scholarly journals Response of Slowly Adapting Pulmonary Stretch Receptors in Surfactant Depleted Cat Lungs: Before and After Surfactant Replacement 226

1996 ◽  
Vol 40 (3) ◽  
pp. 552-552 ◽  
Author(s):  
R. Sindelar ◽  
V. Dammann ◽  
A. Jonzon ◽  
P. Schaller ◽  
A. Schulze ◽  
...  
Keyword(s):  
Surfactant Replacement ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Before And After

Surfactant replacement partially restores the activity of pulmonary stretch receptors in surfactant-depleted cats

2006 ◽  
Vol 100 (2) ◽  
pp. 594-601 ◽  
Author(s):  
Richard Sindelar ◽  
Anders Jonzon ◽  
Andreas Schulze ◽  
Gunnar Sedin
Keyword(s):  
Respiratory Rate ◽  
Spontaneous Breathing ◽  
Lung Lavage ◽  
Lung Compliance ◽  
High Threshold ◽  
Inspiratory Time ◽  
Impulse Frequency ◽  
Surfactant Replacement ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors

Single units of slowly adapting pulmonary stretch receptors (PSRs) were investigated in anesthetized cats during spontaneous breathing on continuous positive airway pressure (2–5 cmH2O), before and after lung lavage and then after instillation of surfactant to determine the PSR response to surfactant replacement. PSRs were classified as high threshold (HT) and low threshold (LT), and their instantaneous impulse frequency ( fimp) was related to transpulmonary pressure (Ptp) and tidal volume (Vt). Both the total number of impulses and maximal fimp of HT and LT PSRs decreased after lung lavage (55 and 45%, respectively) in the presence of increased Ptp and decreased Vt. While Ptp decreased markedly and Vt remained unchanged after surfactant instillation, all except one PSR responded with increased total number of impulses and maximal fimp (42 and 26%, respectively). Some HT PSRs ceased to discharge after lung lavage but recovered after surfactant instillation. The end-expiratory activity of LT PSRs increased or was regained after surfactant instillation. After instillation of surfactant, respiratory rate increased further with a shorter inspiratory time, resulting in a lower inspiratory-to-expiratory time ratio. Arterial pH decreased (7.31 ± 0.04 vs. 7.22 ± 0.06) and Pco2 increased (5.5 ± 0.7 vs. 7.2 ± 1.3 kPa) after lung lavage, but they were the same after as before instillation of surfactant (pH = 7.21 ± 0.08 and Pco2 = 7.6 ± 1.4 kPa) during spontaneous breathing. In conclusion, surfactant instillation increased lung compliance, which, in turn, increased the activity of both HT and LT PSRs. A further increase in respiratory rate due to a shorter inspiratory time after surfactant instillation suggests that the partially restored PSR activity after surfactant instillation affected the breathing pattern.

Reflex control of the tracheal vasculature of sheep

1993 ◽  
Vol 75 (5) ◽  
pp. 2173-2179 ◽  
Author(s):  
S. E. Webber ◽  
J. G. Widdicombe
Keyword(s):  
Carotid Body ◽  
Muscle Tone ◽  
Intravenous Injections ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Before And After ◽  
Cervical Trachea ◽  
Carotid Body Chemoreceptors ◽  
Reflex Stimulation ◽  
Stimulation Of

Arteries to the cervical trachea were perfused at constant flow in anesthetized sheep. Perfusion pressures (PP), blood pressure (BP), and changes in tracheal smooth muscle tone (Ptr) were measured. Stimulation of pulmonary C-fiber receptors decreased PP (-6.5%) and BP (-16.8%) and increased Ptr (+61.5%), changes prevented by vagotomy and therefore reflex. Stimulation of cardiac receptors and slowly adapting pulmonary stretch receptors decreased PP (-7.9%) and BP (-21.0) and increased Ptr (+19.0%), changes reversed by vagotomy and therefore reflex. Stimulation and inhibition of slowly adapting pulmonary stretch receptors had no vagal-dependent effect on PP and BP, but inflation decreased (-20.3%) and deflation increased Ptr (+35.2%), effects abolished by vagotomy and therefore reflex. Systemic hypoxia increased PP and BP before and after vagotomy (+12.2 and +40.3%), effects greatly reduced by cutting the carotid body nerves; it increased Ptr (+29.8%), an effect abolished by vagotomy and cutting the carotid body nerves. Systemic hypercapnia increased PP (+16.9%), BP (+20.5%), and Ptr (+36.2%), the first two responses being unaffected by vagotomy and the last almost abolished. Stimulation of carotid body chemoreceptors by KCN increased PP (+22.5%), BP (+104.7%), and Ptr (+8.5%), all responses prevented by cutting the carotid body nerves. Responses to intravenous injections of KCN were similar.

