Surface-Active Agent in Eustachian Tube Function Philip
N.
Rapport; David J. Lim, MD; Harold S. Weiss, PhD
Using 15 fresh guinea pig temporal bones, Eustachian tubal function was repeatedly before and after saline washing to demonstrate the effect of surface-active agent. Although tubal opening tested
pressures for the 15 ears varied considin each ear tested, a higher pressure was required to open the Eustachian tube after saline washing (P
Chamber outlet valve
opened
Pump stopped O
TO
> TD 0)
o
LU
Tubai Trial
—r
>
100
200
400 300 Pressure in Bulla (mmH20)
opening pressures
500
Downloaded From: http://archotol.jamanetwork.com/ by a University of Arizona Health Sciences Library User on 05/30/2015
600
tension in the tube was virtually eliminated by abolishing the mucusair interface. In discussing the use of urea for "exudative otitis media," Bauer16 suggested the possible pres¬ ence of a lining complex or surfac¬ tant, similar to the lining of lung alveoli, that would reduce surface tension on the middle ear mucosa. Birken and Brookler15 demonstrated evidence of surface tension lowering substance (STLS) in canine Eusta¬ chian tube washings by a bubblestability technique that has been used to demonstrate pulmonary surfac¬ tant.24 In the
lung, the acellular lining layer lies over the plasma membrane of the epithelial cells of alveoli, so that air does not contact the cell surface directly. Histochemical study showed that the alveolar lining layer contains lipids and carbohydrates.25 Autoradiographic study showed that type II cells are actively engaged in phospholipid synthesis.26 Chemical analysis showed further that the lin¬ ing layer contains phospholipids
Gas phase
Lining layer
substance.27 These constituents of the lin¬ ing layer and make up the surfactant system of the lung. Using tricomplex floccular technique that preserves phospholipids in the surfactant, it was possible to demonstrate the pres¬ ence of pulmonary surfactant by elec¬ tron microscopy.28 Lim,29 using the same method, demonstrated small lamellar granules resembling pulmo¬ nary surfactant lamellae (or pure leci¬ thin lamellae) in the dark cores of the secretory granules in the Eustachian tube, and in the lining layer of the middle ear, mastoid, and tubai mu¬ cosa. On this basis, he suggested that there may be an auditory surfactant that has functions similar to that of pulmonary surfactant. In the absence of direct biochemical data, it cannot be concluded whether or not the pos¬ tulated auditory surfactant is chem¬ ically identical to pulmonary surfac¬
Interface and adsorbed
n
surfactant
Hypophase
cf
b
Surfactant in unassocjated molecules or micelles
¿
Surfactant molecule
Fig 4.—Theoretical
surfactant
"
^
Some basic concepts
concerning
Hypophase
¿
system modified after Scarpelli.1
Formation of film (1st expansion)
ex¬
±±f-^~
1st compression
*
are
tant.
o-
Liquid phase
^.Non-polar
common
chemicals
*" Interface
Fig 5.—Theoretical concept showing changes of surfactant system with repeated pansion and compression of surface.
(including lecithin, lysolecithin, phosphatidyl dimethylethanolamine, sphingomyelin, phosphatidyl inositol), neutral lipids, mucopolysaccharides, and protein, with lecithin being the most
0¿¿¿¿¿¿¿¿¿
Surface film
2nd
expansion
ooo¿o¿¿oo t., ;f
A 2nd
t/
compression
pulmonary surfactant
are relevant to discussion. It is postulated that the surfactant system exists in two phases in the alveolar lining layer: the interface or junction between the lining layer and alveolar air, and the our
underlying hypophase (liquid phase),
which is in contact with epithelial cell surfaces.27 Surfactant molecules are adsorbed from the hypophase into the interface forming the "surface film." The concept of alveolar lining layer that includes this surface film plus
the hypophase is illustrated in Fig 4. Pattle24 pictures the process of aera¬ tion of the lung during a normal in¬ fant's first breaths, or an expansion after atelectasis, as follows. During the initial expansion, the surface ten¬ sion is very high because most of surfactant is in the hypophase (liquid phase). As the alveolar surface is stretched, a lining film is formed with adsorption of surfactant from the underlying hypophase. When the inspiratory effort ceases, the surfaee
Downloaded From: http://archotol.jamanetwork.com/ by a University of Arizona Health Sciences Library User on 05/30/2015
area of the alveolus decreases and the surface film is compressed, result¬ ing in greater concentration of sur¬ factant in the surface film and decreased surface tension so that collapse is prevented. At the second inspiration, the surface tension in¬ creases again, and more surfactant is added to the surface film as il¬ lustrated in Fig 5. After repeated breathing, the surface film is com¬ pleted and surface tension oscillates at a low level. It is possible that the auditory surfactant stays in the (inactive) hypophase as in the mature fetal lung,27 but with repeated tubai openings, surfactant is adsorbed into the surface film to become effective in facilitating tubai opening. These characteristics of surfactant may ex¬ plain the Naunton-Galluser phenom¬ enon, that is, initial opening of the Eustachian tube is hardest but be¬ comes easier with succeeding opening
attempts.
