Middle Ear Gas Research Articles

Panel 2: Anatomy (Eustachian Tube, Middle Ear, and Mastoid-Anatomy, Physiology, Pathophysiology, and Pathogenesis).

Objective In this report, we review the recent literature (ie, past 4 years) to identify advances in our understanding of the middle ear-mastoid-eustachian tube system. We use this review to determine whether the short-term goals elaborated in the last report were achieved, and we propose updated goals to guide future otitis media research. Data Sources PubMed, Web of Science, Medline. Review Methods The panel topic was subdivided, and each contributor performed a literature search within the given time frame. The keywords searched included middle ear, eustachian tube, and mastoid for their intersection with anatomy, physiology, pathophysiology, and pathology. Preliminary reports from each panel member were consolidated and discussed when the panel met on June 11, 2015. At that meeting, the progress was evaluated and new short-term goals proposed. Conclusions Progress was made on 13 of the 20 short-term goals proposed in 2011. Significant advances were made in the characterization of middle ear gas exchange pathways, modeling eustachian tube function, and preliminary testing of treatments for eustachian tube dysfunction. Implications for Practice In the future, imaging technologies should be developed to noninvasively assess middle ear/eustachian tube structure and physiology with respect to their role in otitis media pathogenesis. The new data derived from these structure/function experiments should be integrated into computational models that can then be used to develop specific hypotheses concerning otitis media pathogenesis and persistence. Finally, rigorous studies on medical or surgical treatments for eustachian tube dysfunction should be undertaken.

Middle ear gas exchange problems in OME and cholesteatoma

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Congestion of mastoid mucosa and influence on middle ear pressure – Effect of retroauricular injection of adrenaline

Micro-CT scanning of temporal bones has revealed numerous retroauricular microchannels, which connect the outer bone surface directly to the underlying mastoid air cells. Their structure and dimensions have suggested a separate vascular supply to the mastoid mucosa, which may play a role in middle ear (ME) pressure regulation. This role may be accomplished by changes in the mucosa congestion resulting in volumetric changes, which ultimately affect the pressure of the enclosed ME gas pocket (Boyle's law). Further, such mucosa congestion may be susceptible to α-adrenergic stimulation similar to the mucosa of the nose. The purpose of our study was to investigate these hypotheses by recording the ME pressure in response to adrenergic stimulation administered by retroauricular injections at the surface of the microchannels.In a group of 20 healthy adults we measured the ME pressure by tympanometry initially in the sitting position, and then in the supine position over a 5 min period with 30 s intervals. In each subject, the study included 1) a control reference experiment with no intervention, 2) a control experiment with subcutaneously retroauricular injection of 1 ml isotonic NaCl solution, and 3) a test experiment with subcutaneously retroauricular injection of 1 ml NaCl-adrenaline solution. In both control experiments the ME pressure displayed an immediate increase in response to changing body position; this pressure increase remained stable for the entire period up to five minutes. In the test experiments the ME pressure also showed an initial pressure increase, but it was followed by a distinct significant pressure decrease with a maximum after 90 s. The test group was injected with both a 5 and 10% adrenaline solution, but the responses appeared similar for the two concentrations.Subcutaneous retroauricular injection of adrenaline caused a significant pressure decrease in ME pressure compared with control ears. This may be explained by the microchannels conveying the adrenaline to the underlying mastoid mucosa, where it may result in a vascular constriction and decongestion, ultimately resulting in a ME pressure decrease. These findings suggest that the microchannels contain vascular connections to the mastoid mucosa, and that the mastoid mucosa is susceptible to vasoactive mediators, which may play a role in ME pressure regulation. Further anatomical and physiological experiments should be carried out to confirm these suggestions including pharmacological interactions with the mastoid mucosa.