Connectivity of slowly adapting pulmonary stretch receptors with dorsal medullary respiratory neurons

1987 ◽  
Vol 58 (6) ◽  
pp. 1259-1274 ◽  
Author(s):  
A. J. Berger ◽  
T. E. Dick
Keyword(s):  
Electrical Stimulation ◽  
Membrane Potential ◽  
Beta Cells ◽  
Spike Activity ◽  
Alpha Cells ◽  
Drg Neurons ◽  
Lung Inflation ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
P Cells

1. Intracellular recordings were made from 50 dorsal respiratory group (DRG) neurons in the region of the ventrolateral nucleus of the solitary tract in anesthetized, paralyzed cats ventilated with a cycle-triggered pump whose inflation stroke was triggered by the onset of phrenic nerve inspiratory (I) discharge. Activity was recorded simultaneously in the ipsilateral nodose ganglion from sensory cell bodies of slowly adapting pulmonary stretch receptors (PSRs). 2. Respiratory cycle-related membrane potential changes of DRG neurons were recorded. Twenty-six neurons that did not exhibit spikes were classified as I alpha, I beta or pump (P)-cells by comparing their membrane potential trajectories during I in the presence of lung inflation with that observed during I, but with lung inflation withheld. The remaining 24 neurons were classified similarly, but the classification was based upon a comparison of their I-phase spike activity responses with and without lung inflation. I phase-related histograms of either membrane potential or spike activity were constructed to facilitate DRG neuronal classification. Additionally, steady lung inflation of varying magnitudes was applied during the expiratory phase. This prolonged expiration and produced different responses in the neurons. Generally, I beta and P-cells were depolarized, whereas I alpha cells were hyperpolarized. 3. Low-intensity electrical stimulation of the ipsilateral vagus nerve evoked excitatory postsynaptic potentials (EPSPs) in all three DRG neuronal types. P-cells and I beta cells exhibited EPSPs in response to the lowest intensity; generally this intensity was below threshold for the simultaneously recorded PSR. Overall, EPSPs in I alpha cells had the highest thresholds, but some EPSPs could be evoked at thresholds similar to those of the I beta cells. The distributions of the average onset latency of the evoked EPSP overlapped considerably. Thus vagal electrical stimulation cannot be used for unequivocal classification of DRG neurons into I alpha, I beta, and P-cell subpopulations. 4. Using intracellular spike-triggered averaging, single PSRs were shown to generate monosynaptic EPSPs in I beta neurons and P-cells but not I alpha cells. Divergence of single PSR afferents also was observed. Relationships between EPSP shape factors, amplitudes, and PSR afferent conduction velocity are similar to those previously observed for monosynaptic EPSPs in hindlimb motoneurons generated by spinal afferents.

Effect of central CO2 drive on lung inflation responses of expiratory bulbospinal neurons in dogs

2000 ◽  
Vol 279 (5) ◽  
pp. R1606-R1618 ◽  
Author(s):  
Mislav Tonkovic-Capin ◽  
Edward J. Zuperku ◽  
Eckehard A. Stuth ◽  
Jurica Bajic ◽  
Zoran Dogas ◽  
...  
Keyword(s):  
Empirical Model ◽  
Time Course ◽  
Transpulmonary Pressure ◽  
Neuronal Responses ◽  
Lung Inflation ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Thiopental Sodium ◽  
Inhibitory Components ◽  
Discharge Patterns