The above-mentioned basic concept be directly applied to bubble for¬ mation, which is an important aspect of surfactant function. Foam is formed by agitation of a liquid and a gas together in the presence of a sur¬ factant, as in the formation of soap suds. The foam is made up of tiny bubbles that are stabilized by the can
Fig 6.—Author's concept
of fluid
dynamics
surface tension lowering property of the surfactant. Birken and Brookler,15 using this phenomenon, demon¬ strated the presence of surfactant in canine tubai washings. This charac¬ teristic of fluid-containing surfactant may explain why bubbles may be ob¬ served behind the tympanic mem¬ brane in some patients with middle ear effusions. It is also tempting to speculate that a ventilating tube, in¬ serted for the treatment of serous otitis media, provides the gas needed to form a liquid-gas interface that is a prerequisite to formation of the sur¬ face film. It has been well recognized that poor tubai function is a common find¬ ing among patients with inflamma¬ tory disease of the middle ear.14·30·31 Obviously, tissue edema in the tube must play an important role in these cases. However, it was postulated that a decrease in auditory surfactant can precipitate serous otitis media32 and make the ear more susceptible to barotrauma.33 By injecting polytef into the soft tissue of the torus tubarius in the pharyngeal recess of the dogs, Birken and Brookler34 produced serous effusions in the injected side. The levels of "STLS" (or surfactant) on the side with the effusion were not changed when compared to the conof middle
ear mucosa.
trol side. However, one of the dogs that developed suppurative otitis media on the injected side showed a decrease of surfactant. Since pulmo¬ nary surfactant deficiency is linked to respiratory distress of the newborn35 and to pulmonary atelectasis due to pneumonia,16 Birken and Brookler34 suggested that the destruction of surfactant by proteolytic enzyme pro¬ duced by a bacterial organism might be the reason for the decrease of sur¬ factant in an infected ear. Substan¬ tially increased levels of proteolytic enzymes in middle ear effusions have been reported by many investiga¬ tors.374" Whether or not auditory surfactant deficiency is an underlying cause of middle ear effusions needs additional study. However, it is rea¬ sonable to postulate that an auditory surfactant deficiency could result in poor Eustachian tube function with¬ out obvious morphological evidence. This postulation is supported by the present experiment in which tubai washing, which presumably removed surfactant, resulted in a substantial increase in the pressure required to open the Eustachian tube, indicating poor tubai function. It is known that sustained high negative pressure in the middle ear cavity can produce serous effusions by transudation.41-43 Flisberg et al14 found that 20 to 30 mm H g (272 to 408 mm H,0) of negative pressure in the normal human middle ear and mas¬ toid produced clear yellow fluid in 15 minutes. However, Bluestone et al31 found that 45 out of 104 ears with concurrent or recent middle ear ef¬ fusions showed no effusions even though the middle ear was under neg¬ ative pressure up to —400 mm , . Why some ears with negative middle ear pressure developed effusion while others did not may be partially ex¬ plained by the effect of surface ten¬ sion. It is well established that the pulmonary surfactant deficiency can produce pulmonary transudation.44 In the normal lung, transudation does not occur because of a balance be¬ tween opposing forces; the force op¬ posing transudation is plasma oncotic pressure, the forces favoring trans¬ udation are capillary blood pressure, tissue fluid oncotic pressure, and sur-
Downloaded From: http://archotol.jamanetwork.com/ by a University of Arizona Health Sciences Library User on 05/30/2015
