Effect of pulmonary arterial PCO2 on slowly adapting pulmonary stretch receptors

1986 ◽  
Vol 60 (6) ◽  
pp. 2048-2055 ◽  
Author(s):  
J. F. Green ◽  
E. R. Schertel ◽  
H. M. Coleridge ◽  
J. C. Coleridge
Keyword(s):  
Lung Mechanics ◽  
Right Heart ◽  
Arterial Pco2 ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Venous Pco2 ◽  
Anesthetized Dogs ◽  
Pulmonary Arterial ◽  
Right Heart Bypass ◽  
Pulmonary Stretch Receptor

We recorded pulmonary stretch receptor (PSR) activity in anesthetized dogs and examined the effect of varying pulmonary arterial PCO2 (PpCO2) in both the naturally perfused and vascularly isolated pulmonary circulations while ventilating the lungs with room air. Steady-state increases in PpCO2 from approximately 25 to 50 Torr and from 50 to 70 Torr decreased PSR activity (impulses/ventilatory cycle) by 15 and 9%, respectively (P less than 0.001). Rapid increases in PpCO2 from approximately 50 to 80 Torr in a right-heart bypass preparation (with pulmonary blood flow constant) decreased PSR activity by 27%. Depression of firing, which was proportionately greater in deflation, was not dependent on changes in lung mechanics. Results show that loading CO2 intravascularly depresses PSR activity, the effects extending above as well as below resting PpCO2. Rapidly increasing PpCO2 above the resting level markedly depresses PSR activity during the transient. We conclude that PSRs may contribute to altered breathing resulting from changes in mixed venous PCO2 over the physiological range.

Reflex effects of lung inflation on tracheal volume

1963 ◽  
Vol 18 (4) ◽  
pp. 681-686 ◽  
Author(s):  
J. G. Widdicombe ◽  
J. A. Nadel
Keyword(s):  
Carotid Body ◽  
Artificial Ventilation ◽  
Vagus Nerves ◽  
Right Heart ◽  
Lung Inflation ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Anesthetized Dogs ◽  
The Right ◽  
Spontaneously Breathing

Transient lung inflation increased the volume of a bypassed tracheal segment in anesthetized dogs, whether spontaneously breathing or paralyzed and artificially ventilated. The degree of dilation during inflation varied with the state of “tone” of the tracheal muscle and with the inflation volume. Pulmonary denervation caused maintained constriction of the trachea and blocked the dilation during lung inflation. Cooling the cervical vagus nerves to between 7 and 12 C had the same effect. Both of these procedures blocked the Hering-Breuer inflation reflex, but the trachea still constricted following carotid body chemoreceptor stimulation by KCN. In paralyzed dogs, injection of veratrine into the right heart caused tracheal dilation, presumably by stimulating pulmonary stretch receptors. Left heart injection dilated the trachea much less. The former effect was abolished by pulmonary denervation. In anesthetized spontaneously breathing dogs carotid body chemoreceptor stimulation by KCN constricted the trachea; this was followed by increased ventilation and secondary tracheal dilation. Pulmonary denervation or muscular paralysis and artificial ventilation prevented the secondary dilation. These results establish the reflex nature of tracheal dilation during transient lung inflation and suggest that Hering-Breuer stretch receptors are the responsible end organs. Submitted on January 15, 1963

Interaction of interval-force relationship with aortic pressure and stroke volume

1976 ◽  
Vol 230 (4) ◽  
pp. 893-900 ◽  
Author(s):  
ER Powers ◽  
Foster ◽  
Powell WJ
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Cardiac Performance ◽  
Right Heart ◽  
Anesthetized Dogs ◽  
Right Heart Bypass ◽  
Force Relationship

The modification by aortic pressure and stroke volume of the response in cardiac performance to increases in heart rate (interval-force relationship) has not been previously studied. To investigate this interaction, 30 adrenergically blocked anesthetized dogs on right heart bypass were studied. At constant low aortic pressure and stroke volume, increasing heart rate (over the entire range 60-180) is associated with a continuously increasing stroke power, decreasing systolic ejection period, and an unchanging left ventricular end-diastolic pressure and circumference. At increased aortic pressure or stroke volume at low rates (60-120), increases in heart rate were associated with an increased performance. However, at increased aortic pressure or stroke volume at high rates (120-180), increases in heart rate were associated with a leveling or decrease in performance. Thus, an increase in aortic pressure or stroke volume results in an accentuation of the improvement in cardiac performance observed with increases in heart rate, but this response is limited to a low heart rate range. Therefore, the hemodynamic response to given increases in heart rate is critically dependent on aortic pressure and stroke volume.