Middle Ear Gas Pressure Regulation

To establish a mathematical model of middle ear gas pressure regulation and to discuss potential implications for pathophysiology-oriented theoretical approach to middle ear surgery, with particular attention to mastoid obliteration. Numerous studies support that small mastoid volume is associated with cholesteatoma. Latest studies show that mastoid obliteration is an effective technique to lower the recurrence rate in these ears. A mathematical model was used to predict the development of gas pressure balance in the function of different middle ear volumes (VME), considering normal and dysfunctional Eustachian tube. Published data as gas pressure input values and our 3D CT reconstruction data in healthy and pathologic middle ears of children were applied. The model predicted ≤6.66 daPa pressure fluctuations in VME ≥3 ml, compared to ≥16 daPa of a VME ≤1 ml at perfect ET function, because of the different pressure change rate and pressure buffer effect of the MEs. Substantially larger fluctuations can be expected in a VME <3 ml with malfunctioning ET. Modeling mastoid obliteration predicts similar pressure fluctuations to a VME ≥3 ml resulting from elimination of gas exchange surface. Pressure change is faster in smaller MEs than in larger ones. Healthy MEs between 3 and 6 ml are very sensitive to the duration of a potential ET dysfunction to develop ME pathology. In MEs with poor mastoid pneumatization and dysfunctional ET, typical in cholesteatoma cases, mastoid obliteration as surgical reduction of mucosal surface for gas exchange can improve ME gas pressure balance resulting in better long-term outcome.

Panel 2: Eustachian Tube, Middle Ear, and Mastoid—Anatomy, Physiology, Pathophysiology, and Pathogenesis

This report reviews the literature to identify the advances in our understanding of the middle ear (ME)-Eustachian tube (ET) system during the past 4 years and, on that basis, to determine whether the short-term goals elaborated in the last report were achieved and propose updated goals to guide future otitis media (OM) research. Databases searched included PubMed, Web of Science (1945-present), Medline (1950 to present), Biosis Previews (1969-present), and the Zoological Record (1978 to present). The initial literature search covered the time interval from January 2007 to June 2011, with a supplementary search completed in February 2012. The panel topic was subdivided; each contributor performed a literature search and provided a preliminary report. Those reports were consolidated and discussed when the panel met on June 9, 2011. At that meeting, the progress was evaluated and new short-term goals proposed. Progress was made on 16 of the 19 short-term goals proposed in 2007. Significant advances were made in the characterization of ME gas exchange pathways, modeling ET function, and preliminary testing of treatments for ET dysfunction. In the future, imaging technologies should be developed to noninvasively assess ME/ET structure and physiology with respect to their role in OM pathogenesis. The new data derived from form/function experiments should be integrated into the finite element models and used to develop specific hypotheses concerning OM pathogenesis and persistence. Finally, rigorous studies of treatments, medical or surgical, of ET dysfunction should be undertaken.

Role of the mastoid in middle ear pressure regulation

Determine the role of mastoid volume in middle ear pressure (MEP) regulation. The hypothesis was that inert gas exchange between blood and middle ear (ME) is slower for larger mastoid volumes. Prospective. For 21 enrolled subjects, the bilateral surface areas and volumes of the mastoid and tympanum were measured from computed tomography scans in 20 subjects with a wide range of mastoid volumes. Then, 19 subjects were reclined in a chair, fitted with a non-rebreathing mask and breathed room air for 20 minutes (acclimation), a gas composition of 25% N(2)O, 20% O(2), balance N(2) for 30 minutes (experiment), and room air for 30 minutes (recovery). Bilateral MEPs were recorded by tympanometry every 2 minutes. The slopes of the MEP-time functions during N(2)O breathing were calculated to the first observation of eustachian tube opening and divided by the estimated blood-ME N(2)O gradient to yield a N(2)O time constant. Sufficient data were available for 16 right and 11 left MEs to calculate the time constant. MEP did not change during the baseline period, but within 10 minutes of breathing the N(2)O mixture showed a progressive increase. The right-left correlation for the time constant was 0.87 (n = 10 ears, P = .001). Regression of the time constants on ME volume showed an inverse relationship (n = 23 ears, r = -41, P = .05). A better data fit was the curvilinear relationship predicted by a mathematical model of the mastoid acting as a ME ear gas reserve. These results support the tested hypothesis that the mastoid could serve as ME gas reserve.