The purpose of these studies is to better understand the nature of the reflex interactions that control the discharge patterns of caudal medullary, expiratory (E) bulbospinal neurons. We examined the effect of central chemodrive inputs measured as arterial CO2 tension (PaCO2 ) during hyperoxia on the excitatory and inhibitory components of the lung inflation responses of these neurons in thiopental sodium-anesthetized, paralyzed dogs. Data from slow ramp inflation and deflation test patterns, which were separated by several control inflation cycles, were used to produce plots of neuronal discharge frequency ( F n) versus transpulmonary pressure (Pt). Pt was used as an index of the activity arising from the slowly adapting pulmonary stretch receptors (PSRs). Changes in inspired CO2 concentrations were used to produce PaCO2 levels that ranged from 20 to 80 mmHg. The data obtained from 41 E neurons were used to derive an empirical model that quantifies the average relationship for F n versus both Pt and PaCO2 . This model can be used to predict the time course and magnitude of E neuronal responses to these inputs. These data suggest that the interaction between PaCO2 and PSR-mediated excitation and inhibition of F n is mainly additive, but synergism between PaCO2 and excitatory inputs is also present. The implications of these findings are discussed.

Consequences of capsaicin treatment on pulmonary vagal reflexes and chemoreceptor activity in lambs

2000 ◽  
Vol 89 (5) ◽  
pp. 1709-1718 ◽  
Author(s):  
Véronique Diaz ◽  
Julie Arsenault ◽  
Jean-Paul Praud ◽  
Keyword(s):  
Ventilatory Response ◽  
Ventilatory Responses ◽  
Body Activity ◽  
Pulmonary Receptor ◽  
Stretch Receptors ◽  
C Fiber ◽  
Pulmonary Stretch Receptors ◽  
Bolus Intravenous Injection ◽  
To Receive ◽  
Stimulation Of

The aim of this study was to test the hypothesis that capsaicin treatment in lambs selectively inhibits bronchopulmonary C-fiber function but does not alter other vagal pulmonary receptor functions or peripheral and central chemoreceptor functions. Eleven lambs were randomized to receive a subcutaneous injection of either 25 mg/kg capsaicin (6 lambs) or solvent (5 lambs) under general anesthesia. Capsaicin-treated lambs did not demonstrate the classical ventilatory response consistently observed in response to capsaicin bolus intravenous injection in control lambs. Moreover, the ventilatory responses to stimulation of the rapidly adapting pulmonary stretch receptors (intratracheal water instillation) and slowly adapting pulmonary stretch receptors (Hering-Breuer inflation reflex) were similar in both groups of lambs. Finally, the ventilatory responses to various stimuli and depressants of carotid body activity and to central chemoreceptor stimulation (CO2 rebreathing) were identical in control and capsaicin-treated lambs. We conclude that 25 mg/kg capsaicin treatment in lambs selectively inhibits bronchopulmonary C-fiber function without significantly affecting the other vagal pulmonary receptor functions or that of peripheral and central chemoreceptors.

Vasomotor inhibition in rabbits by vagal nonmedullated fibers from cardiopulmonary area

1975 ◽  
Vol 229 (5) ◽  
pp. 1410-1413 ◽  
Author(s):  
PN Thoren ◽  
G Mancia ◽  
JT Shepherd
Keyword(s):  
Blood Pressure ◽  
Vagal Afferents ◽  
Total Contribution ◽  
C Fibers ◽  
Aortic Blood ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Vagal Nerves ◽  
Aortic Blood Pressure ◽  
Aortic Baroreceptors

In anesthetized rabbits with sinus and aortic nerve cut, when the cervical vagal nerves were cooled to 12, 8, 6, and 0degreeC, there were progressive increases in aortic blood pressure of 7 +/- 1, 15 +/- 2, 25 +/- 1, and 41 +/- 2 mmHg (SE), respectively. For comparison, during cooling of the aortic and vagal nerves, at 12degreesC there was a decrease in firing in the afferent fibers from aortic baroreceptors (48 +/- 4%) and pulmonary stretch receptors (57 +/- 5%), and at 6degreesC all activity was abolished. Thus, at 6degreesC the activity in medullated fibers from the aortic baroreceptors and pulmonary stretch receptors is blocked, but the increase in aortic blood pressure with vagal cooling is only 60% of that with cooling to 0degreeC. This demonstrates that cardiopulmonary receptors with nonmedullated vagal afferents (C fibers) contribute to the tonic inhibition of the vasomotor center. Because of overlap in sensitivity of different vagal fibers to cooling, the total contribution of these C fibers cannot be evaluated.

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