face tension of the lining film.45 When surface tension is high due to sur¬ factant deficiency, as in respiratory distress syndrome of the newborn,27 the forces are out of balance in favor of transudation into the alveoli. As¬ suming the same fluid moving forces are active in the middle ear, as shown in Fig 6, absence or substantial de¬ crease of auditory surfactant may throw the balance in favor of trans¬ udation resulting in middle ear effu¬ sion. This phenomenon may explain how some ears fail to develop effu¬ sions even with relatively high nega¬ tive pressure in the middle ear if an adequate amount of surfactant is present. On the other hand, auditory surfactant deficiency may result in middle ear effusions even in ears with normal or low negative middle ear
pressure. Additional correlative study using biochemical and physiological data is needed to verify this concept. We have considered the possibility
that the present findings are the re¬ sults of postmortem changes in the Eustachian tube. However, there was no difference between results ob¬ tained from the specimens examined about two hours after dissection and those examined about five hours post¬ mortem. Regardless of the length of the postmortem period, the values ob¬ tained before and after saline wash¬ ing were consistently different. It is unlikely that the postmortem changes could have taken place in such a short time. It is also known that the pulmo¬ nary surfactant system is very stable. Lung tissue can be refrigerated up to six weeks without altering surface
property.27 In view of these consid¬
erations, we have tentatively con¬ cluded that the present findings are real rather than the results of post¬ mortem artifacts. Additional experi¬ ments to determine whether or not the phenomena, observed in the pres¬ ent investigation, can be restored by introducing an artificial surfactant to the saline-washed Eustachian tube is
underway. This study is supported in part by National In¬ stitutes of Health, National Institute of Neuro¬ logical Diseases and Stroke research grant NS08854-5 and by the Roessler Fund. Catherine Morstatter assisted with the open¬ ing pressure measurement apparatus; Charles Stockwell, PhD, provided statistical analysis; Nancy Sally provided illustrations; Dorothea Loftquist provided the photography; and Vir¬ ginia Holford assisted with manuscript prepara¬ tion.
References 1. Rich AR: The Eustachian tube and its related muscles. Johns Hopkins Hosp Bull 352:206\x=req-\ 214, 1920. 2. Toynbee J: On the muscles that open the Eustachian tube. Proc Roy Soc Med 6:286, 1853. 3. Politzer A: The Anatomical and Histological Dissection of the Human Ear in the Normal and Diseased Condition. London, Bailliere Tindall and Cox, 1892. 4. Wolff D: The microscopic anatomy of the Eutachian tube. Ann Otol Rhinol Laryngol 43:483\x=req-\ 494, 1934. 5. Zollner F: Anatomie, Physiologie, Pathologie, und Klinik der Ohrtompete. Berlin, Springer-Verlag, 1942. 6. Graves GO, Edwards LF: The Eustachian tube. Arch Otolaryngol 39:359-397, 1944. 7. von Gyergay A: Neue Wege zur Erkennung der Physiologie und Pathologie der Ohrtrompete. Mschr Ohrenheilk 66:769, 1932. 8. von Dishoeck HAE: Resistance-measuring of the Eustachian tube and the ostium and isthmus valve mechanism. Acta Otolaryngol 35:317, 1947. 9. Aschan G: The Eustachian tube. Acta Otolaryngol 44:295, 1954. 10. Guild SR: Elastic tissue of the Eustachian tube. Ann Otol Rhinol Laryngol 64:537, 1944. 11. Perlman HB: Observations on the Eustachian tube. Arch Otolaryngol 53:370-385,1951. 12. Ingelstedt S, Ortegren U: The ear snorkelpressure chamber technique: Volumetric determination of tubal ventilation. Acta Otolaryngol,
suppl 182, pp 1-7, 1963. 13. Flisberg K: Ventilatory studies on the Eustachian tube. Acta Otolaryngol, suppl 219, pp 1\x=req-\ 82, 1966.
14. Flisberg K, Ingelsted S, Ortegren U: On middle ear pressure. Acta Otolaryngol, suppl 182, pp 43-56, 1963. 15. Birken EA, Brookler KH: Surface tension lowering substance of the canine Eustachian tube. Ann Otol Rhinol Laryngol 81:268-271, 1972. 16. Bauer F: The use of urea in exudative otitis media. Otol Clin North Am 3:67-78, 1970. 17. Pattle RE: Surface lining of lung alveoli. Physiol Rev 45:48-79, 1965.
