Reflex tracheal contraction during pulmonary venous congestion in the dog.

Kappagoda, C. T.; Man, Godfrey C.W.; Ravindran, Krishnan; Teo, Koon K.

doi:10.1113/jphysiol.1988.sp017207

Cited by 20 publications

(12 citation statements)

References 32 publications

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“…Several studies have suggested that airway narrowing during pulmonary congestion was vagally-mediated, because airway obstruction during pulmonary congestion was abolished with either atropine or vagotomy [8][9][10]. However, pretreatment with a dose of atropine that totally blocks muscarinic receptor activity [32] does not affect the increase in canine Rp associated with volume loading in our model.…”

Section: Discussionmentioning

confidence: 39%

“…However, pretreatment with a dose of atropine that totally blocks muscarinic receptor activity [32] does not affect the increase in canine Rp associated with volume loading in our model. This difference may be due to either: 1) differences between canine trachea and peripheral airway [10]; 2) differences in the time of treatment (we pretreated with atropine whereas the other investigators used this drug to reverse pulmonary congestion [8,9]); or 3) differences in protocols, e.g. ISHII et al [6] abruptly increased left atrial pressure by inflating a balloon to 30 mmHg, whereas we gradually increased PCWP to 15 mmHg with a 20 min infusion of normal saline.…”

Section: Discussionmentioning

confidence: 99%

“…The mechanism for this effect remains an issue of debate [7]. The fact that airway obstruction can be abolished by vagotomy or atropine suggests that this response is mediated by a vagal reflex [8][9][10]. Alternatively, vascular congestion and engorgement may increase peripheral airway resistance (Rp) by altering airway geometry [1,5].…”

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confidence: 99%

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The role of submucosal oedema in increased peripheral airway resistance by intravenous volume loading in dogs

Freed

1994

Eur Respir J

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Pulmonary congestion leads to an increase in airway resistance. It is still unknown whether this is due to vascular engorgement or to submucosal oedema. The present study was designed to determine the relative contribution of these two potential mechanisms. We examined the effect of intravenous volume loading on canine peripheral airway resistance (Rp). Bronchoscopes were wedged in contralateral sublobar segments and used to record Rp during rapid infusion of normal saline. Volume loading with normal saline increased pulmonary capillary wedge pressure (PCWP) and Rp. Unlike normal saline, dextran 70 did not increase Rp when infused at a rate that produced similar changes in PCWP. During infusion of normal saline, delta Rp was significantly enhanced in lung segments previously challenged with dry air when compared to contralateral control lungs, unexposed to dry air, and the use of dextran 70 significantly reduced this effect. Vasoconstriction with phenylephrine significantly decreased baseline Rp, but did not completely reverse the effect of fluid infusion. In addition, in lung segments exposed to dry air, delta Rp was significantly greater after volume loading and treatment with phenylephrine when compared to contralateral control lung. Finally, muscarinic receptor blockade was ineffective in preventing Rp from increasing during infusion of normal saline. Our results suggest that volume loading-induced increases in Rp are not caused by either vascular engorgement or the stimulation of muscarinic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 39%

Section: Discussionmentioning

confidence: 99%

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The role of submucosal oedema in increased peripheral airway resistance by intravenous volume loading in dogs

Freed

1994

Eur Respir J

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“…In the present study, one vagus was intact and the other, from which recordings were made, was partly so. The increase observed in peak intratracheal pressure during congestion could be due to (a) a passive stiffening of the lung due to vascular congestion, (b) a reflex bronchoconstriction (Kappagoda, Man, Ravi & Teo, 1988) and (c) a combination of the above. An earlier study examined the effect of bilateral vagotomy on the peak intratracheal pressure changes observed during pulmonary vascular congestion (Kappagoda et al 1987).…”

Section: Lymphflowmentioning

confidence: 99%

Plasmapheresis affects responses of slowly and rapidly adapting airway receptors to pulmonary venous congestion in dogs.

