Biomedical subjects

M R Fedde

Publications and source records attributed to M R Fedde.

At least 55 records · Page 3Linked to original sources

PubMed1988

Absence of CO2-sensitive venous chemoreceptors in the cat.

We tested for the presence of CO2-sensitive venous chemoreceptors in anesthetized, paralyzed, artificially ventilated cats (N = 8). Systemic venous PCO2 was elevated (venous CO2 loading) by continuously passing blood withdrawn from the femoral artery (20 ml/min) through an extracorporeal gas exchanger, ventilated with 50% CO2 and 50% O2, and returning this hypercapnic blood to the femoral vein. Respiratory output was assessed by means of the amplitude of the integrated phrenic neurogram. Results of venous CO2 loading were compared to those of airway CO2 loading in which inspired CO2 levels were adjusted to give the same arterial PCO2 (PaCO2) as in venous loading. Despite large differences in mixed venous PCO2 (PvCO2) during venous CO2 loading (PvCO2 = 55 Torr, PaCO2 = 37 Torr) compared to airway CO2 loading (PvCO2 = 45 Torr, PaCO2 = 37 Torr), phrenic output was unchanged. However, phrenic output was elevated 33% when PaCO2 was increased 6-7 Torr by raising inspired CO2 and reduced 50% when PaCO2 was lowered 6-7 Torr by lowering inspired CO2, thereby substantiating the responsiveness of the respiratory control system to changes in PaCO2. The respiratory output response to changes in venous CO2 was also tested at a higher PaCO2 (40 Torr, created by adding 1% CO2 to the inspired air) and, as before, no change in phrenic output occurred when PvCO2 was elevated at a constant PaCO2. These experiments provide direct evidence for the absence of chemoreceptors in the central veins, right heart, and pulmonary arterial system of the cat that would respond to changes in PvCO2.

Animals↗

PubMed1988

Changes in serum potassium concentration with exercise in Hereford calves: effects of adrenalectomy.

1. Serum potassium concentration [K+] was measured pre- and postadrenalectomy in three Hereford steer calves before, during and following 3.5 min exercise at their maximal speed capability. 2. Both before and after adrenalectomy, serum [K+] increased an average of 2.4 mEq.1(-1) during exercise and was at control levels 10 min postexercise. 3. Hormones from neither the adrenal cortex nor the adrenal medulla influence serum [K+] dynamics during acute exercise.

Adrenal Glands↗

PubMed1988

Serum potassium during exercise in Hereford calves: influence of physical conditioning.

We determined how rapidly serum potassium concentration ([K+]) increased, its magnitude, and how quickly it decreased during and after a 3.5-min exercise bout at maximal speed capability in eight Hereford steers, before and after physical conditioning. Serum [K+] values rose rapidly after the start of exercise and declined rapidly to within 7% of preexercise values 5 min after exercise ceased. Before physical conditioning, serum [K+] increased from an average of 4.19 meq/l at rest to 6.71 meq/l at the highest treadmill speed the animals could sustain (1.8-2.4 m/s at a 3 degrees incline). After physical conditioning, the serum [K+] increase at comparable treadmill speeds was approximately 5% lower than before conditioning (average of 6.37 meq/l); however, the animals could now exercise from 0.6 to 0.8 m/s faster than before conditioning, and their maximal serum [K+] rose to an average of 7.47 meq/l, a 10% increase over preconditioned maximal values. We conclude that higher speeds and accompanying increases in serum [K+] attained by conditioned animals may place them at greater risk of cardiotoxicity than before conditioning.

Animals↗

PubMed1987

Cardiorespiratory changes during HCl infusion unrelated to decreases in circulating blood pH.