Effect of pulmonary arterial PCO2 on breathing pattern

1988 ◽  
Vol 64 (5) ◽  
pp. 1844-1850 ◽  
Author(s):  
E. R. Schertel ◽  
D. A. Schneider ◽  
L. Adams ◽  
J. F. Green
Keyword(s):  
Breathing Pattern ◽  
Minute Ventilation ◽  
Blood Gases ◽  
Middle Level ◽  
Positive Pressure ◽  
Breathing Patterns ◽  
Arterial Pco2 ◽  
Anesthetized Dogs ◽  
Steady State Levels ◽  
Pulmonary Arterial

We studied breathing patterns and tidal volume (VT)-inspiratory time (TI) relationships at three steady-state levels of pulmonary arterial PCO2 (PpCO2) in 10 anesthetized dogs. To accomplish this we isolated and then separately pump perfused the pulmonary and systemic circulations, which allowed us to control blood gases in each circuit independently. To ventilate the lungs at a rate and depth determined by central drive, we used an electronically controlled positive-pressure ventilator driven by inspiratory phrenic neural activity. Expiratory time (TE) varied inversely with PpCO2 over the range of PpCO2 from approximately 20 to 80 Torr. VT and TI increased with rising PpCO2 over the range from approximately 20 to 45 Torr but did not change further as PpCO2 was raised above the middle level of approximately 45 Torr. Thus minute ventilation increased as a function of TE and VT as PpCO2 was increased over the lower range and increased solely as a function of TE as PpCO2 was increased over the upper range. The VT-TI relationship shifted leftward on the time axis as PpCO2 was lowered below the middle level but did not shift in the opposite direction as PpCO2 was raised above the middle level. In addition to its effect on breathing pattern, we found that pulmonary hypocapnia depressed inspiratory drive.

Responses of pulmonary vagal mechanoreceptors to high-frequency oscillatory ventilation

1988 ◽  
Vol 65 (2) ◽  
pp. 633-639 ◽  
Author(s):  
J. A. Wozniak ◽  
P. W. Davenport ◽  
P. C. Kosch
Keyword(s):  
High Frequency ◽  
Spontaneous Breathing ◽  
High Frequency Oscillatory Ventilation ◽  
Oscillatory Ventilation ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Residual Capacity ◽  
Anesthetized Dogs ◽  
Increased Activity ◽  
High Frequency Oscillatory

The discharge of 57 slowly adapting pulmonary stretch receptors (PSR's) and 16 rapidly adapting receptors (RAR's) was recorded from thin vagal filaments in anesthetized dogs. The receptors were localized and separated into three groups: extrathoracic tracheal, intrathoracic tracheal, and intrapulmonary receptors. The influence of high-frequency oscillatory ventilation (HFO) at 29 Hz on receptor discharge was analyzed by separating the response to the associated shift in functional residual capacity (FRC) from the oscillatory component of the response. PSR activity during HFO was increased from spontaneous breathing (49%) and from the static FRC shift (25%). PSR activity during the static inflation was increased 19% over spontaneous breathing. RAR activity was also increased with HFO. These results demonstrate that 1) the increased activity of PSR and RAR during HFO is due primarily to the oscillating action of the ventilator and secondarily to the shift in FRC associated with HFO, 2) the increased PSR activity during HFO may account for the observed apneic response, and 3) PSR response generally decreases with increasing distance from the tracheal opening.

Effect of expiratory loading on expiratory duration and pulmonary stretch receptor discharge

1986 ◽  
Vol 61 (5) ◽  
pp. 1857-1863 ◽  
Author(s):  
P. W. Davenport ◽  
J. A. Wozniak
Keyword(s):  
Linear Relationship ◽  
Temporal Summation ◽  
Spatial Summation ◽  
Stretch Receptor ◽  
Single Breath ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Temporal And Spatial ◽  
Resistive Loads ◽  
Pulmonary Stretch Receptor

Slowly adapting pulmonary stretch receptors have been hypothesized to be the afferents mediating the vagally dependent, volume-related prolongation of expiratory time (TE) during expiratory loading. It has been further suggested that the vagal component of this prolongation of TE is due to the temporal summation of pulmonary stretch receptor (PSR) activity during expiratory loading. This hypothesis was tested in rabbits exposed to resistive and elastic single-breath expiratory loading while PSR′s were simultaneously recorded. Both types of loads resulted in a decreased expired volume (VE) and increased expiratory duration (TE). The TE for resistive loads were significantly greater than for elastic loads for equivalent VE. Thus two different VE-TE relationships were found for resistive and elastic loads. When TE was plotted against the area under the expired volume trajectory, a single linear relationship was observed. PSR activity recorded during expiratory loading increased as VE decreased and TE increased. A single linear relationship resulted when the number of PSR spikes during the expiration was plotted against the associated TE for all types of loads. These findings demonstrate that the volume-related prolongation of TE with single-breath expiratory loads is associated with an increase in PSR discharge. These results support the hypothesis that the vagal component of load-dependent prolongation of TE is a function of both the temporal and spatial summation of PSR activity during the expiratory phase.