18. Morstatter C, Glaser R, Jurrus ER, et al: Compliance characteristics of excised lungs, abstracted. Physiologist 17:291, 1974. 19. von Neergaard K: Neue Auffassungen \l=u"\ber einen Grundbegriff der Atemmechanik: Die Retraktionskraft der Lunge, abhangig von der
Oberflachen spannung in den Alveolen. Z Ges 1929. 20. Winer BJ: Statistical Principles in Experimental Design. New York, McGraw-Hill Book Co Inc, 1962, pp 105-113. 21. Naunton RF, Galluser J: Measurements of Eustachian tube function (human). Ann Otol Rhinol Laryngol 76:455-471, 1967. 22. Riu R, Le Den R, Guillerm R, et al: Electromyographic study of opening of the Eustachian tube. Ann Otolaryngol 83:645-658,1966. 23. Perlman HB: Normal tubal function. Arch Otolaryngol 86:632-638, 1967. 24. Pattle RE: Properties, function and origin of the alveolar lining layer. Proc Roy Soc Med 148:217-240, 1958. 25. Luke JL, Spicer SS: Histochemistry of surface epithelial and pleural mucins in mammalian lung. Lab Invest 14:2101-2109, 1965. 26. Buckingham SH, Heinemann S, Sommer S, et al: Phospholipid synthesis in the large pulmonary alveolar cell. Am J Pathol 48:1027-1041, 1966. 27. Scarpelli EM: The Surfactant System of the Lung. Lea & Febiger, Philadelphia, 1968. 28. Dermer GB: The fixation of pulmonary surfactant for electron microscopy: I. The alveolar surface lining layer. J Ultrastruct Res 27:88\x=req-\ 104, 1969. 29. Lim DJ: Functional morphology of the lining membrane of the middle ear and Eustachian tube: An overview. Ann Otol Rhinol Laryngol 83:5-26, 1974. 30. Holmquist J, Renwall U: Eustachian tube function in secretory otitis media. Arch Otolaryngol 99:59-61, 1974. 31. Bluestone CD, Berry QC, Andrus WS: Mechanics of the Eustachian tube as it influences susceptibility to and resistance of middle ear effusions in children. Ann Otol Rhinol Laryngol 83:27-34, 1974.
Exp Med 66:373-394,
32. Brookler KH, Birken EA: Surface tension
lowering substance of the Eustachian tube. Laryngoscope 81:1671-1673, 1971. 33. Brookler KH: Otitis barotrauma. Laryngo-
scope 83:966-968, 1973. 34. Birken EA, Brookler KH: Surface tension lowering substance of the Eustachian tube in non-suppurative otitis media: An experiment with dogs. Laryngoscope 83:255-258, 1973. 35. Avery ME, Mead J: Surface properties in relation to atelectasis and hyaline membrane disease. Am J Dis Child 97:517-523, 1959. 36. Sutnick AI, Soloff LA: Atelectasis with pneumonia: A pathophysiologic study. Ann Intern Med 60:39-46, 1964. 37. Lupovich P, Harkins M: The pathophysiology of effusion in otitis media. Laryngoscope 82:1647-1653, 1972. 38. Juhn SK, Huff JS, Paparella MM: Biochemical analysis of middle ear effusions: Preliminary report. Ann Otol Rhinol Laryngol 80:347-353, 1971. 39. Veltri RW, Sprinkle PM: Serous otitis media\p=m-\Immunologlobulinand lysozyme levels in middle ear fluids and serum. Ann Otol Rhinol
Laryngol 82:297-301, 40. Palva
1973.
T, Raunio V, Nousianen R: Secretory
otitis media: Protein and enzyme analyses. Ann Otol Rhinol Laryngol 83:35-43, 1974. 41. Holmgren L: Experimental tubal occlusion. Acta Otolaryngol 28:587-592, 1940. 42. Paparella MM, Hiraide F, Juhn S, et al: Cellular events involved in middle ear fluid production. Ann Otol Rhinol Laryngol 79:766-780, 1970. 43. Proud GO, Odoi H: Effects of Eustachian tube ligation. Ann Otol Rhinol Laryngol 79:30\x=req-\ 32, 1970. 44. Clements JA: Pulmonary edema and permeability of alveolar membranes. Arch Environ Health 2:280-283, 1961. 45. Gruenwald P, Johnson RP, Hustead RF, et al: Correlation of mechanical properties of infant lungs with surface activity of extracts. Proc Soc Exp Biol Med 109:369-371, 1962.
Downloaded From: http://archotol.jamanetwork.com/ by a University of Arizona Health Sciences Library User on 05/30/2015
N.
