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Biomedical subjects

W K Milsom

Publications and source records attributed to W K Milsom.

At least 73 records · Page 4Linked to original sources
PubMed1989

Effects of prolonged inflation on pulmonary stretch receptor discharge in turtles.

The tonic and phasic discharge characteristics of single, slowly adapting pulmonary stretch receptors (SAR) were examined before and after 1 h periods of constant pressure inflation to normal resting (VLr, pressure = 0 cm H2O) and elevated (VLe, pressure = 10 cm H2O) lung volumes in turtles (Chrysemys sp.). Based on their discharge at VLr, SAR were classified as either low (n = 13) or high threshold (n = 4) receptors. Inflations were performed with both air and 5% CO2 in air. Lung gas composition and arterial PCO2 and pH were measured during the maintained inflations. In animals ventilated with air, low and high threshold receptors adapted by 57 and 30% respectively over the first 3 min at VLe. During the remainder of the 1 h period, the discharge of low threshold SAR fell an additional 20% while that of the high threshold SAR remained relatively constant. There were significant increases in both alveolar and arterial PCO2 during the maintained inflations. Ventilation with 5% CO2 reduced the static discharge levels of low and high threshold SAR by 10 and 25% respectively, suggesting that a part of the apparent adaptation of these receptors to maintained inflation for 1 h with air was due to the accumulation of metabolic CO2. Following 1 h of maintained inflation, the phasic responses to pump ventilation were decreased in low threshold SAR but remained unchanged in high threshold SAR. The static discharge associated with step inflation was unchanged in both receptor groups. The data suggest that increased SAR discharge is sustained indefinitely during increased lung volume and may account for persistent changes in breathing pattern previously observed during chronic changes in lung volume.

Adaptation, Physiological↗
PubMed1989

Temperature effects on pulmonary receptor responses to airway pressure and CO2 in Alligator mississippiensis.

The effects of body temperature (Tb) on pulmonary stretch receptor (PSR) and CO2-sensitive intrapulmonary chemoreceptor (IPC) response characteristics may have important effects on ventilatory control in reptiles. In this study, three questions were addressed: (1) what are the effects of Tb on PSR and IPC responses to airway pressure (Paw) and lung CO2 (PCO2); (2) what are the effects of acute (less than 12 h) vs chronic (greater than 1 week) changes in Tb on both receptor groups; and (3) can predicted changes in the fractional dissociation of imidazole (alpha im), calculated via independent changes in Tb and PCO2, explain the CO2-sensitivity of either IPC or PSR? Single fiber PSR and IPC responses to Paw, PCO2 and Tb were determined in 11 anesthetized Alligator mississippiensis (pentobarbital; 30 mg/kg), acclimated at 20 degrees C (N = 5) or at 30 degrees C (N = 6). PSR activity increased as Paw increased at both Tb, but PSR activity and sensitivity to Paw were lower at 20 degrees C. The average Q10 was 2.1. Increasing inhaled CO2 from 1 to 7% decreased PSR activity by 27 +/- 6% at 20 degrees C and 18 +/- 5% at 30 degrees C. IPC activity decreased as PCO2 increased at both Tb, but IPC activity and sensitivity were reduced at 20 degrees C. The average Q10 was 3.2. Increasing Paw from 2 to 10 cm H2O had inconsistent effects on IPC activity. There were no differences between the effects of acute or chronic changes in Tb on either PSR or IPC responses. Predicted changes in alpha im could not explain the CO2-sensitivity of either IPC or PSR. We conclude that PSR and IPC adapt rapidly to Tb changes. The larger Q10 of IPC suggests that the relative role of IPC vs PSR in ventilatory control may be greater at elevated body temperatures.

Alligators and Crocodiles↗
PubMed1988

Effects of intrapulmonary CO2 and airway pressure on pulmonary vagal afferent activity in the alligator.