To test the hypothesis that infusion of HCl changes blood pressure and respiration independent of decreases in circulating blood pH, an extracorporeal arteriovenous shunt (20 ml/min) between the femoral artery and vein was installed in anesthetized cats. Into this loop, acid (0.25 M HCl) and, approximately 10 cm downstream, base (0.25 M NaOH) could be infused simultaneously. Likewise, either acid or base could be infused individually. Right ventricular (Prv) and arterial (Pa) blood pressure, tidal volume (VT), and respiratory frequency (fresp) were recorded as well as blood gases and pH in arterial, right ventricular, and shunt loop blood at the reentrance into the animal. When HCl and NaOH were infused simultaneously and at equimolar rates (0.2 mmol/min for 10 min), there was a large increase in Prv, with little change or decrease in Pa. Respiratory frequency was increased, but total ventilation was not elevated because of a concomitant fall in VT. The rise in Prv and increase in fresp were transient in that they could only be evoked during the first HCl-NaOH infusion in a given animal. Repetitive infusions of HCl-NaOH into the same animal failed to elicit the response. Similar transient acid effects were evoked when HCl was infused without NaOH but not when NaOH was infused without HCl. During the second and third infusion of HCl, ventilatory responses were elicited that were explainable by stimulation of known chemoreceptors. The transient rise in Prv and fresp evoked by acid infusion might be explained by release of an agent from blood elements at the tip of the HCl infusion catheter, which in turn would constrict pulmonary vessels and influence breathing.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Biological effects of short-term, high-concentration exposure to methyl isocyanate. III. Influence on gas exchange in the guinea pig lung.

The influence of methyl isocyanate (MIC) inhalation on the gas exchange function of the lungs in guinea pigs was studied by measuring arterial blood gases, pH, and tracheal pressure during constant-volume, artificial ventilation with air or 100% O2 at 40 and 120 min after exposure. A 15 min exposure to MIC at concentrations of 240 to 628 ppm caused a marked reduction in PaO2 and pHa and an elevated tracheal pressure during artificial ventilation. The low PaO2 was only slightly elevated when the animals were ventilated with 100% O2. Although the dry-wet lung weight ratio was reduced at the highest exposure concentration, the effect was not severe and no significant increase in lung water was found at the lower concentrations. MIC inhalation caused severe pulmonary blood shunting and ventilation/perfusion imbalance. This, in turn, led to hypoxemia, metabolic acidosis, and tissue hypoxia, which could produce death. The pulmonary gas exchange deficit likely resulted from bronchial and bronchiolar obstruction caused by sloughed epithelium and other debris from intra- and extrapulmonary airways.

Animals↗

PubMed1986

Effects of altering dead space volume on respiration and air sac gases in geese.

Dead space volume (VD) was altered in spontaneously breathing, anesthetized geese from values far above (about 115 ml) to those far below (about 3 ml) the normal VD (approximately 40 ml). Respiratory gases were measured in cranial (CrS) and caudal air sacs (CdS) and in blood. The major findings were as follows: Ventilation increased linearly with VD, by increases in tidal volume (VT) at constant breathing rate (fresp); effective parabronchial ventilation, (VT-VD) X fresp, remained constant and so did arterial blood gases. No changes occurred in CrS gas composition. CdS PCO2 declined with decreasing VD, and the respiratory exchange ratio increased, reaching values above unity at the lowest VD. The gas composition in CrS, and particularly its relation to end-expired gas composition, is in agreement with current models of the gas flow pattern in the avian lung. The PCO2 values in CdS are higher than expected by simple models, e.g. by dead space re-inhalation. Neopulmonic gas exchange and incomplete gas mixing are suggested to contribute significantly to the gas composition of CdS.

Air Sacs↗

PubMed1986

Regional circulatory responses to hypocapnia and hypercapnia in bar-headed geese.

To investigate mechanisms that may allow birds to tolerate extreme high altitude (hypocapnic hypoxia), we examined the effects of severe hypocapnia and moderate hypercapnia on regional blood flow in bar-headed geese (Anser indicus), a species that flies at altitudes up to 9,000 m. Cerebral, coronary, and pectoral muscle blood flows were measured using radioactive microspheres, while arterial CO2 tension (PaCO2) was varied from 7 to 62 Torr in awake normoxic birds. Arterial blood pressure was not affected by hypocapnia but increased slightly during hypercapnia. Heart rate did not change during alterations in PaCO2. Severe hypocapnia did not significantly alter cerebral, coronary, or pectoral muscle blood flow. Hypercapnia markedly increased cerebral and coronary blood flow, but pectoral muscle blood flow was unaffected. The lack of a blood flow reduction during severe hypocapnia may represent an important adaptation in these birds, enabling them to increase O2 delivery to the heart and brain at extreme altitude despite the presence of a very low PaCO2.

Acid-Base Equilibrium↗

PubMed1985

Gas exchange during exercise in hypoxic ducks.

