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Biomedical subjects

C B Wolff

Publications and source records attributed to C B Wolff.

At least 19 recordsLinked to original sources
PubMed2000

Cerebral blood flow and oxygen delivery at high altitude.

During acclimatization to moderate altitudes, a simple calculation from data of others shows that the rise in cerebral blood flow (CBF) is sufficient that oxygen delivery to brain (DaO2) is constant as arterial oxygen content (CaO2) falls. This balance occurs on average even though the hypocapnia caused by hypoxic hyperventilation causes cerebral vasoconstriction, conflicting with hypoxic cerebral vasodilation. The relative strengths of the ventilatory and cerebral vascular sensitivities may affect this balance in individual subjects. There is no evidence for a mechanism to detect or respond directly to DaO2. Hypoxic cerebral vasodilation is believed to depend upon tissue and capillary PO2 and content, not arterial. Despite these reservations it is of interest that the average resultant DO2 remains constant. I speculate here that this match may relate to the well-known local hyperemic response to neuronal activity which now has been shown to initially overcompensate, in that tissue PO2 and pH rise in the first few seconds after neural activity. Analysis of results from the paper by Severinghaus et al. (Circ. Res. 1966;19:274-282) shows that in their subjects, despite approximately 20% reductions in arterial oxygen content at 3,810 m altitude, the data does not show any significant fall in DaO2 as a result of increased cerebral blood flows.

Altitude↗
PubMed1995

Cerebral microvascular permeability and CSF pH in anaesthetized rats.

The idea that the blood-brain barrier (BBB) may be made slightly permeable by an acid load on the brain side was tested in single pial venular capillaries of anaesthetized young rats. The fluorescent dye, Lucifer Yellow (457 Da), was used as a fluid-phase marker to measure permeability in the presence of a free radical scavenger. Tight microvessels were unresponsive to pH changes of 0.3-0.5 units. Vessels that were permeable showed small, significant increases in permeability with decreasing pH (2.19 +/- 0.562 x 10(-6) cm s-1 (pH unit)-1). This effect increased with increasing permeability.

Animals↗
PubMed1995

Maternal eating patterns and birth weight of Mexican American infants.

Eating patterns of 549 Mexican American mothers were identified using dietary data from the United States Hispanic Health and Nutrition Examination Survey. These eating patterns were then used to investigate the relationship between maternal diet and infant birth weight. Principle components factor analysis was used to determine the structure of the maternal eating patterns. Seven distinct eating patterns were identified: nutrient dense, traditional, transitional, nutrient dilute, protein rich, high fat dairy, and mixed dishes. Stepwise multiple regression analysis was used to identify those eating patterns associated with birth weight. In addition to eating patterns, regression variables included body mass index, hemoglobin, gestational age at delivery, maternal age, infant gender, acculturation, marital status, income, education, and smoking during pregnancy. Regression results indicated that the nutrient dense (fruits, vegetables, low fat dairy, etc.) and protein rich (low fat meats, processed meats, and dairy desserts, etc.) eating patterns were associated with increased birth weight and that the transitional eating pattern (fats and oils, breads and cereals, high fat meats, sugar, etc.) was associated with decreased birth weight. Study findings suggest that the eating pattern methodology may be an appropriate tool for analyzing food frequency data in the investigation of diet and health relationships and for targeting dietary interventions.

Acculturation↗
PubMed1992

Carotid chemoreceptor discharge during epinephrine infusion in anesthetized cats.

It is known that during exercise there is an increase in plasma epinephrine. The purpose of the present investigation was to determine whether stimulation of carotid chemoreceptors by epinephrine is a direct effect or secondary to epinephrine-induced increases in arterial plasma [K+] and whole body CO2 production (VCO2). Chemoreceptor discharge was recorded from single fiber preparations of the carotid sinus nerves in anesthetized cats ventilated to a constant arterial PCO2 (PaCO2). Infusion of epinephrine (1 microgram.kg-1 x min-1) caused arterial [K+] to increase from a mean of 2.7 to 3.8 mM. VCO2 increased so that ventilation had to be increased by 60% to maintain PaCO2 constant. Mean chemoreceptor discharge increased by 50%, but this was no greater than would be predicted on the basis of the increases in arterial [K+] and VCO2. In a further group of experiments epinephrine was infused at 0.1 microgram.kg-1 x min-1 and produced no significant increase in chemoreceptor firing. These experiments provide no evidence for epinephrine having a direct effect on the carotid chemoreceptor.

Anesthesia, Intravenous↗
PubMed1985

Ventilatory changes during exercise and arterial PCO2 oscillations in chronic airway obstruction patients.