Pulmonary stretch receptor discharge patterns in eupnea, hypercapnia, and hypoxia

1982 ◽  
Vol 53 (2) ◽  
pp. 346-354 ◽  
Author(s):  
S. Iscoe
Keyword(s):  
Tidal Volume ◽  
Linear Equations ◽  
Discharge Frequency ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Residual Capacity ◽  
Instantaneous Discharge ◽  
Discharge Patterns ◽  
Spontaneously Breathing ◽  
Pulmonary Stretch Receptor

The discharge properties of pulmonary stretch receptors (PSR) were studied in spontaneously breathing, pentobarbital sodium-anesthetized cats. During eupneic breathing, 105 of 116 PSR (both tonically and phasically active) were recruited in the first third of inspiration; none were recruited in the last third. Linear equations adequately expressed the relation between instantaneous discharge frequency and inspired volume in eupnea. During CO2 rebreathing, both tidal volume and peak PSR discharge frequency were inversely related to inspiratory duration. At fixed volumes less than 40 ml above functional residual capacity, instantaneous PSR discharge frequency either did not change or decreased with increases in flow. Above 40 ml, increases in discharge frequency accompanied increases in flow (0.033 spikes/s per ml/s). During progressive hypocapnic hypoxia, discharge frequency increased, on average, at all volumes with increases in flow (0.206 spikes/s per ml/s). During both conditions, as with eupnea, increases in frequency were linearly related to increments in tidal volume. Therefore, tidal volume alone can be used to estimate PSR feedback to the respiratory centers, provided that its instantaneous value is appropriately scaled to account for the different effects of CO2 and hypocapnic hypoxia on PSR discharge.

Mechanism of action of isoproterenol on venous return

1977 ◽  
Vol 232 (2) ◽  
pp. H152-H156 ◽  
Author(s):  
J. F. Green
Keyword(s):  
Venous Return ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Vascular Effects ◽  
Right Heart ◽  
Control Value ◽  
Anesthetized Dogs ◽  
Venous Resistance ◽  
Right Heart Bypass ◽  
Transient And Steady State

The systemic vascular effects of isoproterenol infused in a dose of 1 mug-kg-1-min-1 was studied in 10 anesthetized dogs. A right heart bypass preparation allowed the separation of venous return into splanchnic and extrasplanchnic flows. Each channel was drained by gravity into an external reservoir. Venous return was then pumped into the pulmonary artery. During the infusion of isoproterenol, the pump was set at sufficient speed to maintain a constant level of blood in the external reservoir. Venous resistances and compliances of both channels were calculated from transient and steady-state volume shifts that occurred after rapid drops in splanchnic and then extrasplanchnic venous pressures. Isoproterenol affected both arterial and venous systems. Venous return increased from 1.62+/-0.11 to 2.40+/-0.19 liter/min (P less than 0.001) while arterial pressure fell from 97.5+/-3.8 to 70.2+/-5.9 mmHg (P less than 0.01). The compliances of the splanchnic and extrasplanchnic channels did not change significantly from their control values of 0.025+/-0.004 and 0.024+/-0.002 liter/mmHg. The venous resistance of the extrasplanchnic channel also did not change from its control value of 5.0 mmHg-liter-1-min-1; however, the splanchnic venous resistance decreased from 16.3+/-3.2 to 9.4+/-2.8 mmHg-liter-1-min-1 (P less than 0.001). The effective splanchnic back pressure, estimated by measuring the level to which hepatic venous pressure had to be raised to cause a change in portal pressure, decreased from 3.9 to 3.0 mmHg (P less than 0.01).

Hypocapnic-hypoglycemic interactions on cerebral high-energy phosphates and pH in dogs

1992 ◽  
Vol 263 (6) ◽  
pp. H1864-H1871 ◽  
Author(s):  
F. E. Sieber ◽  
S. A. Derrer ◽  
S. M. Eleff ◽  
R. C. Koehler ◽  
R. J. Traystman
Keyword(s):  
Glucose Uptake ◽  
High Energy ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
O2 Uptake ◽  
Arterial Pco2 ◽  
Eeg Abnormalities ◽  
Active Regulation ◽  
Venous Pco2 ◽  
Anesthetized Dogs