We quantitatively assessed pulmonary gas exchange in Pekin ducks (Anas platyrhynchos) during running exercise (1.44 km X h-1 at 3 degrees incline) while the ducks spontaneously breathed either air (FIO2 = 0.21) or a hypoxic gas mixture (FIO2 = 0.12). During exercise, oxygen consumption increased 3 times above the resting value in normoxia and 3.6 times above rest in hypoxia. The convection requirement rose 34% and 20% in running normoxic and hypoxic ducks, respectively. The O2 extraction coefficient was the same in resting normoxic and hypoxic ducks (0.19 vs 0.18) and decreased by the same amount under exercise conditions (0.14 vs 0.15). Arterial PO2 was maintained during exercise in normoxia but increased slightly during exercise in hypoxia. Cardiac output increased by 73% and 111% during exercise in normoxic and hypoxic ducks, respectively. Calculations indicate that both the O2-diffusing capacity and the total conductance for O2 of the gas exchange system increased markedly during exercise in normoxia and hypoxia. We conclude that at this level of exercise, there was no apparent limitation to gas exchange in either the normoxic or hypoxic Pekin duck.

Acid-Base Equilibrium↗

PubMed1985

Blood flow distribution during hypocapnic hypoxia in Pekin ducks and bar-headed geese.

The purpose of this study was to determine the effects of hypocapnic hypoxia on regional blood flow in birds. Regional blood flow was measured using the radioactive microsphere method in unanesthetized Pekin ducks (Anas platyrhynchos) and bar-headed geese (Anser indicus) breathing 21, 10 and 5% O2. In both birds, arterial PO2 was reduced from about 96 Torr during normoxia to about 28 Torr during severe hypoxia. Severe hypocapnic hypoxia produced a change in the pattern of blood flow in ducks; blood flow to some organs increased (brain, adrenal glands, heart, and eyes) while flow to other organs decreased (liver, spleen, small intestine, shell gland). Compared with ducks, bar-headed geese were able to provide higher levels of O2 delivery to their tissues since blood flow to a variety of organs and skeletal muscles was either unchanged or increased during severe hypoxia. The redistribution of blood flow in Pekin ducks during severe hypocapnic hypoxia may help to support large increases in cerebral and coronary blood flow but may also contribute to the development of a metabolic acidosis.

Animals↗

PubMed1985

Ventilatory and intrapulmonary chemoreceptor sensitivity to CO2 in the burrowing owl.

We measured the ventilatory response of anesthetized, unidirectionally ventilated pigeons and burrowing owls to changes in intrapulmonary CO2 concentration and the static CO2 sensitivity of intrapulmonary chemoreceptors (IPC) in these species and the domestic goose. Compared with pigeons, burrowing owls showed a significantly reduced respiratory frequency and amplitude response to increases in FICO2 from 0.05 to 0.10, which corroborates similar findings in intact, awake individuals of the same species. The average static CO2 sensitivity of IPC in geese, pigeons, and burrowing owls, as reflected by the average slope of the linear regressions of receptor discharge frequency on ln(PICO2), was -7.96, -11.1 and -6.87 imp/sec . ln(PICO2), respectively. The sensitivities of individual receptors were normally distributed in geese and pigeons, but skewed in burrowing owls. Therefore, the median CO2 sensitivity [-5.50 imp/sec . ln(PICO2)] is a more appropriate measure of the typical CO2 sensitivity of IPC in burrowing owls. The static CO2 sensitivity of IPC in burrowing owls is the lowest reported for euthermic birds with a normal acid-base balance and may materially contribute to the blunted ventilatory response of these birds to the elevated CO2 levels they encounter in nature.

Animals↗

PubMed1985

Breathing pattern in anesthetized chickens: CO2 inhalation and vagotomy.

The breathing patterns of 20 anesthetized chickens were studied during progressive suppression of intrapulmonary chemoreceptors (IPC) by various concentrations of CO2 and following bilateral vagotomy. The vagotomy breathing pattern, characterized by a marked accentuation of expiratory times with prolonged expiratory pauses, was markedly different from that induced by CO2 inhalation. Removal of neural input to the central respiratory centers from IPC does not appear to be solely responsible for the altered breathing pattern following vagotomy in birds.

Anesthesia↗

PubMed1985

Respiratory, cardiovascular, and metabolic adjustments to exercise in the Hereford calf.