Ventilatory kinetics during exercise (30 W for 6 min) were studied in 3 asthmatics, 14 patients with chronic airway obstruction (11 with bronchial or type B disease, 3 with emphysematous or type A disease), and in 5 normal age-matched controls. The measure of ventilatory increase during early exercise, alpha 1-3%, was calculated as (avg minute ventilation over 1st-3rd min of exercise--resting minute ventilation)/(avg minute ventilation over 4th-6th min of exercise--resting minute ventilation) X 100. Arterial pH, PO2, and PCO2 (PaCO2) were measured in vitro at rest and within 20 s of termination of exercise. Respiratory PaCO2 oscillations had previously been monitored at rest in the patients (indirectly as in vivo arterial pH, using a fast-response pH electrode) and quantified by upslope (delta PaCO2/delta t). alpha 1-3% was normal in asthmatics (whose respiratory oscillations as a group showed least attenuation) and in type A patients (whose respiratory oscillations as a group were most attenuated). In type B patients reduction in alpha 1-3% correlated with attenuation of delta PaCO2/delta t (r = 0.75; P less than 0.01). There was no significant correlation between delta PaCO2/delta t and change of in vitro PaCO2 from rest to the immediate postexercise period. These findings are consistent with the hypothesis that attenuation of delta PaCO2/delta t slows ventilatory kinetics during exercise in type B but not type A patients. Intact respiratory oscillations are not necessary for CO2 homeostasis after the first few minutes of exercise.

Aged↗
PubMed1984

Arterial plasma potassium measured continuously during exercise in man.

Five continuous records of arterial plasma potassium were obtained from three normal subjects during brief periods (5-7 min) of exercise (100 W). In two of these subjects hepatic venous blood samples were withdrawn at 0.5-1.0 min intervals and analysed in vitro for plasma potassium. Arterial plasma potassium rose rapidly at the start of exercise from 3.8 +/- 0.3 mmol/l (mean +/- SD) to plateau levels of 5.4 +/- 0.1 mmol/l. One of the above subjects and a further subject were studied after beta-blockade with propranolol. This resulted in an exaggerated rise in arterial plasma potassium during exercise. Hepatic venous potassium measurements indicated that the liver probably had little effect on potassium changes during exercise. The changes in arterial plasma potassium during exercise are rapid and substantial. If transmitted to the extracellular fluid these changes would alter cell transmembrane potential and might as a result alter receptor sensitivity.

Adult↗
PubMed1983

The effect of increased lung volume on the expiratory rate of rise of alveolar carbon dioxide tension in normal man.

The rate at which alveolar PCO2 (PA, CO2) rises during expiration has been measured in seven healthy medical students. PA, CO2 rate of rise [delta PA, CO2/delta t] was measured by a method utilizing constant expiratory flow rates in individual breaths in two subjects, and was calculated from airway PCO2 and expiratory tidal volume in the remaining five subjects. Steady-state runs were recorded at two or more metabolic rates with the subject making no special effort to control mean lung volume. This was done to establish the relationship between delta PA, CO2/delta t and the rate of CO2 production (VCO2) at normal lung volume in individual subjects. Steady-state runs were also recorded at high lung volume. In each subject delta PA, CO2/delta t was less than would have been obtained at normal lung volume. Inversion of a hypothetical relation between delta PA, CO2/delta t, VCO2 and average lung volume (VLa; DuBois, Britt & Fenn, 1952) yielded calculated values of VLa for both the normal and the high lung volume states. Lung gas volume was measured in a whole body plethysmograph, ('box volume') both for the normal and high lung volume states, in each subject. Mean VLa and 'box volume' estimates showed only moderately good agreement, whereas the estimated differences between normal and high lung volume obtained by the two methods were virtually identical. These experiments suggest that the expiratory PA, CO2 rate of rise is determined, in the steady state, partly by the rate of CO2 production (a directly proportional relationship) and partly by the mean lung volume (an inversely proportional relationship).

Carbon Dioxide↗
PubMed1982

The rate of rise of alveolar carbon dioxide pressure during expiration in man.

1. The purpose of the study was to see whether the rate of rise of alveolar PCO2 (PA, CO2) in expiration was directly proportional to the rate of pulmonary elimination of CO2 (VCO2) in man in the steady state. 2. Alveolar ventilation at rest and during exercise in man was calculated from the difference between total ventilation and dead space ventilation, and from the ratio of the rate of pulmonary CO2 elimination to the mean expired alveolar CO2 (total) fraction. The results were indistinguishable. In agreement with other workers' findings alveolar ventilation changed in direct proportion to the rate of carbon dioxide elimination, confirming the isocapnia of exercise ventilation in man. 3. The rate of rise of expiratory alveolar PCO2 in individual breaths has been obtained by two methods. In the first, a pattern of respiration with constant expiratory flow in each breath brought expiratory alveolar profiles to the outermost end of the airway. In the second method, the early part of the alveolar PCO2 during normal expiration was calculated from airway PCO2 and expired volume. 4. The data obtained with both methods show that, in the steady state, expiratory alveolar PCO2 rises at a rate which is directly proportional to the rate of CO2 production.

Carbon Dioxide↗
PubMed1981

Reflex effects on human breathing of breath-by-breath changes of the time profile of alveolar PCO2 during steady hypoxia.