With a level of hypoglycemia (1–1.5 mM) that does not alter cerebral O2 uptake and glucose uptake in dogs, induction of hypocapnia may cause severe electroencephalographic (EEG) abnormalities. The aim of this study was to determine the effect of hypoglycemia (blood glucose = 1.1 +/- 0.1 mM) and hypocapnia (arterial PCO2 = 15 +/- 1 mmHg) on cerebral ATP, phosphocreatine, and intracellular pH (pHi; 31P magnetic resonance spectroscopy), cerebral blood flow (CBF; radiolabeled microspheres), global O2 uptake, and glucose uptake in anesthetized dogs. Neither hypoglycemia nor hypocapnia alone altered brain high-energy phosphates, pHi, O2 or glucose uptake or caused major EEG abnormalities. Hypocapnia alone decreased CBF to 62 +/- 4% of control. The combination of hypoglycemia and hypocapnia did not decrease CBF (85 +/- 6% of control), and O2 and glucose uptake were unchanged. During hypocapnic hypoglycemia, isoelectric EEG was seen in 40% of animals, ATP and phosphocreatine decreased to 38 +/- 12 and 43 +/- 12% of control, respectively, while pHi increased from 7.13 +/- 0.05 to 7.43 +/- 0.09. The increase in pHi was related reciprocally to the decrease in venous PCO2, indicating little change in intracellular bicarbonate concentration ([HCO3-]i). With normoglycemic hypocapnia, in contrast, estimated [HCO3-]i decreased 57 +/- 1%. These data suggest that active regulation of pHi during normoglycemic hypocapnia is impaired during hypoglycemic hypocapnia associated with decreased ATP.

Responses of pulmonary stretch receptors during ramp inflations of the lung

1986 ◽  
Vol 61 (1) ◽  
pp. 344-352 ◽  
Author(s):  
A. I. Pack ◽  
M. D. Ogilvie ◽  
R. O. Davies ◽  
R. J. Galante
Keyword(s):  
Transpulmonary Pressure ◽  
Type I ◽  
Single Population ◽  
Lung Inflation ◽  
Lung Expansion ◽  
Constant Rate ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Multiple Levels ◽  
Pulmonary Stretch Receptor

Studies were conducted in anesthetized paralyzed dogs to determine how the dynamic and proportional sensitivity of pulmonary stretch receptors change during lung inflation. The firing of each receptor was examined at multiple levels of static transpulmonary pressure and during multiple identical inflations at each of several rates. The averaged response of the receptor was computed and receptor activity related to transpulmonary pressure. On the basis of a quantitative criterion, employed to distinguish type I from type II receptors, the receptors could not be divided into distinct subpopulations. Thus all receptors were treated as coming from a single population. For all receptors we observed that their proportional sensitivity (increases in firing produced by increases in lung expansion at a constant rate of inflation) declined as the lung was inflated. In contrast, the dynamic sensitivity (increases in firing produced by increased rates of inflation at constant transpulmonary pressure) increased or remained relatively constant with increasing lung expansion. Thus, as inflation volume increases, the pulmonary stretch receptor acts increasingly as a rate receptor. The rate of inflation may have a more important role in control of the inspiratory duration than previously realized.

Inhibitory effect of inhaled wood smoke on the discharge of pulmonary stretch receptors in rats

1998 ◽  
Vol 84 (4) ◽  
pp. 1138-1143 ◽  
Author(s):  
C. J. Lai ◽  
Y. R. Kou
Keyword(s):  
Carbonic Anhydrase ◽  
Gas Phase ◽  
Transpulmonary Pressure ◽  
Inhibitory Effect ◽  
Lung Mechanics ◽  
Wood Smoke ◽  
Gas Mixture ◽  
Afferent Inhibition ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors

We investigated the inhibition of slowly adapting pulmonary stretch receptors (PSRs) by inhaled wood smoke. Impulses were recorded from PSRs in 68 anesthetized, open-chest, and artificially ventilated rats. Eighty-one of one hundred five PSRs were inhibited within one or two breaths when 6 ml of wood smoke were delivered into the lungs. As a group ( n = 105), PSR activity significantly decreased from a baseline of 19.0 ± 1.3 (SE) to a lowest level of 12.9 ± 1.2 impulses/breath at the fourth or fifth breath after smoke delivery. This afferent inhibition usually persisted for 5–18 breaths. In contrast, smoke delivery did not affect transpulmonary pressure. Delivery of gas-phase smoke or a hypercapnic gas mixture containing CO2 at a concentration (15%) matching that in the smoke produced a nearly identical inhibition in the same PSRs ( n = 10). This afferent inhibition was largely prevented by pretreatment with acetazolamide (an inhibitor of carbonic anhydrase; n = 10) but was not affected by pretreatment with the vehicle for acetazolamide ( n = 8) or isoproterenol (a bronchodilator; n = 10). These results suggest that 1) an increase in H+ concentration resulting from hydration of CO2 in the smoke may be responsible for the inhibitory effect of wood smoke on the discharge of PSRs and 2) changes in lung mechanics are not the cause of this afferent inhibition.

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