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.

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

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.

Effects of pulmonary air embolism on discharge of slowly adapting pulmonary stretch receptors

1994 ◽  
Vol 76 (1) ◽  
pp. 97-103 ◽  
Author(s):  
B. P. Lee ◽  
H. F. Chen ◽  
F. C. Hsu ◽  
T. B. Kuo ◽  
M. H. Yang
Keyword(s):  
Fiber Type ◽  
Air Embolism ◽  
Transpulmonary Pressure ◽  
Lung Compliance ◽  
Group I ◽  
Airway Collapse ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Close Relationship ◽  
Dynamic Lung Compliance

Pulmonary air embolism (PAE) usually causes small-airway collapse. Local transpulmonary pressure (Ptr) is thought to be closely associated with the activity of slowly adapting pulmonary stretch receptors (SAPSRs). To test whether discharge of SAPSRs located distal to collapsed airways is closely related to the overall Ptr, we studied 65 SAPSRs in anesthetized paralyzed open-chest dogs that were ventilated at constant tidal volume and frequency. PAE increased both Ptr and total pulmonary resistance but decreased dynamic lung compliance. Three groups of SAPSRs were identified on the basis of their locations in intrapulmonary airways. Group I had 29 SAPSRs located in airways < 1 mm in diameter. Group II had 10 SAPSRs that were found in intrapulmonary airways between 1 and 2 mm in diameter. PAE decreased the activity of 31 of the 39 SAPSRs in these two groups. Their activity during PAE was not related to Ptr. The 26 SAPSRs in group III were in airways > 2 mm in diameter. PAE increased the peak firing rate of 18 of these receptors, and there was a close relationship between the discharge frequency of these SAPSRs and the Ptr during PAE. In groups I and II, the dissociation between Ptr and SAPSR activity during PAE may have been caused by peripheral airway collapse. Activity of central fibers was blocked at higher temperatures than activity of peripheral fibers. We suggest that the response of a SAPSR to PAE depends on the location of the receptor within the lungs, and we speculate that threshold and fiber type are also related to location.

scholarly journals The Effect of Surfactant on Low and High Threshold Slowly Adapting Pulmonary Stretch Receptors(PSR) in Lung Lavaged Cats

1999 ◽  
Vol 45 (4, Part 2 of 2) ◽  
pp. 320A-320A
Author(s):  
R Sindelar ◽  
A Jonzon ◽  
P Schaller ◽  
A Schulze ◽  
G Sedin
Keyword(s):  
High Threshold ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors

Response of slowly adapting pulmonary stretch receptors to reduced lung compliance

1991 ◽  
Vol 71 (2) ◽  
pp. 425-431 ◽  
Author(s):  
J. Yu ◽  
T. E. Pisarri ◽  
J. C. Coleridge ◽  
H. M. Coleridge
Keyword(s):  
Steady State ◽  
Tidal Volume ◽  
Time Constant ◽  
Transpulmonary Pressure ◽  
Lung Compliance ◽  
Steady State Response ◽  
Positive End Expiratory Pressure ◽  
State Response ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors

We examined the steady-state response of slowly adapting pulmonary stretch receptors (SAPSRs) to reduced lung compliance in open-chest cats with lungs ventilated at eupneic rate and tidal volume (VT) and with a positive end-expiratory pressure (PEEP) of 3–4 cmH2O. Transient removal of PEEP decreased compliance by approximately 30% and increased transpulmonary pressure (Ptp) by 1–2.5 cmH2O. Reduction of compliance significantly decreased SAPSR discharge in deflation and caused a small increase in discharge at the peak of inflation; it had little effect on discharge averaged over the ventilatory cycle. Increasing VT to produce a comparable increase in Ptp significantly increased peak discharge. Thus unlike rapidly adapting receptors, whose discharge is increased more effectively by reduced compliance than by increased VT, SAPSRs are stimulated by increased VT but not by reduced compliance. We speculate that the most consistent effect of reduced compliance on SAPSRs (the decrease in deflation discharge) was due to the decreased time constant for deflation in the stiffer lung. This alteration in firing may contribute to the tachypnea evoked as the lungs become stiffer.