The respiratory effects of forced changes of alveolar PCO2 were studied in four healthy human subjects and in one anaesthetized cat. Solenoid valves, triggered by changes in mouth pressure, allowed changes from one inspiratory gas mixture to another, either during expiration (between-breath changes, BBC) or in the middle of inspiration (within-breath changes, WBC). In BBC the subject breathed CO2-free gas in one inspiration, CO2-rich gas in the next, and so on; end-tidal PCO2 alternated regularly from breath to breath by 1.1 kPa. In WBC CO2-free gas was given early in one inspiration and late in the next, with CO2-rich gas late in the former and early in the latter, and so on end-tidal PCO2 was nearly constant from breath to breath. Eight respiratory output variables were analysed. WBC induced small but significant alternation in most of the variables; these effects occurred almost exclusively in runs in hypoxia. The responses were not very different from those seen in BBC. The experiment on the cat showed that the alveolar PCO2 changes predicted during WBC are reflected by changes in pH in the arterial blood. The results confirm predictions based upon observations in the steady state of tube- and reversed-tube breathing in man. It seems likely that the responses are mediated by the arterial chemoreceptors responding to small changes in the profile of the (CO2, H+) oscillation.

Animals↗
PubMed1981

Respiratory arterial pH and PCO2 oscillations in patients with chronic obstructive airways disease.

1. Arterial pH oscillations have been monitored in vivo in patients with well defined chronic obstructive bronchitis, asthma and clinical emphysema. 2. The patients with clinical emphysema were shown to differ from those with chronic obstructive bronchitis on the basis of a number of clinical and physiological criteria. 3. Patients with asthma showed least attenuation of their pH oscillations as a group, in contrast to emphysematous patients who showed most attenuation. In patients with clinical emphysema the attenuation was relatively homogeneous. The patients with chronic obstructive bronchitis showed the full range from normal oscillations (zero attenuation) to zero (complete attenuation). 4. The amplitude and approximate rate of change of upslope of the PaCO2 oscillations in vivo were calculated, from measured pH oscillation amplitudes, using buffer slope values in vitro from Siggaard Anderson [(1962, 1963) Scandinavian Journal of Clinical and Laboratory Investigation, 14, 598-604; 15, 211-217], then dividing the PaCO2 amplitude by half the respiratory period. 5. Mean arterial PCO2 in vitro showed a very strong correlation with the downslope of the pH oscillation in vivo (calculated as for PaCO2 upslope) in patients without clinical emphysema. This correlation would be expected to some extent, owing to the logarithmic relationship of PaCO2 oscillations to pH oscillations. However, the mean arterial PCO2 also showed a very strong correlation with the upslope of the calculated PaCO2 oscillations, again excluding patients with clinical emphysema.

Adult↗
PubMed1980

Chronic stable asthma and the normal arterial pressure of carbon dioxide in hypoxia.

Arterial blood-gas tensions, pH, and peak expiratory flow rate were measured in 29 patients with chronic asthma in a stable state. The hypoxia in these patients was found to be comparable with the hypoxia seen in normal subjects at high altitude in its effects on arterial pressure of carbon dioxide (PaCO2). These results suggest that in patients with asthma the PaCO2 taken as normal should be related to the arterial oxygen tension. Any increase in the observed value compared with this predicted value indicates impaired respiratory control. This may well help in assessing the patients at greatest risk during an attack of asthma.

Adult↗
PubMed1980

Respiratory oscillations in arterial carbon dioxide tension as a control signal in exercise.

We have monitored oscillations in arterial pH (of respiratory frequency) in normal man at rest and during exercise. The pH oscillations are known to reflect respiratory oscillations in arterial carbon dioxide tension generated at the lungs. We have found that the pH oscillations increase in their upslope and downslope during exercise. This means that oscillations in arterial carbon dioxide tension can be considered as a control signal.

Carbon Dioxide↗
PubMed1978

The influence of low, normal and high Pa(O2) on the respiratory effects of Pa(CO2) oscillations in anaesthetised cats.

The present study examines the influence of oxygen tension on the recurrent tidal volume changes caused by oscillations in arterial P(CO2). The oscillations have a period equal to two respiratory cycles, and are produced by giving alternately CO2 -enriched and CO2 -free gas mixtures. The results show alternation of the tidal volume with the same incidence (is greater than 50%) at low, normal and high oxygen tensions. However, the magnitudes of the breath-by-breath changes are significantly greater at low oxygen tension than at normal oxygen tension. Under high oxygen tension breath-by-breath tidal volume changes are indistinguishable from those at normal oxygen tension.

Animals↗
PubMed1978

Respiratory oscillations in discharge frequency of chemoreceptor afferents in sinus nerve and anaesthetized cats at normal and low arterial oxygen tensions.

1. The discharge of chemoreceptor afferents in preparations of the sinus nerve in spontaneously breathing anaesthetized cats has been subjected to an averaging procedure in records obtained when the animals breathed (a) air and (b) a hypoxic gas mixture. 2. The mean discharge frequency was higher in hypoxia than at normal oxygen tension. 3. Oscillations in chemoreceptor discharge frequency with the same period as respiration were obtained by the averaging procedure both at normal arterial oxygen tensions and in hypoxia, but there was no significant increase in oscillation amplitude with hypoxia. 4. The carotid body response to arterial PCO2 oscillations does not therefore appear to be amplified by hypoxia. This finding is discussed in relation to the reported dependence upon hypoxia of the ventilatory effects of tube breathing in man.

Action Potentials↗