Kappagoda

Ravindran

1989

The Journal of Physiology

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SUMMARY1. The effects of plasmapheresis on the responses of rapidly adapting receptors (RARs) and slowly adapting receptors (SARs) of the airways to pulmonary venous congestion were examined in dogs anaesthetized with a-chloralose. Pulmonary venous congestion was produced in a graded manner by partial obstruction of the mitral valve sufficient to raise the mean left atrial pressure by 5, 10 and 15 mmHg. Plasmapheresis was performed by withdrawing 10 % of blood volume twice.2. Both RARs (n = 11) and SARs (n = 5) responded to pulmonary venous congestion by increasing their activities. The responses of the former were proportionately greater.3. After plasmapheresis which reduced the concentration of plasma proteins by 12-3+1-0%, the responses of the RARs to pulmonary venous congestion were enhanced significantly. There was nio significant change in the responses of SARs.4. In another set of six RARs, the effects of graded pulmonary venous congestion were investigated twice with an interval of 45 min between the two observations. No significant differences were noted between the two responses.5. Collection of lymph from the tracheobronchial lymph duct (n = 6) showed that after plasmapheresis, there was an increase in the control lymph flow. In addition, the lymph flow was enhanced during pulmonary venous congestion (mean left atrial pressure increased by 10 mmHg).6. It is suggested that a natural stimulus for the excitation of the RAR is a function of the fluid fluxes in the pulmonary extravascular space.

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“…Authors have addressed the mechanisms responsible for bronchial narrowing in animal models of pulmonary edema. Results variably support a role for reflex vagal efferent tone [3, 7, 9, 10, 11]and the development of airway epithelial edema and peribronchial cuffing [1, 2, 3, 6, 7, 8, 12, 13, 14, 15]. Don and Johnson [13]observed a correlation between airway narrowing on chest radiographs and mucosal edema on histologic examination of human lungs.…”

Section: Introductionmentioning

confidence: 99%

Effect of Pulmonary Edema on Tracheal Diameter

Snapper

Trochtenberg²,

Hwang³

et al. 1999

Respiration

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Background: Though it is well known that cardiogenic and noncardiogenic pulmonary edema can cause changes in lung mechanics, actual alterations in tracheal diameter have not been described. Objective: To evaluate the effects of pulmonary edema induced by increased left atrial pressure (cardiogenic) and Perilla ketone (PK; noncardiogenic) on tracheal diameter in chronically instrumented awake sheep. Methods: We investigated the effects of two mechanistically distinct types of pulmonary edema on tracheal diameter in chronically instrumented awake sheep. Cardiogenic pulmonary edema (analogous to congestive heart failure in humans) was induced by increasing left atrial pressure (↑P_LA) by inflating the balloon on a Foley catheter positioned in the mitral valve annulus to cause partial obstruction to flow across the valve (n = 18). Noncardiogenic pulmonary edema (increased pulmonary microvascular permeability pulmonary edema analogous to the acute respiratory distress syndrome in humans) was produced by the intravenous administration of PK (n = 11). Lateral chest radiographs (CXRs) were scored by a standardized 5-point scoring system for the severity of pulmonary edema, and tracheal diameter was measured at a fixed location in the carina. Three radiologists, blinded to sheep identification number and experimental protocol, evaluated the radiographs independently at different points in time for edema severity and tracheal diameter. The sheep were sacrificed immediately after the final CXR, and wet/dry lung weight ratio (W/D ratio) was determined. Results: Both ↑P_LA and PK were associated with statistically significant tracheal narrowing (↑P_LA: 20.3 ± 0.6 to 15.1 ± 0.9 mm; PK: 20.2 ± 0.6 to 14.1 ± 1.4 mm). Tracheal narrowing correlated with the severity of the pulmonary edema determined radiographically (↑P_LA: r = –0.69, p < 0.01; PK: r = –0.62, p < 0.01) and by W/D ratio (↑P_LA: r = –0.64, p < 0.05; PK: r = –0.54, p < 0.05). Conclusions: We conclude that tracheal narrowing occurs in sheep models of both cardiogenic and noncardiogenic pulmonary edema and that the degree of narrowing correlates with the severity of the edema.

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Reflex tracheal contraction during pulmonary venous congestion in the dog.

Cited by 20 publications

References 32 publications

The role of submucosal oedema in increased peripheral airway resistance by intravenous volume loading in dogs

The role of submucosal oedema in increased peripheral airway resistance by intravenous volume loading in dogs

Plasmapheresis affects responses of slowly and rapidly adapting airway receptors to pulmonary venous congestion in dogs.

Effect of Pulmonary Edema on Tracheal Diameter

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