Acute inhalation of ozone stimulates bronchial C-fibers and rapidly adapting receptors in dogs

1993 ◽  
Vol 74 (5) ◽  
pp. 2345-2352 ◽  
Author(s):  
J. C. Coleridge ◽  
H. M. Coleridge ◽  
E. S. Schelegle ◽  
J. F. Green
Keyword(s):  
Lung Compliance ◽  
Acute Exposure ◽  
Ozone Exposure ◽  
C Fibers ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Lower Trachea ◽  
Afferent Response ◽  
Vagal Cooling ◽  
Stimulation Of

To identify the afferents responsible for initiating the vagally mediated respiratory changes evoked by acute exposure to ozone, we recorded vagal impulses in anesthetized, open-chest, artificially ventilated dogs and examined the pulmonary afferent response to ozone (2–3 ppm in air) delivered to the lower trachea for 20–60 min. Bronchial C-fibers (BrCs) were the lung afferents most susceptible to ozone, the activity of 10 of 11 BrCs increasing from 0.2 +/- 0.2 to 4.6 +/- 1.3 impulses/s within 1–7 min of ozone exposure. Ten of 15 rapidly adapting receptors (RARs) were stimulated by ozone, their activity increasing from 1.5 +/- 0.4 to 4.7 +/- 0.7 impulses/s. Stimulation of RARs (but not of BrCs) appeared secondary to the ozone-induced reduction of lung compliance because it was abolished by hyperinflation of the lungs. Ozone had little effect on pulmonary C-fibers or slowly adapting pulmonary stretch receptors. Our results suggest that both BrCs and RARs contribute to the tachypnea and bronchoconstriction evoked by acute exposure to ozone when vagal conduction is intact and that BrCs alone are responsible for the vagally mediated tachypnea that survives vagal cooling to 7 degrees C.

scholarly journals Veno-venous ECMO as a platform to evaluate lung lavage and surfactant replacement therapy in an animal model of severe ARDS

2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Robert Qaqish ◽  
Yui Watanabe ◽  
Marcos Galasso ◽  
Cara Summers ◽  
A adil Ali ◽  
...  
Keyword(s):  
Replacement Therapy ◽  
Lung Lavage ◽  
Post Injury ◽  
Surfactant Replacement ◽  
Recruitment Maneuvers ◽  
Surfactant Replacement Therapy ◽  
Dosing Strategies ◽  
Yorkshire Pigs ◽  
Saline Lavage ◽  
Protective Systems

Abstract Background There are limited therapeutic options directed at the underlying pathological processes in acute respiratory distress syndrome (ARDS). Experimental therapeutic strategies have targeted the protective systems that become deranged in ARDS such as surfactant. Although results of surfactant replacement therapy (SRT) in ARDS have been mixed, questions remain incompletely answered regarding timing and dosing strategies of surfactant. Furthermore, there are only few truly clinically relevant ARDS models in the literature. The primary aim of our study was to create a clinically relevant, reproducible model of severe ARDS requiring extracorporeal membrane oxygenation (ECMO). Secondly, we sought to use this model as a platform to evaluate a bronchoscopic intervention that involved saline lavage and SRT. Methods Yorkshire pigs were tracheostomized and cannulated for veno-venous ECMO support, then subsequently given lung injury using gastric juice via bronchoscopy. Animals were randomized post-injury to either receive bronchoscopic saline lavage combined with SRT and recruitment maneuvers (treatment, n = 5) or recruitment maneuvers alone (control, n = 5) during ECMO. Results PaO2/FiO2 after aspiration injury was 62.6 ± 8 mmHg and 60.9 ± 9.6 mmHg in the control and treatment group, respectively (p = 0.95) satisfying criteria for severe ARDS. ECMO reversed the severe hypoxemia. After treatment with saline lavage and SRT during ECMO, lung physiologic and hemodynamic parameters were not significantly different between treatment and controls. Conclusions A clinically relevant severe ARDS pig model requiring ECMO was established. Bronchoscopic saline lavage and SRT during ECMO did not provide a significant physiologic benefit compared to controls.

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