Vagal afferents and active upper airway closure  during pulmonary edema in lambs

The present study was undertaken to gain further insight into the mechanisms responsible for the sustained active expiratory upper airway closure previously observed during high-permeability pulmonary edema in lambs. The experiments were conducted in nonsedated lambs, in which airflow and thyroarytenoid and inferior pharyngeal constrictor muscle electromyographic activity were recorded. We first studied the consequences of hemodynamic pulmonary edema (induced by impeding pulmonary venous return) on upper airway dynamics in five lambs; under this condition, a sustained expiratory upper airway closure consistently appeared. We then tested whether expiratory upper airway closure was related to vagal afferent activity from bronchopulmonary receptors. Five bivagotomized lambs underwent high-permeability pulmonary edema: no sustained expiratory upper airway closure was observed. Finally, we studied whether a sustained decrease in lung volume induced a sustained expiratory upper airway closure. Five lambs underwent a 250-ml pleural infusion: no sustained expiratory upper airway closure was observed. We conclude that 1) the sustained expiratory upper airway closure observed during pulmonary edema in nonsedated lambs is related to stimulation of vagal afferents by an increase in lung water and 2) a decrease in lung volume does not seem to be the causal factor.

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Inferior pharyngeal constrictor electromyographic activity during permeability pulmonary edema in lambs

Journal of Applied Physiology ◽

10.1152/jappl.1996.81.4.1598 ◽

1996 ◽

Vol 81 (4) ◽

pp. 1598-1604 ◽

Cited By ~ 12

Author(s):

Véronique Diaz ◽

Irenej Kianicka ◽

Patrick Letourneau ◽

Jean-Paul Praud ◽

Keyword(s):

Pulmonary Edema ◽

Upper Airway ◽

Emg Activity ◽

Lung Edema ◽

Electromyographic Activity ◽

Airway Closure ◽

Constrictor Muscle ◽

Glottic Closure ◽

Permeability Pulmonary Edema ◽

Inferior Pharyngeal Constrictor

Diaz, Véronique, Irenej Kianicka, Patrick Letourneau, and Jean-Paul Praud. Inferior pharyngeal constrictor electromyographic activity during permeability pulmonary edema in lambs. J. Appl. Physiol. 81(4): 1598–1604, 1996.—Newborn mammals exhibit an active expiratory upper airway closure during the first hours of extrauterine life. We have recently shown that permeability pulmonary edema led to active expiratory glottic closure in awake newborn lambs while hypoxia (inspired O2 fraction 8%; 15 min) did not. In the present study, we tested the hypothesis that expiratory glottic closure was accompanied by an increase in pharyngeal constrictor muscle expiratory electromyographic (EMG) activity. We studied seven awake nonsedated lambs aged 8–20 days. Airflow (facial mask + pneumotachograph), blood gases (arterial catheter), and EMG activity of both the thyroarytenoid muscle (a glottic adductor) and the inferior pharyngeal constrictor muscle were recorded before and after intravenous injection of halothane (0.05 ml/kg) to induce a permeability pulmonary edema. A central apnea (duration 15 s to 5 min) with continuous thyroarytenoid and inferior pharyngeal constrictor activity was observed within seconds after halothane injection. One lamb died despite rescuing maneuvers. An expiratory phasic thyroarytenoid and inferior pharyngeal constrictor muscle activity with simultaneous zero airflow gradually took place and, by 30 min after halothane injection, was present at each expiration in the six remaining lambs. Expiratory glottic and pharyngeal constrictor muscle EMG activity was subsequently present during the whole study period (1.5–5 h), even after correction of the initial hypoxia. Permeability lung edema was present at postmortem examination in all seven lambs. We conclude that a permeability pulmonary edema induced by intravenous halothane in nonsedated lambs enhances both glottic and pharyngeal constrictor muscle expiratory EMG. We hypothesize that expiratory contraction of the inferior pharyngeal constrictor muscle could participate in the active expiratory upper airway closure; this, in turn, might improve alveolocapillary gas exchange by increasing the end-expiratory lung volume.

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Effects of capsaicin pretreatment on expiratory laryngeal closure during pulmonary edema in lambs

Journal of Applied Physiology ◽

10.1152/jappl.1999.86.5.1570 ◽

1999 ◽

Vol 86 (5) ◽

pp. 1570-1577 ◽

Cited By ~ 24

Author(s):

Véronique Diaz ◽

Dominique Dorion ◽

Sylvain Renolleau ◽

Patrick Létourneau ◽

Irenej Kianicka ◽

...

