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Biomedical subjects

M Gleeson

Publications and source records attributed to M Gleeson.

At least 73 records · Page 4Linked to original sources

Breast feeding conditions a differential developmental pattern of mucosal immunity.

A prospective study of 146 children was conducted to evaluate the influence of infant feeding patterns on the development of mucosal immunity. First, there was a trend towards lower IgG concentrations in the breast-fed neonate, indicating a possible earlier 'closure' mechanism of membrane permeability. Second, the post-natal increase in IgA was earlier and greater in formula-fed infants. Third, IgM was detected earlier, more frequently, and at higher levels in formula-fed infants.

Aging

Effects of changes in tidal volume on avian intrapulmonary chemoreceptor discharge.

It has been suggested that avian intrapulmonary CO2-sensitive receptors (IPC) may be capable of monitoring the rate and extent of CO2 washout from the lung during spontaneous breathing. The purpose of this study was to analyse IPC discharge activity (using computerised bin-averaging and counting techniques) in spontaneously breathing domestic fowl when VT was elevated from resting levels. This was accomplished by administration of almitrine (2 mg X kg-1 i.v.), a respiratory stimulant drug that has been shown to have a specific long-lasting stimulatory action on carotid body chemoreceptors. Unanaesthetized decerebrate chickens were tracheotomized and single unit activity was recorded from 14 IPC. When VT progressively increased following administration of almitrine (with little or no change in TI or TE), IPC activity increased in a linear relationship with the increased VT. IPC activity in expiration was also increased, and the delay period before the onset of IPC discharge in inspiration was shortened. It is concluded that IPC discharge is increased when VT is elevated in the spontaneously breathing chicken and hence the IPC are capable of monitoring the extent of each ventilatory effort. It is well known that IPC have strong inhibitory effects on ventilatory motor output and conceivably they could originate reflexogenic information to the respiratory centres in response to intrapulmonary PCO2 changes. The latter could arise from changes in CO2 delivery by the mixed venous blood or from changes in the extent of CO2 washout with each breath.

Almitrine

Ventilatory and cardiovascular responses of the unanaesthetized chicken, Gallus domesticus, to the respiratory stimulants etamiphylline and almitrine.

The ventilatory and cardiovascular effects of i.v. administration of the respiratory stimulants etamiphylline and almitrine were investigated in conscious or decerebrate adult female domestic fowl. Infusion of etamiphylline (100 mg . kg-1) or injection of almitrine (2 mg . kg-1) evoked a potent long-lasting stimulation of ventilation in both conscious and decerebrate fowl. The pattern of the respiratory response was characteristically different to that observed in mammals in that the increased minute volume of ventilation was attained by large increases in respiratory frequency accompanied by a reduction in tidal volume. The pattern of respiration following drug-induced stimulation was, in some birds, typical of thermal panting although neither etamiphylline nor almitrine caused significant increases in body temperature. Differences in the pattern of responses of the rate and depth of breathing may be attributed in part to the differences in pulmonary receptor systems involved in the control of breathing in birds and mammals.

Almitrine

Changes in intrapulmonary chemoreceptor discharge in response to the adjustment of respiratory pattern during hyperventilation in domestic fowl.

It has been suggested that avian vagal intrapulmonary CO2-sensitive receptors (i.p.c.) may be capable of monitoring the rate and extent of CO2 wash-out from the lung during spontaneous breathing. The purpose of this study was to record i.p.c. discharge activity in spontaneously breathing domestic fowl when minute volume (VI) was elevated from resting levels. This was accomplished by administration of almitrine (2 mg X kg-1 I.V.), a respiratory stimulant drug that has been shown to have a specific long-lasting stimulatory action on carotid body chemoreceptors. Unanaesthetized decerebrate fowl were tracheotomized and single-unit activity was recorded from sixteen vagal i.p.c. When ventilation was elevated 2.2-fold by almitrine (initially by increases in tidal volume (VT)) i.p.c. discharge was increased in both inspiration and expiration, and the delay period before the onset of i.p.c. discharge in inspiration was markedly shortened. Within 5-10 min after the administration of almitrine, the breathing pattern changed to one of rapid, shallow breathing, although the 2.2-fold elevation of the rate of gas flow through the parabronchi (V) and mean inspiratory flow rate (VT/TI) were maintained. The i.p.c. continued to fire phasically, with peaks of discharge in both inspiration and expiration, though there were fewer spikes per breath and mean inspiratory peak discharge rate returned to control (eupnoeic) levels. It is concluded that i.p.c. discharge is increased when VI is elevated in the spontaneously breathing fowl and that the pattern of discharge is dependent on the pattern of breathing. I.p.c. show high dynamic sensitivity to changes in the PCO2 of their microenvironment and it is possible to explain the changes in discharge pattern observed in terms of the PCO2 changes in the lungs and air sacs. These results support proposals that the pattern of breathing is to some extent dependent upon the intensity and timing of i.p.c. activity.