Six Hereford steers were studied before, during, and after short exercise bouts on a motor-driven treadmill (3 degrees incline) at four speeds (1.0, 1.4, 1.8, and 2.2 m X s-1). Oxygen consumption (MO2) and carbon dioxide production (MCO2) were measured by collecting the expired gas. Arterial and mixed venous blood samples were obtained simultaneously from indwelling catheters in the aorta and pulmonary artery. A 10-fold increase was observed in MO2 and MCO2 at the highest work load. Minute ventilation increased proportionately less than MO2 and MCO2 with increasing work loads, but alveolar ventilation was found to increase in proportion to both MO2 and MCO2. The highest work load produced a threefold increase in cardiac output primarily as a result of increased heart rate. A 10-fold increase in lactate and a 63% increase in serum potassium concentration were observed at the highest work load. Plasma cortisol levels were highest at 10 min postexercise and reached levels of seven times the resting values following exercise at the highest speed. The responses to exercise in the calf are qualitatively similar to those observed in other species, but quantitative differences exist in some cardiovascular and metabolic responses which may limit this animal's ability to perform strenuous exercise.

Animals↗

PubMed1985

Effect of ruminal CO2 on gas exchange and ventilation in the Hereford calf.

The contribution of ruminal CO2 to gas exchange measurements and ventilation was determined in four rumen-fistulated Hereford steers at rest and during exercise. The calves were exercised at 1.4 and 2.2m X s-1 under three treatments: 1)full rumen with fistula sealed, 2) full rumen with fistula open, and 3) empty rumen. Measurements also were made at rest while flushing the empty rumen with either 100% N2 or a mixture of 50% CO2-50% N2. O2 consumption, CO2 production (Mco2), and ventilation were measured by collecting the expired gas. Absorption across the ruminal epithelium during rest increased Mco2 by 3%, whereas absorption and eructation together increased Mco2 by 15%. The respiratory exchange ratio (R) was significantly different among the three treatments at rest, but no differences were observed in R among the treatments during exercise. No changes were observed in minute ventilation among the three conditions, but a decrease in respiratory frequency and an increase in tidal volume occurred when the rumen was empty. These changes in ventilatory pattern may have been due to a decrease in body temperature when the rumen was empty. When the empty rumen was flushed with 50% CO2, Mco2 was increased 21% over the value observed when flushing with 100% N2. CO2 of fermentation origin is added to the expired gas by both eructation and absorption and has a significant effect on R in the resting animal, but no effect on R during exercise.

Animals↗

PubMed1984

Chemoreflex drive of ventilation during exercise in ducks.

To determine if arterial chemoreceptors contribute to the ventilatory response during exercise, we measured minute ventilation (VI) in spontaneously breathing Pekin ducks (Anas platyrhynchos) during rest and running exercise when the inspired gas was switched from either 21% or 12% O2 to 100% O2 for 45 s (O2-test). In normoxia at rest (PaO2 = 99 Torr), inhaling 100% O2 reduced VI by 30%, while during resting hypoxic conditions (PaO2 = 56 Torr), 100% O2 inhalation reduced VI by 66%. During exercise, abruptly inhaling 100% O2 decreased VI by only 14% and 33% in normoxic and hypoxic conditions, respectively. Thus, only a small fraction of the ventilatory response during exercise under normoxic conditions is due to an arterial chemoreceptor input. However, during exercise in hypoxic conditions, arterial chemoreceptors provide a substantial portion of the total drive to ventilation.

Animals↗

PubMed1984

Oxygen delivery to the heart and brain during hypoxia: Pekin duck vs. bar-headed goose.

To investigate mechanisms that may allow birds to tolerate extreme high altitude, we acutely exposed unanesthetized bar-headed geese (Anser indicus) and Pekin ducks (Anas platyrhynchos) to 0.21, 0.10, and 0.05 inspired fractional concentrations of O2 (FIO2). In both birds, arterial O2 partial pressure (PaO2) was about 95 Torr at 0.21 FIO2, 45 Torr at 0.10 FIO2, and 28 Torr at 0.05 FIO2. Hyperventilation occurred at both levels of hypoxia, with PaCO2 decreasing to about 7 Torr at 28 Torr PaO2. At 28 Torr PaO2, arterial O2 content (CaO2) in geese (10.4 vol%) was significantly higher than in ducks (4.1 vol%). As PaO2 declined from about 95 to 28 Torr, both cerebral and coronary blood flow (determined by using the radioactive microsphere method) increased more than fivefold in ducks but less than threefold in geese. At both levels of hypoxia, O2 delivery (flow X CaO2) to the heart and brain of geese was the same as or higher than that of ducks. The unique control of cerebral and coronary O2 delivery exhibited by both species of birds may be related to their remarkable tolerance to severe hypocapnic hypoxia.