The effects of airway CO2 and pressure on pulmonary vagal afferent fibers were studied in seven anesthetized alligators Alligator mississippiensis, at room temperature (24 degrees C). Of 49 receptors which fired in phase with ventilation, 13 behaved like mammalian rapidly adapting pulmonary stretch receptors, 19 like mammalian slowly adapting pulmonary stretch receptors (PSR), and 17 like avian intrapulmonary CO2-sensitive chemoreceptors (IPC). PSR and IPC were positively localized to the lung by punctate stimulation or response to airway CO2 changes during pulmonary artery occlusion. PSR discharge frequency (fPSR) was measured at airway pressures (Paw) from 0 to 15 cm H2O at FICO2 = 0.01 in 14 receptors. fPSR increased in all receptors throughout the range of Paw studied. In 13 PSR, increasing FICO2 from 0.01 to 0.07 decreased fPSR 23 +/- 13% (+/- SEM) at Paw = 2 cm H2O and 14 +/- 7% at 15 cm H2O. IPC discharge frequency (fIPC) decreased as FICO2 increased and most discharged less than 1 sec-1 at FICO2 = 0.03. In 7 IPC at FICO2 = 0.01, increasing Paw from 2 to 15 cm H2O increased fIPC 17 +/- 5% after pulmonary artery occlusion demonstrating some mechanosensitivity in alligator IPC. Although both IPC and PSR showed mechanosensitivity and CO2-sensitivity, the two receptor types were distinct. PSR were 13 times more sensitive to Paw changes than IPC and IPC were 14 times more sensitive to FICO2 changes than PSR. We did not find any receptors with intermediate CO2- or mechanosensitivities that could represent a transitional form of receptor. These results predict that IPC and PSR may have different roles in reflex ventilatory control.

Alligators and Crocodiles↗
PubMed1987

Changes in ventilation and breathing pattern produced by changing body temperature and inspired CO2 concentration in turtles.

Respiratory minute ventilation (VE), breathing pattern, oxygen consumption (VO2) and arterial blood gases and pH were measured in freshwater turtles (Chrysemys picta) at 10, 20 and 30 degrees C while the animals breathed gases of varying CO2 concentration (FICO2 = 0, 2, 4, 6 and 8%). Increasing body temperature produced unequal increases in VE and VO2 such that VE/VO2 decreased. This relative hypoventilation led to a rise in PaCO2 and fall in pHa. Increasing FICO2 at all temperatures greatly elevated VE. The magnitude of this response increased with increasing temperature. Thus, paradoxically, there was an increase in both PaCO2 and CO2 sensitivity with increasing temperature. Increases in VE due to increases in temperature were primarily due to a shortening of the periods of breath holding. Although changes in VT contributed to changes in VE with increasing FICO2, the changes in f, due to shortening the periods of breath holding, contributed twice as much. In relative terms, increasing temperature had no effect on the CO2 response of any respiratory variable. Analysis of the data indicates that all changes which occurred in VE, PaCO2 and pHa with changes in body temperature can be explained by equal Q10 effects of roughly two on both metabolic rate and ventilatory sensitivity to changes in PaCO2.

Animals↗
PubMed1987

Effects of H+ versus CO2 on ventilation in the Pekin duck.

Measurements were made of ventilation (VE) and arterial blood gases (PCO2 and PO2) and pH in awake Pekin ducks, Anas platyrhynchos, exposed to sequential cycles of 1% step changes in inspired CO2 from 0 to 5 and back to 0% CO2, as well as to a sustained period (5 h) of 5% CO2 breathing. Changing the background level of inspired PO2 was used to alter the range of PaCO2 over which CO2 response curves were obtained. The initial increase in minute ventilation following a sustained step increase in inspired CO2 (5%) began to decline immediately at a rate of approximately 1% every 5 min. This was closely paralleled by increases in both pH and [HCO-3] while arterial PaCO2 remained constant or increased slightly. CO2 response curves (VE vs PaCO2) generated in a sequential fashion shifted down and to the right (a paradoxical decrease in VE associated with an increase in PaCO2) while the relationship between VE and pH remained constant. These data suggest that VE is a single function of pH in birds under these conditions and that the relationship between VE and PaCO2 is altered due to metabolic acid-base compensation even during acute CO2 exposure.

Acidosis, Respiratory↗
PubMed1986

Oxygen sensitive afferent information arising from the first gill arch of yellowfin tuna.

Single nerve fiber discharge was recorded from O2 sensitive receptors in the first gill arch of the yellowfin tuna, Thunnus albacares, in vitro. These receptors were innervated by the vagus nerve and increased their discharge in response to decreasing perfusion rate, decreasing perfusion PO2 and, in most fibers, to decreasing external PO2. Fibers responding to environmental hypoxia exhibited an exponential increase in discharge to decreasing external PO2 with a sensitivity similar to that exhibited by cat carotid body chemoreceptors. Indirect evidence suggests that these receptors are located near the gill vasculature and are more sensitive to changes in arterial PO2 than water PO2. Their response characteristics and hypoxic sensitivity strongly implicate them as the afferent limb in the cardiac responses and perhaps also the ventilatory responses exhibited by tuna to environmental hypoxia.