Almitrine

Respiratory and cardiovascular responses of the exercising chicken to spinal cord cooling at different ambient temperatures. I. Cardiovascular responses and blood gases.

We measured oxygen consumption (VO2), heart rate (HR), stroke volume (SV), cardiac output (CO) and mean arterial blood pressure (MBPa) of chickens during 15 min treadmill exercise at 0.5 ms-1 and 0.8 ms-1 at thermoneutral (23 degrees C), low (9 degrees C) and high (34 degrees C) ambient temperature (Ta); the vertebral canal was cooled to 34 degrees C during the middle 5 min of each exercise period. PO2, PCO2, pH and oxygen content (CO2) of the arterial and mixed venous blood were also measured. VO2 during exercise was not significantly affected by Ta. Spinal cord cooling produced definite increases in VO2, CO and SV during 0.5 ms-1 exercise at 9 degrees C; otherwise, effects of spinal cord cooling were not significant. HR, SV and CO were all linearly related to VO2; these relationships were unaffected by spinal cord cooling or Ta. Blood pressure did not increase during exercise. PaCO2 and P-vCO2 did not increase significantly during exercise. The arterial-venous CO2 difference was increased by exercise only at 34 degrees C. The chickens generally hyperventilated at 34 degrees C Ta compared to the other Ta values. No consistent effect on blood gases or on pH and CO2 of the blood could be attributed to spinal cord cooling.

Animals

Respiratory and cardiovascular responses of the exercising chicken to spinal cord cooling at different ambient temperatures. II. Respiratory responses.

We measured oxygen consumption (VO2), carbon dioxide production (VCO2), minute volume (VE), respiratory frequency (f) and tidal volume (VT) of chickens during 15 min treadmill exercise at 0.5 ms-1 and 0.8 ms-1 at thermoneutral (23 degrees C), low (9 degrees C) and high (34 degrees C) ambient temperature (Ta); the vertebral canal was cooled to 34 degrees C during the middle 5 min of each exercise period. Temperatures of the vertebral canal (TVC) and rectum (Tre) were also measured. Exercise at 0.5 ms-1 caused increases in O2 consumption, CO2 production, minute volume and tidal volume compared to resting controls at each Ta. Minute volume and respiratory frequency were higher and tidal volume was lower in birds exercising at 34 degrees C than at 23 or 9 degrees C. Spinal cord cooling during exercise (0.5 ms-1) at 9 degrees C caused further increases in O2 consumption, tidal volume and respiratory frequency almost equivalent to those produced by an increase in the running speed to 0.8 ms-1. Spinal cord cooling during exercise (0.5 ms-1) at 23 degrees C did not significantly affect O2 consumption, CO2 production, minute volume, tidal volume or respiratory frequency. Spinal cord cooling during exercise (0.5 ms-1) at 34 degrees C did not affect O2 consumption or CO2 production, but caused decreases in minute volume and respiratory frequency and an increase in tidal volume. We conclude that the domestic fowl exhibits spinal thermosensitivity during exercise, although these responses appear to be smaller than those previously reported for the resting bird. Decreased external temperature potentiates the effects of spinal cord cooling during exercise.

Animals

The relationship between atopy and salivary IgA deficiency in infancy.

In a prospective study, infants born to atopic parents had a significantly higher prevalence of salivary IgA deficiency at all ages studied than control infants, and the mean non zero IgA level of the potentially atopic infants was significantly lower at 8 and 12 months than of control infants. Of the infants with atopic parents, the prevalence of IgA deficiency was not significantly greater in those who manifested atopic disease during the study period than in those who did not, but the levels were significantly lower at 4 months.

Aging

Effects of body temperature on ventilation, blood gases and acid-base balance in exercising fowl.