Rapport; David J. Lim, MD; Harold S. Weiss, PhD
Using 15 fresh guinea pig temporal bones, Eustachian tubal function was repeatedly before and after saline washing to demonstrate the effect of surface-active agent. Although tubal opening tested
pressures for the 15 ears varied considin each ear tested, a higher pressure was required to open the Eustachian tube after saline washing (P
Chamber outlet valve
opened
Pump stopped O
TO
> TD 0)
o
LU
Tubai Trial
—r
>
100
200
400 300 Pressure in Bulla (mmH20)
opening pressures
500
Downloaded From: http://archotol.jamanetwork.com/ by a University of Arizona Health Sciences Library User on 05/30/2015
600
tension in the tube was virtually eliminated by abolishing the mucusair interface. In discussing the use of urea for "exudative otitis media," Bauer16 suggested the possible pres¬ ence of a lining complex or surfac¬ tant, similar to the lining of lung alveoli, that would reduce surface tension on the middle ear mucosa. Birken and Brookler15 demonstrated evidence of surface tension lowering substance (STLS) in canine Eusta¬ chian tube washings by a bubblestability technique that has been used to demonstrate pulmonary surfac¬ tant.24 In the
lung, the acellular lining layer lies over the plasma membrane of the epithelial cells of alveoli, so that air does not contact the cell surface directly. Histochemical study showed that the alveolar lining layer contains lipids and carbohydrates.25 Autoradiographic study showed that type II cells are actively engaged in phospholipid synthesis.26 Chemical analysis showed further that the lin¬ ing layer contains phospholipids
Gas phase
Lining layer
substance.27 These constituents of the lin¬ ing layer and make up the surfactant system of the lung. Using tricomplex floccular technique that preserves phospholipids in the surfactant, it was possible to demonstrate the pres¬ ence of pulmonary surfactant by elec¬ tron microscopy.28 Lim,29 using the same method, demonstrated small lamellar granules resembling pulmo¬ nary surfactant lamellae (or pure leci¬ thin lamellae) in the dark cores of the secretory granules in the Eustachian tube, and in the lining layer of the middle ear, mastoid, and tubai mu¬ cosa. On this basis, he suggested that there may be an auditory surfactant that has functions similar to that of pulmonary surfactant. In the absence of direct biochemical data, it cannot be concluded whether or not the pos¬ tulated auditory surfactant is chem¬ ically identical to pulmonary surfac¬
Interface and adsorbed
n
surfactant
Hypophase
cf
b
Surfactant in unassocjated molecules or micelles
¿
Surfactant molecule
Fig 4.—Theoretical
surfactant
"
^
Some basic concepts
concerning
Hypophase
¿
system modified after Scarpelli.1
Formation of film (1st expansion)
ex¬
±±f-^~
1st compression
*
are
tant.
o-
Liquid phase
^.Non-polar
common
chemicals
*" Interface
Fig 5.—Theoretical concept showing changes of surfactant system with repeated pansion and compression of surface.
(including lecithin, lysolecithin, phosphatidyl dimethylethanolamine, sphingomyelin, phosphatidyl inositol), neutral lipids, mucopolysaccharides, and protein, with lecithin being the most
0¿¿¿¿¿¿¿¿¿
Surface film
2nd
expansion
ooo¿o¿¿oo t., ;f
A 2nd
t/
compression
pulmonary surfactant
are relevant to discussion. It is postulated that the surfactant system exists in two phases in the alveolar lining layer: the interface or junction between the lining layer and alveolar air, and the our
underlying hypophase (liquid phase),
which is in contact with epithelial cell surfaces.27 Surfactant molecules are adsorbed from the hypophase into the interface forming the "surface film." The concept of alveolar lining layer that includes this surface film plus
the hypophase is illustrated in Fig 4. Pattle24 pictures the process of aera¬ tion of the lung during a normal in¬ fant's first breaths, or an expansion after atelectasis, as follows. During the initial expansion, the surface ten¬ sion is very high because most of surfactant is in the hypophase (liquid phase). As the alveolar surface is stretched, a lining film is formed with adsorption of surfactant from the underlying hypophase. When the inspiratory effort ceases, the surfaee
Downloaded From: http://archotol.jamanetwork.com/ by a University of Arizona Health Sciences Library User on 05/30/2015
area of the alveolus decreases and the surface film is compressed, result¬ ing in greater concentration of sur¬ factant in the surface film and decreased surface tension so that collapse is prevented. At the second inspiration, the surface tension in¬ creases again, and more surfactant is added to the surface film as il¬ lustrated in Fig 5. After repeated breathing, the surface film is com¬ pleted and surface tension oscillates at a low level. It is possible that the auditory surfactant stays in the (inactive) hypophase as in the mature fetal lung,27 but with repeated tubai openings, surfactant is adsorbed into the surface film to become effective in facilitating tubai opening. These characteristics of surfactant may ex¬ plain the Naunton-Galluser phenom¬ enon, that is, initial opening of the Eustachian tube is hardest but be¬ comes easier with succeeding opening
attempts.