Surface area-volume relationships for the mastoid air cell system and tympanum in adult humans: Implications for mastoid function

Conclusions: The middle ear (ME) surface area/volume ratio (SA/V) is greater than that of the tympanum. The rate of ME pressure decrease is proportional to the ME SA/V. The mastoid air-cell system (MACS) will not function as an ME gas reserve unless the blood perfusion/surface area is much greater for the tympanum than the MACS and decreases as MACS volume increases. Objective: To measure the MACS and tympanum surface areas and volumes and ascertain whether the MACS could function as an ME gas reserve. Methods: Twenty adult subjects with a wide range of MACS volumes underwent CT of their MEs. The left and right surface areas and volumes of the tympanum and MACS were reconstructed and entered into a simple perfusion-limited model of transmucosal gas exchange. In this model the MACS would be a gas reserve if ME SA/V was less than the tympanum SA/V or equivalently, if their ratio was less than a critical value of 1. Results: Both MACS and tympanum SA were linearly related to their volumes. MACS SA/V and the ME SA/V were significantly greater than those for the tympanum. Inputting the measured values into the model yielded a critical value of 1.4, which was significantly greater than 1.

Perfusion and diffusion limitations in middle ear gas exchange: The exchange of CO 2 as a test case

A long standing debate on perfusion/diffusion limitations in the context of middle ear (ME) gas exchange was revisited using data obtained from previous iso-pressure gas-exchange measurements in different mammals. We tried to determine whether the exchange of CO 2 in the ME is limited by perfusion or by diffusion by comparing the mass specific cardiac output ( ms Q ˙ ) and the mass specific initial CO 2 flow rate into air-washed MEs ( ms V i ˙ CO 2 ) of rabbits and rats. Based on previously published allometry at rest, the ms Q ˙ was 0.154 mL/(min g) in rabbits (mean body weight: 2800 g) and 0.259 mL/(min g) in rats (mean body weight: 179.1 g); ms V i ˙ CO 2 (Δ t = 0) was 0.109 ± 0.047 μL/(h g) in rabbits ( n = 16) and 0.170 ± 0.094 μL/(h g) in rats ( n = 9). Similar ratios were found when an allometric comparison was made between the ratio of ms V i ˙ CO 2 (Δ t = 0) (∼0.64), and the ratio of ms Q ˙ s (∼0.59) in rabbits and rats. If the active mucosal surface areas of MEs of rabbits and rats are directly proportional to their masses as are the masses of their hearts and if their ms Q ˙ s are proportional to the rates of blood flows in the ME mucosa, these results support the assumption that the exchange of CO 2 in the ME of mammals is mainly perfusion (and not diffusion) dependent.

Tympanometric experiments on retracted ear drums – does tympanometry reflect the true middle ear pressure?

Conclusions: Tympanometry in ears with retracted or partially atelectatic tympanic membranes does not reflect the true middle ear (ME) pressure. The position of the tympanogram peak depends on the size of a retraction pocket and the remaining ME gas volume. Thus tympanometry in such cases cannot be used for measurements of ME pressure. Objective: To prove the hypothesis that tympanometry in ears with retraction pockets or atelectasis does not measure ME pressure correctly. Materials and methods: Tympanometry was performed in a simplified artificial ME model, in which different ‘tympanic membranes’ with pockets could be integrated. Results: We found a shift of the tympanogram peaks, either towards negative or positive pressures, depending on the position of the pocket: in case of an ‘inward’ direction (towards the ME like a retraction pocket) the peak was in the negative pressure range, in case of an ‘outward’ direction (bulging into the ear canal) the shift was towards positive pressures. The shift increased with decreasing volume behind the tympanic membrane. The effect cannot be simply be explained by hysteresis but by the air ‘cushion’ that is ‘trapped’ behind the membrane, limiting its excursions during the tympanometric sweep.