Keyword(s):

Pulmonary Edema ◽

Intravenous Injection ◽

Upper Airway ◽

Airway Closure ◽

Respiratory Response ◽

C Fibers ◽

Bolus Intravenous Injection ◽

Series Of Experiments ◽

Permeability Pulmonary Edema ◽

First Time

The present study, performed in nonsedated, conscious lambs, consisted of two parts. In the first part, we 1) examined for the first time whether a respiratory response to pulmonary C-fiber stimulation could be elicited in nonsedated newborns and 2) determined whether this response could be abolished by capsaicin pretreatment. Then, by using capsaicin-desensitized lambs, we studied whether pulmonary C fibers were involved in the sustained, active expiratory upper airway closure previously observed during pulmonary edema. Airflow and thyroarytenoid and inferior pharyngeal constrictor muscle electromyographic activities were recorded. In the first set of experiments, a 5–10 μg/kg capsaicin bolus intravenous injection in seven intact lambs consistently led to a typical pulmonary chemoreflex, showing that C fibers are functionally mature in newborn lambs. In the second series of experiments, eight lambs pretreated with 25–50 mg/kg subcutaneous capsaicin did not exhibit any respiratory response to 10–50 μg/kg intravenous capsaicin injection, implicating C fibers in the response. Finally, in the above capsaicin-desensitized lambs, we observed that halothane-induced high-permeability pulmonary edema did not cause the typical response of sustained expiratory upper airway closure seen in the intact lamb. We conclude that functionally mature C fibers are present and responsible for a pulmonary chemoreflex in response to capsaicin intravenous injection in nonsedated lambs. Capsaicin pretreatment abolishes this reflex. Furthermore, the sustained expiratory upper airway closure observed during halothane-induced pulmonary edema in intact nonsedated lambs appears to be related to a reflex involving stimulation of pulmonary C fibers.

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Edema from cyclooxygenase products of endogenous arachidonic acid in isolated lung

Journal of Applied Physiology ◽

10.1152/jappl.1989.67.2.846 ◽

1989 ◽

Vol 67 (2) ◽

pp. 846-855 ◽

Cited By ~ 13

Author(s):

M. R. Littner ◽

F. D. Lott

Keyword(s):

Arachidonic Acid ◽

Pulmonary Edema ◽

Enzyme Inhibitor ◽

Calcium Ionophore ◽

Dry Weight ◽

Lung Water ◽

Isolated Lung ◽

Pulmonary Arterial ◽

Area Product ◽

Permeability Pulmonary Edema

We infused A23187, a calcium ionophore, into the pulmonary circulation of dextran-salt-perfused isolated rabbit lungs to release endogenous arachidonic acid. This led to elevations in pulmonary arterial pressure and to pulmonary edema as measured by extravascular wet-to-dry weight ratios. The increase in pressure and edema was prevented by indomethacin, a cyclooxygenase enzyme inhibitor, and by 1-benzylimidazole, a selective inhibitor of thromboxane (Tx) A2 synthesis. Transvascular flux of 125I-albumin from vascular to extravascular spaces of the lung was not elevated by A23187 but was elevated by infusion of oleic acid, an agent known to produce permeability pulmonary edema. We confirmed that A23187 leads to elevations in cyclooxygenase products and that indomethacin and 1-benzylimidazole inhibit synthesis of all cyclooxygenase products and TxA2, respectively, by measuring perfusate levels of prostaglandin (PG) I2 as 6-ketoprostaglandin F1 alpha, PGE2, and PGF2 alpha and TxA2 as TxB2. We conclude that release of endogenous pulmonary arachidonic acid can lead to pulmonary edema from conversion of such arachidonic acid to cyclooxygenase products, most notably TxA2. This edema was most likely from a net hydrostatic accumulation of extravascular lung water with an unchanged permeability of the vascular space, since an index of permeability-surface area product (i.e., transvascular albumin flux) was not increased.