The above-mentioned basic concept be directly applied to bubble for¬ mation, which is an important aspect of surfactant function. Foam is formed by agitation of a liquid and a gas together in the presence of a sur¬ factant, as in the formation of soap suds. The foam is made up of tiny bubbles that are stabilized by the can
Fig 6.—Author's concept
of fluid
dynamics
surface tension lowering property of the surfactant. Birken and Brookler,15 using this phenomenon, demon¬ strated the presence of surfactant in canine tubai washings. This charac¬ teristic of fluid-containing surfactant may explain why bubbles may be ob¬ served behind the tympanic mem¬ brane in some patients with middle ear effusions. It is also tempting to speculate that a ventilating tube, in¬ serted for the treatment of serous otitis media, provides the gas needed to form a liquid-gas interface that is a prerequisite to formation of the sur¬ face film. It has been well recognized that poor tubai function is a common find¬ ing among patients with inflamma¬ tory disease of the middle ear.14·30·31 Obviously, tissue edema in the tube must play an important role in these cases. However, it was postulated that a decrease in auditory surfactant can precipitate serous otitis media32 and make the ear more susceptible to barotrauma.33 By injecting polytef into the soft tissue of the torus tubarius in the pharyngeal recess of the dogs, Birken and Brookler34 produced serous effusions in the injected side. The levels of "STLS" (or surfactant) on the side with the effusion were not changed when compared to the conof middle
ear mucosa.
trol side. However, one of the dogs that developed suppurative otitis media on the injected side showed a decrease of surfactant. Since pulmo¬ nary surfactant deficiency is linked to respiratory distress of the newborn35 and to pulmonary atelectasis due to pneumonia,16 Birken and Brookler34 suggested that the destruction of surfactant by proteolytic enzyme pro¬ duced by a bacterial organism might be the reason for the decrease of sur¬ factant in an infected ear. Substan¬ tially increased levels of proteolytic enzymes in middle ear effusions have been reported by many investiga¬ tors.374" Whether or not auditory surfactant deficiency is an underlying cause of middle ear effusions needs additional study. However, it is rea¬ sonable to postulate that an auditory surfactant deficiency could result in poor Eustachian tube function with¬ out obvious morphological evidence. This postulation is supported by the present experiment in which tubai washing, which presumably removed surfactant, resulted in a substantial increase in the pressure required to open the Eustachian tube, indicating poor tubai function. It is known that sustained high negative pressure in the middle ear cavity can produce serous effusions by transudation.41-43 Flisberg et al14 found that 20 to 30 mm H g (272 to 408 mm H,0) of negative pressure in the normal human middle ear and mas¬ toid produced clear yellow fluid in 15 minutes. However, Bluestone et al31 found that 45 out of 104 ears with concurrent or recent middle ear ef¬ fusions showed no effusions even though the middle ear was under neg¬ ative pressure up to —400 mm , . Why some ears with negative middle ear pressure developed effusion while others did not may be partially ex¬ plained by the effect of surface ten¬ sion. It is well established that the pulmonary surfactant deficiency can produce pulmonary transudation.44 In the normal lung, transudation does not occur because of a balance be¬ tween opposing forces; the force op¬ posing transudation is plasma oncotic pressure, the forces favoring trans¬ udation are capillary blood pressure, tissue fluid oncotic pressure, and sur-
Downloaded From: http://archotol.jamanetwork.com/ by a University of Arizona Health Sciences Library User on 05/30/2015