Interaction of pneumococcal phase variation and middle ear pressure/gas composition: An in vitro model of simulated otitis media

Streptococcus pneumoniae, a leading cause of otitis media (OM), undergoes spontaneous intra-strain variations in colony morphology. Transparent (T) variant is more efficient in colonizing the nasopharynx while the opaque (O) variant exhibits greater virulence during systemic infections. We hypothesized that changes in middle ear (ME) gas pressure/composition during Eustachian tube (ET) dysfunction and the treatment of that dysfunction, e.g., tympanostomy tube (TT) insertion, play a role in selecting the S. pneumoniae variant that can efficiently colonize/infect the ME mucosa. Human ME epithelial cells were preconditioned for 24 h under one of three conditions that simulated (1) normal ME, (2) ME with ET obstruction (ETO) and (3) ME with TT; subsequently exposed to a dose (∼10 7 CFU/ml) of either T or O variant of S. pneumoniae, and then incubated for 1 h and 3 h. Under the simulated ETO and TT conditions, T variant exhibited a higher growth rate and greater epithelial adherence and killing than did O variants. Attachment of T variant to epithelial cells was documented by scanning electron microscopy. These results suggest that the T variant is more highly adapted to various ME environments than the O variants.

Middle ear gas exchange via the mucosa: estimation by hyperventilation

Conclusion: It is thought that gas exchange via the mucosa occurred in relation to the partial pressure gradient, and it was impaired mainly by inflammatory changes in the mastoid mucosa. It was verified that gas exchange via the mucosa is less likely to be impaired than gas exchange via the eustachian tube. Objectives: To evaluate the capacity of middle ear gas exchange via the mucosa by examining the effect of hyperventilation on middle ear pressure. Subjects and methods: A total of 55 patients, 40 patients with a type A tympanogram and 15 with type C, were selected. Tympanometry was performed in one ear every 2 min while hyperventilation was forcibly continued for 4–6 min in the supine position. The middle ear pressure and the pressure of end-tidal carbon dioxide (PETCO2) was measured, and sonotubometry was performed. Results: PETCO2 decreased gradually as hyperventilation continued in all cases. Although middle ear pressure decreased by hyperventilation in 49 of 55 patients, in 6 patients it hardly decreased despite the decrease in PETCO2. These six patients were treated for otitis media with effusion within 1 month before this examination.

High-resolution gas volume change measurements bring new insights in pressure regulation of the middle ear

in this issue, the paper by Kania et al. ([7][1]) presents measurements and modeling results on the role of nitrogen in the gas exchange processes in the middle ear. The middle ear is a semirigid biological gas pocket that is closed most of the time. External influences, such as changing weather

Role of nitrogen in transmucosal gas exchange rate in the rat middle ear

This study investigates the role of nitrogen (N2) in transmucosal gas exchange of the middle ear (ME). We used an experimental rat model to measure gas volume variations in the ME cavity at constant pressure. We disturbed the steady-state gas composition with either air or N2 to measure resulting changes in volume at ambient pressure. Changes in gas volume over time could be characterized by three phases: a primary transient increase with time (phase I), followed by a linear decrease (phase II), and then a gradual decrease (phase III). The mean slope of phase II was -0.128 microl/min (SD 0.023) in the air group (n = 10) and -0.105 microl/min (SD 0.032) in the N2 group (n = 10), but the difference was not significant (P = 0.13), which suggests that the rate of gas loss can be attributed mainly to the same steady-state partial pressure gradient of N2 reached in this phase. Furthermore, a mathematical model was developed analyzing the transmucosal N2 exchange in phase II. The model takes gas diffusion into account, predicting that, in the absence of change in mucosal blood flow rate, gas volume in the ME should show a linear decrease with time after steady-state conditions and gas composition are established. In accordance with the experimental results, the mathematical model also suggested that transmucosal gas absorption of the rat ME during steady-state conditions is governed mainly by diffusive N2 exchange between the ME gas and its mucosal blood circulation.

Middle ear gas loss in inflammatory conditions: The role of mucosa thickness and blood flow