In order to determine the influence of hyperthermia on respiratory, blood gas and acid-base changes in exercising birds, we exercised domestic fowl on a treadmill at ambient temperatures of 5, 20, 30 and 35 degrees C for 10 min at graded running speeds up to 4.3 km.h-1. Ventilation and gas exchange were measured continuously and arterial blood gases, pH and the concentration of lactic acid in arterial blood were measured in samples taken during the last minute of each run. During exercise at 5 degrees C rectal temperature did not change significantly from rest (isothermic condition) and there was no sign of thermal influence on respiratory pattern, such as was observed at higher ambient temperatures. At any given running speed, increased ambient temperature caused increased ventilation by an increase in respiratory frequency (f) together with a decrease in tidal volume (VT). Under isothermic conditions, at low running speeds, birds maintained an isocapnic hyperpnoea: arterial PCO2, PO2 and pH and oxygen extraction were unchanged. However at higher speeds (ca. greater than 2.5 km.h-1) some hyperventilation occurred with subsequent falls in arterial PCO2 and oxygen extraction. Arterial pH also fell significantly (P less than 0.01). During hyperthermic exercise, oxygen extraction, arterial PCO2 and bicarbonate concentration all fell significantly (P less than 0.01) and progressively with increasing work load, and birds hyperventilated at all running speeds. This produced a significant arterial hypocapnia and alkalosis at the lower speeds (P less than 0.05) but this was replaced by a hypocapnic metabolic acidosis at the higher running speeds. Blood lactate concentration rose steeply at speeds above ca. 2.5 km.h-1 but arterial pH fell by only 0.1 units or less partly as a result of buffering by blood bicarbonate. It is concluded that both hyperthermia and lactacidosis are causes of hyperventilation and arterial hypocapnia during heavy running exercise in birds. However, ventilatory adjustments similar to those observed in resting hyperthermic birds, viz. increased f and reduced VT prevent severe arterial hypocapnia from occurring in hyperthermic exercising birds.

Acid-Base Equilibrium

Vagal control of respiratory pattern during hyperpnea in domestic fowl.

Minute volume, tidal volume, and respiratory frequency were measured during hyperpnea induced by exercise, increased body temperature, and CO2 inhalation. Ventilatory characteristics were compared before and after the vagus nerve had been blocked. In normal birds exercise produced increases in both tidal volume and respiratory frequency; hyperthermia produced a typical thermal polypnea consisting of greatly increased respiratory frequency and reduced tidal volume; CO2 inhalation produced increases in tidal volume and respiratory frequency when the birds were euthermic but a slowing of respiratory rate when the birds were hyperthermic. After vagal block these pronounced differences in the pattern of ventilatory response to the various respiratory stimuli were abolished. Instead there was a uniform ventilatory response to all three stimuli consisting mainly of increases in tidal volume combined with small increases in respiratory frequency. It is concluded that in the normal animal control of the varied pattern of ventilatory response to different respiratory stimuli is dependent on vagal fiber activity.

Animals

Effects of PCO2 on respiratory pattern during thermal and exercise hyperventilation in domestic fowl.

The relationship between respiratory pattern and arterial PCO2 was investigated during hyperventilation induced by graded exercise and hyperthermia. Treadmill exercise was performed both in isothermic and hyperthermic conditions. Isothermic exercise was induced by spraying the birds with water before exercise at environmental temperatures of 18 +/- 2 degrees C. Hyperthermic exercise was performed in unsprayed birds at temperatures of 18 +/- 2 degrees C and 30 +/- 2 degrees C. During isothermic exercise there was no significant change in arterial PCO2 at moderate work loads and only a small drop in PCO2 at the heaviest work loads; ventilation was increased by coupled increases in tidal volume and respiratory frequency. During exercise in unsprayed birds rectal temperature rose progressively and arterial PCO2 fell progressively with work load. At each work load ventilation was higher and breathing was more rapid and shallow than during isothermic exercise. These effects were more pronounced during exercise at 30 +/- 2 degrees C than at 18 +/- 2 degrees C. When normal PCO2 was maintained during hyperthermic exercise, as a result of the administration of CO2-enriched air, polypnea was suppressed and the tidal volume-respiratory frequency relationship became identical to that observed during graded isothermic exercise. Maintenance of normal PCO2 in resting birds subjected to a gradual increase in environmental temperature also resulted in changes in respiratory pattern identical to those obtained during eucapnic exercise. It is concluded that, provided arterial PCO2 is held constant, the pattern of breathing is the same for hyperventilation induced by exercise or by body temperature increases.

Animals

Respiratory and blood gas responses in exercising birds.

The effects of exercise in birds on changes in body temperature, ventilation, blood gases and air-sac gases are reviewed. Except in the case of isothermic exercise below the anaerobic threshold, birds hyperventilate during exercise. Exercise hyperventilation is greater at higher exercise intensities and at higher environmental temperatures. The domestic fowl appears to be a suitable model for the study of physiological responses to exercise in running birds. A prior period of training is necessary to accustom the birds to laboratory procedures. The possible neural and/or humoral mechanisms controlling exercise hyperpnea are listed. Intrapulmonary hypocapnia seems to exclude the possibility that lung chemoreceptors are responsible for the hyperpnea during exercise, but these receptors probably play a predominant role in the determination of ventilatory pattern.

