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Biomedical subjects

D J Cunningham

Publications and source records attributed to D J Cunningham.

At least 37 records · Page 2Linked to original sources
PubMed1977

Very small, very short-latency changes in human breathing induced by step changes of alveolar gas composition.

1. Three healthy young males were maintained for sessions of about 1 hr in a state of mild asphyxia (PA,O2 approximately 55, PA,CO2 approximately 45 torr), i.e. with moderately strong drives from both arterial and intracranial chemoreceptors. Tidal volume (VT), breath duration (TT) and duration of inspiration (TI) were recorded, and ventilation (VE) and duration of expiration (TE) were derived breath by breath. 2. The arterial chemoreceptor component of the drive was briefly and abruptly reduced, perhaps silenced, by three separate procedures: the inspiratory pathway was connected for two breaths to a second gas supply line containing, B, hypoxia with Pi,CO2 zero (removal of hypercapnia with maintained hypoxia); C, pure oxygen (removal of asphyxia); and D, oxygen with 40 torr added PCO2 (removal of hypoxia with maintained hypercapnia). In controls, A, the second inspiratory line contained the maintenance mixture so that the switch involved no change of inspiratory gas composition. Each type of test was repeated twenty-four times on each subject. 3. Responses attributable to silencing of arterial chemoreceptors (i.e. with 1 1/2--3 breath latencies about equal to the lung-to-ear circulation time) are reported elsewhere. 4. Very small responses, occurring only half a respiratory cycle after first inhalation of the test mixture, were detected by pooling all responses of each kind from all subjects. When hypoxia was withdrawn, with (C) or without (D) simultaneous withdrawal of hypercapnia, VT and VE were reduced by 3 and 2% respectively, probably because gas mixtures containing high oxygen concentrations are appreciably more viscous than hypoxic mixtures and so require more effort to breathe in and out. When hypercapnia was withdrawn with (C) or without (B) simultaneous withdrawal of hypoxia, TE was significantly lengthened (mean, + 65 +/- 18 msec), 5. The change of TE was discussed in relation to known effects of CO2 on airway receptors in the dog.

Carbon Dioxide↗
PubMed1977

A quantitative description of the pattern of breathing during steady-state CO2 inhalation in man, with special emphasis on expiration.

1. Quantitative data on the pattern of breathing in normal men and women (Gardner, 1977) have been used to derive expressions that are based on known physiological mechanisms.2. The relations between the applied chemical drive to breathing (expressed as DeltaP(A, CO2) in high O(2)) and the several components of the volume-time patterns described in the companion paper were examined. Neither mean tidal volume (V(T)), nor mean inspiratory nor mean expiratory times (T(I), T(E)) were uniquely related to the chemical drive across the breakpoint, which could be demonstrated in two and suspected in the third of these plots.3. Mean inspiratory flow (V(T)/T(I)) was linearly related to P(A, CO2) over the whole range and, like minute ventilation (V), showed no breakpoint. The mean relation was V(T)/T(I) = 0.11 (P(A, CO2) - 35.2). V(T)/T(I) was highly correlated with V; in individuals with healthy lungs and under relatively stable conditions of compliance and resistance it may be accepted as a wholly inspiratory alternative to V as an index, on the efferent side, of the total prevailing chemical drive.4. The description of the relation between T(I) and V(T) was essentially the same as that of Clark & Euler (1972): in range 1, T(I) = either 1.29 - 0.07 V(T)or the constant 1.24 sec, and in range 2, T(I) = 0.65/(V(T) - 0.88) + 0.59.5. Expiration was described by an equation based on the inverse linkage between T(E) and chemical drive and the direct link between both mean and breath-by-breath values of T(I) and T(E): T(E) = pT(I) + q/(drive - r) in which p was 0.64 +/- 0.09, q was 11.1 +/- 2.64 sec. (torr CO(2))(-1) and r was -2.73 +/- 1.09 torr CO(2). All three parameters were necessary for an adequate description.6. It is argued that the first term of the T(E) equation represents influences related to lung volume exerted through the vagus, and that the second represents the effects of over-all chemical stimulation exerted through other pathways.

Adult↗
PubMed1975

The chronic toxicity of methiocarb to grackles, doves, and quail and reproductive effect in quail.

Methiocarb (4-methylthio-3, 5-xylyl N-methyl carbamate, Mesurol, Bay (3744), a bird repellent, was fed in concentrations of 100 to 1,000 ppm to common grackles (Quiscalus quiscula), mourning doves (Zenaida macroura), and breeding pairs of coturnix quail (Coturnix coturnix) to investigate the possibility of cumulative intoxication. Although aversion to treated diets was readily apparent in most of the tests, the 28- to 30-day median lethal concentration (LC50) was determined to be greater than 100 ppm for grackles, 630 ppm (95% confidence limits, 480-830 ppm) for doves, and greater than 1,000 ppm for coturnix quail. Methiocarb appeared to be noncumulative when measured by an index of chronicity: birds consumed several LD50 doses during a day's feeding, and when deaths occurred, they appeared to be due to acute intoxication. Egg production and live chick production were not affected in coturnix fed 100 ppm but were reduced at 316 and 1,000 ppm.