Several middle ear (ME) pathologies are associated with ME gas deficit. These include in particular the chronic otitis media diseases that are associated with inflammation (hence, increased ME mucosal blood flow) and/or reduced Eustachian tube (ET) function. The present study models the trans-mucosal gas exchange in normal and inflamed middle ears of rats. The model evaluates the role of the gas diffusion path in the ME mucosa using mucosa thickness as its index and the role of the mucosal blood flow rate on ME gas economy in order to compare between normal and inflamed MEs. An experimental method employing ME gas volume changes at constant pressure due to trans-mucosal gas exchange, and blood gas values from the literature, was used in anaesthetized rats to corroborate the model. Mucosa thickness was measured as an index of the gas diffusion path between the ME space and the ME circulation. ME inner surface area was estimated from its measured gas volume. Inflammation was inflicted by applying lipopolysaccharide (LPS) into one ear. The contralateral ear served as control. ME gas volume decreased significantly faster with time (p=0.02) in inflamed ears (-0.107 microL min(-1) +/- 0.034 S.D., n=10) versus control ears (-0.067 microL min(-1) +/- 0.036 S.D., n=10). Mucosa thickness was significantly thicker in inflamed ears (48.4 microm +/- 11.0 S.D.) versus controls (20.5 microm +/- 10.1 S.D.). The mathematical model, the experimental results, and the blood gas values were used to estimate the relative effective mucosal blood flow rate. The model predicts that in spite of almost doubling mucosa thickness in LPS treated ears, the increased gas loss in inflamed ears may be explained by increased mucosal blood flow rate. We suggest that the ability to estimate ME blood flow as obtained by applying the model to the measurements, is relevant to medical management of inflamed ME.

High-resolution measurements of middle ear gas volume changes in the rabbit enables estimation of its mucosal CO(2) conductance.

Transmucosal CO(2) exchange in the middle ear (ME) of the New Zealand White rabbit (Oryctolagus cuniculus) was studied using an accurate novel detecting and recording system for measuring gas volume changes at constant pressure, based on a principle that was previously used by Kania et al. (Acta Otolaryngol 124:408-410, 2004). After the ME cavity was washed with ambient air, the initial diffusion rate of CO(2) (V(.-)(i)CO(2)) from the blood perfusing the ME mucosa was calculated from gas volume change measurements. In nine cases, the (V(.-)(i)CO(2))calculated after normalization due to shifts in baseline was 314+/-112 microL x h(-1) (mean +/- SD). In two cases where normalization was not needed, (V(.-)(i)CO(2)) was 409 microL x h(-1) (276 and 543 microL x h(-1)). Normalization of (V(.-)(i)CO(2)) data was also made in five additional cases where secretion of fluids from the lining of the ear canal was observed. In these cases (V(.-)(i)CO(2)) was 245 +/- 142 microL x h(-1). No differences were found between results obtained in the three groups. Thus, an overall mean value of (V(.-)(i)CO(2)) of 305 +/- 131 microL x h(-1) (n = 16) was calculated. An effective coefficient of conductance of CO(2) (G(CO(2))) between the mucosal circulation and the ME gas cavity of the New Zealand White rabbit was estimated to be approximately 0.05 microL (h x Pa)(-1) and compared to the G(CO(2)) estimated for humans in a different study.

Technical pitfalls in middle ear gas studies: Errors introduced by the gas permeability of tubing and additional dead space

ConclusionsWe demonstrated errors introduced by the gas permeability of the tubing and additional dead space. Materials with practically no permeability, such as glass, must be used to overcome the loss or gain of gas through the walls of tubes used for studying ME gas variations. Experiments conducted at a constant volume (variable pressure) require the smallest possible tubing volume in order to obtain good sensitivity and improve the accuracy of the results.ObjectivesExperimental studies that investigate middle ear (ME) gas exchanges, using either pressure measurements or volume changes, are conducted using various tubing connections between the ME and a measuring device. The aims of this study were to highlight experimental problems due to the errors introduced by (i) the gas permeability of the tubing used and (ii) additional dead space in experiments conducted at constant volume.Material and methodsThe problem of the gas permeability of the tubing was addressed by comparing three types of tube (silicone, polyethylene, PVC) with a glass tube. Horizontally placed tubes were connected to a syringe filled with pure CO2 via a gas-tight valve. The end of each tube tested was plunged into colored water (5% Coomassie Brilliant Blue R-250). The tube was washed out with CO2 until gas bubbles were seen leaving it. The valve was then closed and the movement of water in the tube was observed. The same experiments were repeated for pure O2. The problem of the error introduced by the additional dead space volume was addressed at a theoretical level using the well-known gas laws. Two conditions were studied: condition A, in which the experiment was conducted at constant pressure and the volume was measured; and condition B, in which the experiment was conducted at constant volume and the pressure was measured. The main outcome measure of each condition was the calculated variation in the final number of moles of gas involved.ResultsNo water movement was observed in glass tubes. In contrast, plastic tubes exhibited significant gas permeability effects for both CO2 and O2. The colored solution advanced at a faster rate with CO2 than O2 but differently for each type of tubing. For condition A, gas transfer was independent of the volume of the external tubing and was accurately measured by the displacement of the droplet in the lumen. In contrast, for condition B, the pressure variations were influenced by the volume of the tubing.