face tension of the lining film.45 When surface tension is high due to sur¬ factant deficiency, as in respiratory distress syndrome of the newborn,27 the forces are out of balance in favor of transudation into the alveoli. As¬ suming the same fluid moving forces are active in the middle ear, as shown in Fig 6, absence or substantial de¬ crease of auditory surfactant may throw the balance in favor of trans¬ udation resulting in middle ear effu¬ sion. This phenomenon may explain how some ears fail to develop effu¬ sions even with relatively high nega¬ tive pressure in the middle ear if an adequate amount of surfactant is present. On the other hand, auditory surfactant deficiency may result in middle ear effusions even in ears with normal or low negative middle ear
pressure. Additional correlative study using biochemical and physiological data is needed to verify this concept. We have considered the possibility
that the present findings are the re¬ sults of postmortem changes in the Eustachian tube. However, there was no difference between results ob¬ tained from the specimens examined about two hours after dissection and those examined about five hours post¬ mortem. Regardless of the length of the postmortem period, the values ob¬ tained before and after saline wash¬ ing were consistently different. It is unlikely that the postmortem changes could have taken place in such a short time. It is also known that the pulmo¬ nary surfactant system is very stable. Lung tissue can be refrigerated up to six weeks without altering surface
property.27 In view of these consid¬
erations, we have tentatively con¬ cluded that the present findings are real rather than the results of post¬ mortem artifacts. Additional experi¬ ments to determine whether or not the phenomena, observed in the pres¬ ent investigation, can be restored by introducing an artificial surfactant to the saline-washed Eustachian tube is
underway. This study is supported in part by National In¬ stitutes of Health, National Institute of Neuro¬ logical Diseases and Stroke research grant NS08854-5 and by the Roessler Fund. Catherine Morstatter assisted with the open¬ ing pressure measurement apparatus; Charles Stockwell, PhD, provided statistical analysis; Nancy Sally provided illustrations; Dorothea Loftquist provided the photography; and Vir¬ ginia Holford assisted with manuscript prepara¬ tion.
References 1. Rich AR: The Eustachian tube and its related muscles. Johns Hopkins Hosp Bull 352:206\x=req-\ 214, 1920. 2. Toynbee J: On the muscles that open the Eustachian tube. Proc Roy Soc Med 6:286, 1853. 3. Politzer A: The Anatomical and Histological Dissection of the Human Ear in the Normal and Diseased Condition. London, Bailliere Tindall and Cox, 1892. 4. Wolff D: The microscopic anatomy of the Eutachian tube. Ann Otol Rhinol Laryngol 43:483\x=req-\ 494, 1934. 5. Zollner F: Anatomie, Physiologie, Pathologie, und Klinik der Ohrtompete. Berlin, Springer-Verlag, 1942. 6. Graves GO, Edwards LF: The Eustachian tube. Arch Otolaryngol 39:359-397, 1944. 7. von Gyergay A: Neue Wege zur Erkennung der Physiologie und Pathologie der Ohrtrompete. Mschr Ohrenheilk 66:769, 1932. 8. von Dishoeck HAE: Resistance-measuring of the Eustachian tube and the ostium and isthmus valve mechanism. Acta Otolaryngol 35:317, 1947. 9. Aschan G: The Eustachian tube. Acta Otolaryngol 44:295, 1954. 10. Guild SR: Elastic tissue of the Eustachian tube. Ann Otol Rhinol Laryngol 64:537, 1944. 11. Perlman HB: Observations on the Eustachian tube. Arch Otolaryngol 53:370-385,1951. 12. Ingelstedt S, Ortegren U: The ear snorkelpressure chamber technique: Volumetric determination of tubal ventilation. Acta Otolaryngol,
suppl 182, pp 1-7, 1963. 13. Flisberg K: Ventilatory studies on the Eustachian tube. Acta Otolaryngol, suppl 219, pp 1\x=req-\ 82, 1966.
14. Flisberg K, Ingelsted S, Ortegren U: On middle ear pressure. Acta Otolaryngol, suppl 182, pp 43-56, 1963. 15. Birken EA, Brookler KH: Surface tension lowering substance of the canine Eustachian tube. Ann Otol Rhinol Laryngol 81:268-271, 1972. 16. Bauer F: The use of urea in exudative otitis media. Otol Clin North Am 3:67-78, 1970. 17. Pattle RE: Surface lining of lung alveoli. Physiol Rev 45:48-79, 1965.
18. Morstatter C, Glaser R, Jurrus ER, et al: Compliance characteristics of excised lungs, abstracted. Physiologist 17:291, 1974. 19. von Neergaard K: Neue Auffassungen \l=u"\ber einen Grundbegriff der Atemmechanik: Die Retraktionskraft der Lunge, abhangig von der
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