Animals

Ventilation, gaseous exchange and air sac gases during moderate thermal panting in domestic fowl.

Gaseous exchange, ventilatory pattern and gas levels within the interclavicular and abdominal air sacs of domestic fowl were monitored before, during and after periods of moderate hyperthermic panting. O2 consumption (VO2) remained virtually unaltered and CO2 production (VCO2) increased slightly during panting as compared to normal respiration. Resting VO2 was 12.2 ml X kg-1 X min-1. Resting (eupneic) PO2 and PCO2 of the interclavicular and abdominal air sacs were 100.1 and 38.5 torr, and 125.2 and 16.4 torr respectively. During panting the partial pressure of the abdominal air sac Pabs, O2 and Pabs, CO2 fell and rose to extreme values of 109 and 29.8 torr respectively. Simultaneously the partial pressure of the interclavicular air sac Pics, O2 and Pics, CO2 changed by smaller amounts to 107.5 and 32.3 torr respectively. Ventilatory pattern during thermal panting was characterized by rapid, shallow movements which were interrupted at regular intervals by short sequences of slower, deeper breaths. During these intermittent periods of eupneic breathing gas levels returned towards normal and these alterations were reflected in transient variations in VO2 and VCO2 about their mean values. Changes in gas levels within the lung-air sac system are discussed in connexion with the peripheral control of ventilation during panting.

Acid-Base Equilibrium

Effects of temperature on the ventilatory response to inspired CO2 in unanaesthetized domestic fowl.

The influence of raised environmental temperature on the respiratory response to CO2 in awake, spontaneously breathing domestic fowl was investigated. In terms of their effects on ventilation VE temperature and CO2 were additive and non-interactive, VE being approximately 1900 ml . min-1 greater at 33 +/- 1 degree C compared to 18 +/- 1 degree C, regardless of inspired CO2 partial pressure PICO2. Temperature had no effect on the slope of the relationship between VE and both arterial and clavicular air sac PCO2. Blood and clavicular sac PCO2 were regulated within 2-3 Torr of normal at PICO2 levels below approximately 20 Torr as a result of hyperventilation but PCO2 regulation began to fail at higher PICO2. Hypercapnia induced increases in respiratory frequency f at normal temperatures but decreases in f at 33 +/- 1 degree C. There was little change in f at 25 +/- 1 degree C. The ventilatory increase in response to CO2 at 18 +/- 1 degree C and 25 +/- 1 degree C could be described by a linear relationship between VE and tidal volume VT. However, respiration departed from this pattern at temperatures above the panting threshold (32-34 degrees C). These findings are discussed in the context of central and peripheral mechanisms which may be involved in the control of rate and depth of breathing.

Animals

The effects of physical exercise on metabolic rate and dietary-induced thermogenesis.

1. The energy metabolism of ad lib.-fed adult male Wistar rats receiving daily running exercise (0.9 km/d; 8 degrees incline) on a motor-driven treadmill, over a period of 56 d, was compared with that of sedentary ad lib.-fed rats and sedentary restricted-fed rats of similar body-weight (approximately 420 g). 2. The metabolizable energy of the diet (Oxoid 41 B) was 11.44 +/- 0.05 kJ/g. This value was not affected by restricted feeding (70% ad lib.), exercise training or exercise itself. 3. Exercise-trained rats ate 5% more food than the sedentary ad lib.-fed rats but their equilibrium body-weight was 60 g lower than that of the latter group. 4. Resting metabolic rate, measured over 22 h in a respiration chamber was increased by 10% in exercise-trained animals. 5. Feeding increased energy expenditure (dietary-induced thermogenesis) and this effect was potentiated by performance of an exercise task. 6. Exercise-trained rats exhibited anticipatory rises in energy expenditure (approximately 40%) when placed on a stationary treadmill. 7. Treadmill work increased energy expenditure by a factor of 1.9-2.4. 8. The energy cost of the exercise, determined by respiration calorimetry was 66-80 J/g per km. These energy costs did not account for all the differences observed in food energy consumption of exercise-trained and sedentary rats of equal body-weight. 9. It is concluded that regular physical exercise increases energy expenditure by factors additional to the energy requirement directly related to the physical work. These factors include an increased resting metabolic rate in exercise-trained rats, increased dietary thermogenesis induced by exercise and anticipatory increases in energy metabolism during the period preceding exercise.

Animals