Aspects of the pathophysiology of maternal lung edema during tocolytic therapy (Comment on: High permeability pulmonary edema (ARDS) during tocolytic therapy, by RUSSI et al.)

Sphingomyelin synthase (SMS) catalyzes the synthesis of sphingomyelin (SM) and is required for maintenance of plasma membrane microdomain fluidity. Of the two isoforms of mammalian SMS, SMS1 is mostly present in the trans-Golgi apparatus, whereas SMS2 is predominantly found at the plasma membrane. SMS2 has a role in receptor mediated response to inflammation in macrophages, however, the role of SMS2 in vascular permeability, pulmonary edema, and lung injury have not been investigated. To define the role of SMS activation in lung injury, we utilized a lipopolysaccharide (LPS)-induced lung edema model. SMS activity was measured and correlated with the severity of lung injury. Within 4 h of LPS treatment, SMS activity was increased significantly and remained upregulated up to 24 h. Comparison of LPS-induced lung injury in SMS2 knockout (SMS2−/−) and wild-type littermate control mice showed that inflammation, cytokine induction, and lung injury were significantly inhibited in SMS2−/− mice. Our results suggest that a deficiency of SMS2 can diminish the extent of pulmonary edema and lung injury. Furthermore, we show that depletion of SMS2 was sufficient to decrease MAP kinase-JNK activation, severity of LPS-induced pulmonary neutrophil influx, and inflammation, suggesting a novel role of SMS2 activation in lung injury.

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Neonatal high-permeability pulmonary edema based on serial cytokine profiles and KL-6 in serum: case report

FUKUSHIMA JOURNAL OF MEDICAL SCIENCE ◽

10.5387/fms.2016-8 ◽

2017 ◽

Vol 63 (1) ◽

pp. 22-27

Author(s):

Toshihiko Nakamura ◽

Mari Nakamura ◽

Naoto Takahashi

Keyword(s):

Case Report ◽

Pulmonary Edema ◽

High Permeability ◽

Cytokine Profiles ◽

Permeability Pulmonary Edema

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Primary (High Permeability) Pulmonary Edema

Seminars in Respiratory and Critical Care Medicine ◽

10.1055/s-2008-1070980 ◽

1983 ◽

Vol 4 (04) ◽

pp. 285-288 ◽

Cited By ~ 2

Author(s):

Kenneth Brigham

Keyword(s):

Pulmonary Edema ◽

High Permeability ◽

Permeability Pulmonary Edema

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

Journal of Applied Physiology ◽

10.1152/jappl.1999.86.5.1561 ◽

1999 ◽

Vol 86 (5) ◽

pp. 1561-1569 ◽

Cited By ~ 9

Author(s):

Véronique Diaz ◽

Dominique Dorion ◽

Irenej Kianicka ◽

Patrick Létourneau ◽

Jean-Paul Praud ◽

...

Keyword(s):

Pulmonary Edema ◽

Lung Volume ◽

Upper Airway ◽

Vagal Afferents ◽

Electromyographic Activity ◽

Airway Closure ◽

High Permeability ◽

Lung Water ◽

Permeability Pulmonary Edema ◽

Insight Into

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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