Animals↗
PubMed1975

Leaching and degradation of 4-aminopyridine-14C in several soil systems.

Leaching and degradation of 4-aminopyridine (a frightening agent for protecting grain crops from blackbirds) was studied in seven soils. Carbon 14-labeled 4-aminopyridine was strongly adsorbed onto soil colloids, with the degree of adsorption related to pH. Application of seven in. of simulated rainfall over 20 days to surface-treated alkaline soils leached to 0.02 percent to 0.18 percent of the -14C; radioactivity was detected in the runoff from only one of the four acidic soils. Degradation of 4-aminopyridine-14C to -14CO(2) was negligible in soils incubated up to two months under anaerobic conditions. Under aerobic incubation, there was a one-week lag before extensive breakdown began. Degradation rates increased with increasing temperature and soil moisture during incubation, but soil composition had a greater influence. After three months at 30 degrees C and 50 percent moisture, evolution of -14CO(2) ranged from 0.4 percent for a highly acidic loam (pH 4.1) to more than 50 percent for a lighter-textured, alkaline, loamy sand (pH 7.8); the half-life of 4-aminopyridine in soils under these test conditions ranged from 3 to more than 22 months. A theoretical scheme is presented for the degradation of 4-aminopyridine in soils.

Aerobiosis↗
PubMed1974

The effects of raising alveolar PCO2 and ventilation separately and together on the sensitivity and setting of the baroreceptor cardiodepressor reflex in man.

1. The effects of changes in ventilation and/or alveolar P(CO2) on the baroreflex control of heart rate have been studied in seven experiments on six young men and women who had been trained to control tidal volume and respiratory frequency at various levels independent of alveolar P(CO2), during hyperoxia.2. Intravenous phenylephrine provoked transient rises of directly measured arterial pressure during which individual systolic pressures (P) were linearly related to the following pulse interval (I). Baroreflex sensitivity was expressed as the slope of the regression of I on P, and reflex setting (I(ref)) as I at a single reference arterial pressure (= mean P for the experiment).3. Voluntary control of breathing had little effect on heart rate and arterial pressure (baroreflex setting), but diminished reflex sensitivity.4. Hypercapnia regularly caused tachycardia at the reference pressure (i.e. baroreflex setting lowered). The response was completely or partly reproduced by change of P(A, CO2) at constant ventilation in four subjects but not in two others; in them change of ventilation at constant P(A, CO2) completely mimicked the effect of free-breathing hypercapnia.5. Values of baroreflex sensitivity were relatively scattered. Hypercapnia caused a fall in baroreflex sensitivity in three subjects whether ventilation was fixed or free to rise. After separating the effect of voluntarily controlling ventilation, ventilation per se was without effect on reflex sensitivity.6. It is concluded that hypercapnia and hyperpnoea have separate effects on the baroreflex, the relative magnitudes of which differ from one subject to another. Baroreflex setting and sensitivity vary independently in response to change of ventilation and of P(A, CO2).

Blood Pressure↗
PubMed1973

The respiratory effects in man of altering the time profile of alveolar carbon dioxide and oxygen within each respiratory cycle.

1. Breathing hypoxic gas through an external dead space (ca. 1200 c.c.) stimulated ventilation disproportionately. A loop (ca. 250 c.c.) in the inspiratory pathway reduced the effect.2. The alveolar time patterns of P(CO) (2) and P(O) (2) characteristic of tube breathing with or without the loop have been simulated in moderate hypoxia by changing the composition of inspired gas at selected intervals after the beginning of inspiration.3. Supplying CO(2)-free gas in late inspiration usually stimulated ventilation, but less than did real tube breathing. Supplying CO(2)-free gas early in inspiration usually depressed ventilation. The difference between the ;CO(2)-free late' and ;CO(2)-free early' effects was 20% of the control ventilation (P < 0.001), i.e. was nearly the same as between the effects of real tube breathing without and with the loop.4. Tube-like P(A, O) (2) time patterns had no effects.5. A-a P(CO) (2) and P(O) (2) gradients remained constant throughout.6. The V(E), f and V(T) relations were unaltered in tube breathing.7. The respiratory system can discriminate between small differences in time patterns of P(A, CO) (2) but not of P(A, O) (2); the signal is amplified by steady hypoxia. The arterial chemoreceptors are probably responsible for these effects.

Adult↗