Adaptation, Physiological↗

PubMed1984

Attenuated pulmonary pressor response to hypoxia in bar-headed geese.

We determined the pulmonary pressor response during hypoxia in bar-headed geese (Anser indicus), a species that flies at altitudes up to 9,000 m, and Pekin ducks (Anas platyrhynchos), a non-flyer. Mean pulmonary arterial blood pressure (PAP) and arterial O2 partial pressure (PaO2) were measured in unanesthetized birds acutely exposed to 21, 10, 5, and, in geese only, 4% O2. PAP in geese did not change as PaO2 was reduced from 95 to 46 Torr and rose only 3 mmHg when PaO2 was reduced to 28 Torr. The same PaO2 decline in ducks (99 to 29 Torr) resulted in an 11-mmHg rise in PAP. The data suggest that very little or no increase in pulmonary vascular resistance occurs in these geese during hypoxia. This bird may provide a unique model in which to study pulmonary vascular control mechanisms.

Animals↗

PubMed1983

Exercise hyperpnea in the duck without intrapulmonary chemoreceptor involvement.

To determine the involvement of intrapulmonary chemoreceptors (IPC) in the control of breathing during exercise, it is necessary to hold the PCO2 in the microenvironment of these receptors constant at the resting value. We accomplished this in unanesthetized Pekin ducks by ligating the left pulmonary artery and diverting all of the cardiac output to the right lung, which was denervated. The ducks were then unidirectionally ventilated with a constant gas stream (5% CO2, 19% O2, balance N2) at a flow rate of 12 L X min-1. This procedure provided a constant microenvironment for the receptors in the left lung despite any changes in the chemical composition or flow rate of the blood going to the right lung during exercise. Ventilatory effort increased during running exercise (1.44 km X h-1 at a 3 degrees incline) by an average of 145% over resting values because of an increase in both respiratory frequency and tidal volume. Because no altered stimuli were presented to the IPC using this procedure, the increased ventilation with exercise could not have resulted from changes in their discharge frequency. We conclude that ventilation can increase during exercise in the duck in the absence of IPC involvement and that other neural input, possibly from muscle, is responsible for the hyperpnea.

Animals↗

PubMed1983

Cardiopulmonary control during exercise in the duck.

To determine the importance of nonhumoral drives to exercise hyperpnea in birds, we exercised adult White Pekin ducks on a treadmill (3 degrees incline) at 1.44 km X h-1 for 15 min during unidirectional artificial ventilation. Intrapulmonary gas concentrations and arterial blood gases could be regulated with this ventilation procedure while allowing ventilatory effort to be measured during both rest and exercise. Ducks were ventilated with gases containing either 4.0 or 5.0% CO2 in 19% O2 (balance N2) at a flow rate of 12 l X min-1. At that flow rate, arterial CO2 partial pressure (PaCO2) could be maintained within +/- 2 Torr of resting values throughout exercise. Arterial O2 partial pressure did not change significantly with exercise. Heart rate, mean arterial blood pressure, and mean right ventricular pressure increased significantly during exercise. On the average, minute ventilation (used as an indicator of the output from the central nervous system) increased approximately 400% over resting levels because of an increase in both tidal volume and respiratory frequency. CO2-sensitivity curves were obtained for each bird during rest. If the CO2 sensitivity remained unchanged during exercise, then the observed 1.5 Torr increase in PaCO2 during exercise would account for only about 6% of the total increase in ventilation over resting levels. During exercise, arterial [H+] increased approximately 4 nmol X l-1; this increase could account for about 18% of the total rise in ventilation. We conclude that only a minor component of the exercise hyperpnea in birds can be accounted for by a humoral mechanism; other factors, possibly from muscle afferents, appear responsible for most of the hyperpnea observed in the running duck.

Animals↗