Afferent Pathways↗
PubMed1983

Diving responses in ducks after acute barodenervation.

The contribution of systemic arterial baroreceptors to the cardiovascular adjustments to diving has been investigated in unanesthetized ducks after acute baroreceptor denervation. Both intact and denervated ducks exhibited bradycardia on diving, although denervated ducks showed a lesser and more variable fall in heart rate. Hindlimb vascular resistance rose significantly in both intact and denervated ducks. Continuous stimulation of one depressor nerve, through miniature electrodes implanted on the cut central end, resulted in a diving bradycardia intermediate between that recorded in intact and denervated animals. Intermittent stimulation of the depressor nerve, for 20-s periods, at intensities high enough to cause a large fall in mean arterial pressure (MAP) predive caused a smaller reduction in MAP as a dive was prolonged, due to a large decline in the ability of the baroreceptor reflex to affect peripheral resistance. There was no change in the effect of stimulation on cardiac control before or during diving. The present experiments indicate that a barostatic reflex, which exerts its effects primarily through cardiac control and not control of total peripheral resistance, is active through the dive but that the majority of the diving response in ducks is independent of baroreceptor integrity.

Animals↗
PubMed1983

Interaction between norepinephrine and hypoxia on carotid body chemoreception in rabbits.

The effects of both bolus injection and constant infusion of various levels of norepinephrine (NE) on the activity of single-carotid chemoreceptor nerve fibers was studied in pentobarbital-anaesthetized rabbits under normoxic and hypoxic conditions. All animals were paralyzed and artificially ventilated. The dominant effect of NE was to excite carotid body chemoreceptor fibers in a dose-dependent fashion. There was an inverse relationship between the effect of NE on afferent fiber discharge and arterial O2 tension at all levels of exogenous NE above threshold levels. Propranolol (PROP) in sufficient dosage abolished the chemoreceptor response to NE and also markedly reduced the chemoreceptor response to hypoxia. These results support suggestions that beta-adrenergic receptors may be an integral part of the O2 chemosensory mechanism. They also demonstrate a nonadditive interaction between the effects of NE and hypoxia on the chemoreceptor afferent fibers. A reduction in resting discharge levels after infusion of PROP further suggests that endogenous catecholamines may contribute to carotid body chemoreceptor activity even under normoxic normocapnic conditions.

Animals↗
PubMed1982

Role of central and peripheral chemoreceptors in diving responses of ducks.

Using techniques of vascular isolation and subsequent perfusion we have investigated the effects of altering blood gas tensions, in the cerebral and carotid body circulations, on some cardiovascular responses to diving in unanesthetized ducks. After denervating the right carotid body, perfusion of the innervated left carotid body with hyperoxic blood significantly reduced diving bradycardia and reduced the increase in hindlimb vascular resistance (HLVR) in 1-min dives compared with dives in which the innervated carotid body was autoperfused. Denervation of systemic arterial baroreceptors reduced the fall in heart rate (HR) and increased the rise in HLVR in all dives. Cross-perfusion of the head, from a donor with blood of normal blood gas tensions, did not significantly affect HR or HLVR in 2-min dives compared with dives in which the head was autoperfused. however, cross-perfusing the cerebral circulation with blood of elevated PaCO2 caused significantly greater increases in HLVR than when high PaCO2 only affected the peripheral circulation. We conclude that peripheral chemoreceptors cause virtually all the bradycardia in the later stages of a dive but only about one-half the increase in HLVR, a significant contribution comes from the stimulation of central chemoreceptors with blood of high PaCO2.

Animals↗
PubMed1981

On chemoreceptor control of ventilatory responses to CO2 in unanesthetized ducks.

