, although the principles used in setting standards for these two pollutants may be applied to photochemical pollutants such as ozone which may effect the lung. It is only when the dose-effect relationships between pollution and disease are more clearly understood that the benefit of reducing air pollution to improve health can be predicted.
The pressure-volume relationship of the mammalian lung is markedly curvilinear and in the normal lung, can be shown to fit an exponential function of the form V = V0(1 - K 0e-K1P) in the range of lung volume from FRC to TLC. A method is presented, using a programmable calculator, of determining the parameters V0, K0, and K1, and of deriving related constants of greater physiological significance. Values calculated from pressure-volume curves of 20 normal human subjects are listed, together with coefficients of determination, to demonstrate the adequacy of fit of the method. Half-inflation pressure (h- ln 2/K1), ranged from 2.65 to 9.21 and coefficients of determination (r2) ranged from 0.851 to 0.9998.
We measured lung mechanics in seven healthy males during acute isocapnic hypoxia (PAO2 = 40-50 Torr; PACO2 = 38-42 Torr). Hypoxia was accompanied by increases in total lung capacity (mean increase +/- SD; 0.40 +/- 0.24 liters; P less than 0.005) functional residual capacity (0.34 +/- 0.25 liters; P less than 0.01) and residual volume (0.56 +/- 0.44 liters; P less than 0.02) in all subjects. Specific conductance of the lung decreased during hypoxia (P less than 0.02). The static deflation pressure-volume curve of the lung was shifted upward during hypoxia in all subjects. Resting end-expiratory recoil pressure of the lung was slightly, but not significantly lower during hypoxtic expiratory lung compliance was greater during hypoxia (0.39 +/- 0.04 l/cmH2O) than control measurements (0.31 +/- 0.05 l/cmH2O; P less than 0.005). No change was noted in dynamic lung compliance. All changes in lung mechanics were reversed within three minutes of reoxygenation. We conclude that acute isocapnic hypoxia increases total lung capacity in man and suggest that this may be due to the effect of hypoxia on the airways and pulmonary circulation.
Tidal volume together with end-inspiratory pressure was measured in four seated healthy men, during normal breathing and during single inspirations taken from a series of rigid containers which provided added elastances (range: 5-70 cmH2O/l). Experiments were performed both during quiet breathing and during ventilation increased by added dead space. Added elastic loads always resulted in a decreased tidal volume. This decrease was partly compensated by increased pressure developed by the inspiratory muscles; being more so with greater added elastance, control ventilation, or both. Analysis of our results indicates that the load-compensatory response may be attributed to changes in mechanical impedance of the ventilatory pump, due to the mechanical arrangement and the intrinsic properties of the inspiratory muscles (force-length and force-velocity relationships), changes in respiratory frequency with increasing ventilation, and to vagally mediated load compensation.
Comparison of published reports on physiological effects of exposure to ozone (O3) suggests that Canadians are more reactive than southern Californians. Responses of subjects and experimental methods were compared in a cooperative investigation of this apparent difference in reactivity. Four Canadians and four Californians were exposed to 0.37 ppm O3 in purified air at 21 degrees C and 50% relative humidity for 2 hours with intermittent light exercise. Exposures to purified air alone served as controls. Responses of subjects were similar to those observed previously: Canadians on the average showed greater clinical and physiological reactivity to exposure than did Californians, who were no more than minimally reactive. Canadians also showed larger increases in erythrocyte fragility following exposure. No methodological differences sufficient to explain different results of previous studies were found. Although other possible explanations have not been ruled out entirely, adaptation of southern Californians to chronic ambient O3 exposure is a rational hypothesis to explain these results.
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