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High permeability pulmonary edema (ARDS) during tocolytic therapy — a case report

Journal of Perinatal Medicine ◽

10.1515/jpme.1988.16.1.45 ◽

1988 ◽

Vol 16 (1) ◽

pp. 45-49 ◽

Cited By ~ 9

Author(s):

Erich W. Russi ◽

Ludwig Spaetling ◽

Jürg Gmür ◽

Henning Schneider

Keyword(s):

Case Report ◽

Pulmonary Edema ◽

High Permeability ◽

Permeability Pulmonary Edema

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Ventilation inhomogeneity in oleic acid-induced pulmonary edema

Journal of Applied Physiology ◽

10.1152/jappl.1997.82.4.1040 ◽

1997 ◽

Vol 82 (4) ◽

pp. 1040-1045 ◽

Cited By ~ 19

Author(s):

John Y. C. Tsang ◽

Michael J. Emery ◽

Michael P. Hlastala

Keyword(s):

Oleic Acid ◽

Pulmonary Edema ◽

Phase Iii ◽

Lung Water ◽

Peripheral Airways ◽

Ventilation Inhomogeneity ◽

Distal Airway ◽

Tissue Compliance ◽

Permeability Pulmonary Edema ◽

The Right

Tsang, John Y. C., Michael J. Emery, and Michael P. Hlastala. Ventilation inhomogeneity in oleic acid-induced pulmonary edema. J. Appl. Physiol.82(4): 1040–1045, 1997.—Oleic acid causes permeability pulmonary edema in the lung, resulting in impairment of gas-exchange and ventilation-perfusion heterogeneity and mismatch. Previous studies have shown that by using the multiple-breath helium washout (MBHW) technique, ventilation inhomogeneity (VI) can be quantitatively partitioned into two components, i.e., convective-dependent inhomogeneity (cdi) and diffusive-convective-dependent inhomogeneity (dcdi). Changes in VI, as represented by the normalized slope of the phase III alveolar plateau, were studied for 120 min in five anesthetized mongrel dogs that were ventilated under paralysis by a constant-flow linear motor ventilator. These animals received oleic acid (0.1 mg/kg) infusion into the right atrium at t = 0. MBHWs were done in duplicate for 18 breaths every 40 min afterward. Three other dogs that received only normal saline served as controls. The data show that, after oleic acid infusion, dcdi, which represents VI in peripheral airways, is responsible for the increasing total VI as lung water accumulates progressively over time. The cdi, which represents VI between larger conductive airways, remains relatively constant throughout. This observation can be explained by increases in the heterogeneity of tissue compliance in the periphery, distal airway closure, or by decreases in ventilation through collateral channels.

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Rebreathing lung tissue volume of sheep with normal and edematous lungs

Journal of Applied Physiology ◽

10.1152/jappl.1986.61.3.1132 ◽

1986 ◽

Vol 61 (3) ◽

pp. 1132-1138 ◽

Cited By ~ 2

Author(s):

G. J. Huchon ◽

A. Lipavsky ◽

J. M. Hoeffel ◽

J. F. Murray

Keyword(s):

Oleic Acid ◽

Pulmonary Edema ◽

Blood Volume ◽

Lung Tissue ◽

Extravascular Lung Water ◽

Lung Water ◽

Lung Weight ◽

Tissue Volume ◽

Accuracy Of Measurements ◽

Permeability Pulmonary Edema

To determine the accuracy of measurements of lung tissue volume (Vlt) by rebreathing acetylene in normal and edematous lungs, we compared gravimetric values of total lung weight (Ql) and extravascular lung water (Qwl) with Vlt in anesthetized control sheep (C) and sheep with hydrostatic pulmonary edema (HPE) or oleic acid-induced permeability pulmonary edema (PPE), five animals each. In eight additional sheep we determined that acetylene solubility in blood (0.117 +/- 0.010 ml X 100 ml-1 X Torr-1) differed significantly from that in lung-blood homogenates (0.095 +/- 0.009 ml X 100 ml-1 X Torr-1, P = 0.0017). The latter value was used in all calculations. In C, Vlt was 194% of Qwl and 98% of Ql; in HPE, Vlt was 144% of Qwl and 87% of Ql; and in PPE, Vlt was 112% of Qwl and 77% of Ql. We conclude that when the lungs are normal, Vlt reasonably measures Ql not Qwl. However in both HPE and PPE, Vlt progressively underestimates Ql and cannot differentiate between increased blood volume and increased Qwl.

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