Using cross perfusion between pairs of animals we examined the effects of increases in arterial CO2 tension (Paco2) at pulmonary, carotid body, and central chemoreceptors on ventilation in unanesthetized, spontaneously breathing White Pekin ducks. By adjusting the level of inspired CO2 of either the experimental or donor animals it was possible to manipulate Paco2 at any one or combination of the receptor groups. Stimulation of central chemosensitive areas alone was three to four times more effective in increasing both frequency and minute ventilation (Ve) than stimulation of the carotid bodies alone. Increases in tidal volume were small in both instances. Increasing PCO2 in the pulmonary circulation of an innervated lung, independent of changes in Paco2 at the carotid body or head, had no effect on VE. We conclude that central chemoreceptors play the major role in a steady-state response of awake ducks to CO2 while the carotid bodies play a smaller but still significant role. The intrapulmonary chemoreceptors play no role in the response per se although their inhibition by high airway CO2 causes marked effects on the pattern of breathing

Animals↗
PubMed1980

The role of vagal afferent information and hypercapnia in control of the breathing pattern in chelonia.

The normal breathing pattern of the turtle, Chrysemys picta (Schneider), consists of periods of continuous breathing interspersed with periods of breath holding. During each ventilatory period respiratory frequency and tidal volume are controlled independently. There is a large variability in inspiratory and expiratory gas-flow rates yet tidal volumes are maintained within narrow limits by adjustments of the lengths of the active inspiratory and expiratory intervals. Lung volume information carried within the vagus nerve is responsible for the careful regulation of tidal volume as well as for modulation of the air flow rates and lowering of the threshold of the mechanism initiating expiration following breath holding. Increases in pulmonary minute ventilation during hypercapnia are caused by increases in respiratory frequency due solely to a shortening of the periods of breath holding. There is some increase in tidal volume but the breath length remains constant and thus the frequency of breathing within each ventilatory period also remains constant. After vagotomy, changes in minute ventilation due to hypercapnia stem primarily from changes in tidal volume while changes in respiratory frequency are greatly reduced.

Afferent Pathways↗
PubMed1979

Pulmonary receptor chemosensitivity and the ventilatory response to inhaled CO2 in the turtle.

Ventilatory responses of unanesthetized turtles to changes in the intrapulmonary CO2 content of a vascularly isolated and an intact lung were measured during spontaneous breathing. The hyperpnea associated with inhalation of CO2 by the vascularly isolated lung was 19% of that associated with inhalation of CO2 by the intact lung. Transection of the vagus nerve supplying the isolated lung abolished this response. We conclude that both inhibition of pulmonary stretch receptor discharge with increasing levels of FICO2 and a functional increase in central inspiratory volume threshold during hypercapnia contribute to tidal volume increases following CO2 inhalation in normal animals. The major component of the ventilatory response of intact turtles to increasing levels of FICO2, however, was an increase in respiratory frequency. When CO2 was inspired only by the vascularly isolated lung the increase in respiratory frequency was only 21% of that recorded when the same levels of CO2 were inspired by the intact lung. Thus the ventilatory response of turtles to increasing levels of FICO2 is primarily dependent upon concomitant hypercapnia.

Animals↗
PubMed1979

Functional characteristics of slowly adapting pulmonary stretch receptors in the turtle (Chrysemys picta).

1. Single nerve fibre discharge has been recorded from slowly adapting pulmonary stretch receptors in single-pithed turtles on artificial ventilation. 2. Receptor discharge during static and dynamic lung inflations showed that lung volume was the major stimulus of these receptors. The rate and degree of change in transpulmonary pressure were without direct effect. 3. The response of these receptors to static and dynamic lung inflation differed only quantitatively from those of bronchopulmonary stretch receptors in mammals. The lower discharge frequencies and sensitivities of the turtle receptors may arise from the low body temperature of these animals. 4. The sensitivity of turtle pulmonary receptors to CO2 was greater than that recorded for bronchopulmonary receptors of mammals although the effects of CO2 on receptor discharge were qualitatively similar. In several instances, receptor discharge was totally inhibited throughout the ventilatory cycle by inflation with 5--10% CO2 in air.

Action Potentials↗
PubMed1977

Carbon dioxide sensitivity of pulmonary receptors in the frog.

Pulmonary mechano-receptors have been found in the frog lung that are sensitive to CO2 concentrations in the lungs and airways comparable to the physiological levels recorded in frogs. These results support the suggestion that a pulmonary receptor with distinct mechano- and chemosensitive properties may represent the functional precursor of the more specialized pulmonary receptor types which have evolved in birds and mammals.

Action Potentials↗