Gas flow into and within the middle ear.

Both a normal and a narrowed eustachian tube (ET) are capable of equilibrating pressures between the middle ear (ME) and the atmosphere almost instantaneously. The objective of this study was to assess experimentally the effect of narrowing a simulated ET isthmus on air passage into the ME. A Perspex ME model (0.5 mL) was constructed in which a 1.5-mm long ET of 0.07- to 1.0-mm diameter and a "mastoid" of 0- to 10-mL volume were changeable. The ET could be opened and closed with a valve. A -5 mm H2O pressure difference between the system and the atmosphere was created by withdrawing gas from the system. The time required to equalize these pressures after opening the valve to the atmosphere were measured with a pressure transducer. A pressure difference of -5 mm H2O was created in the system when 1.3 to 6.5 microL of ME gas was removed. On ET valve opening, the pressure was equalized within 0.1 and 0.15 to 0.3 seconds for ET diameters of 1.00 and 0.07 mm, respectively, depending also on the "mastoid" volume. Similar results were obtained when the pressure was measured through the "tympanic isthmus" and "aditus ad antrum." Our model shows that under ordinary physiological conditions, the amount of gas that can pass through the ET during swallowing time (0.4 sec) is potentially higher than required to equalize a negative pressure. This is also the case when the ET is very narrow and open for a very short time. It is unlikely that any narrowing of the tube will, by itself, hamper gas transfer into or within the ME, as long as the ET is not totally obstructed.

Studying middle ear gas variations needs nonporous materials

Problem: Experimental studies that investigate middle ear (ME) gas exchange, by using either pressure or volume measurements, are conducted using various tubing connections between the ME and a measuring device. The purpose of the present study was to highlight experimental problems encountered when measuring small gas volume or pressure changes, or more specifically, error introduced by the gas permeability of the connecting tube. Methods: Several types of plastic tubes were tested for their gas permeability. Various plastic tubes including pediatric folley probe (Porgès S. A., France) were connected to a syringe filled with pure or 50% CO 2 through a gas-tight valve placed horizontally. The end of the plastic tube was plunged into colored water (Coomassie Brilliant Blue R-250 5%; Sigma®). The tube was purged with the gas until gas bubbles were seen leaving it, the valve was then closed, and the movement of water in the tube was followed with time. The same procedure was repeated with glass tubes. Results: No water movement was observed with glass tubes. In contrast, the colored solution advanced in the plastic tube at a rate twice as fast with 100% CO 2 than with 50% CO 2, a rate that changed according to the different plastic species. In contrast to the gas-tightness of glass tubes, plastic tubes exhibited significant gas permeability. The same experiments were repeated for O 2 with similar results. Conclusion: This study demonstrates the significant influence of the tubing used for connection. Significance: When studying ME gas variations, materials with no permeability such as glass must be used to overcome the loss or gain of gas through the tubing used. Support: No support

A mathematical model of trans-mucosal gas exchanges

Problem: Gas exchanges in the middle ear (ME) are thought to be the cornerstone in the development of atelectasis and cholesteatoma. The purpose of the current study was to validate a mathematical model of trans-mucosal gas exchanges based on ME volume variations. Methods: According to Fick’s law of diffusion, the rate of diffusion of a gas is proportional to the partial pressure difference of the gas between the 2 sides of the diffusion barrier, the solubility and diffusion coefficient of the gas in the diffusion barrier, and the surface area available for diffusion − and inversely proportional to the thickness L of the diffusion barrier. In a first step, we designed an experimental rat model for exclusive study of trans-mucosal gas exchanges. In a second step, a mathematical model of trans-mucosal gas exchanges for N2 was developed. In order to validate both models, 2 assumptions were tested. First, linearity of gas volume variations should be verified, ie, being constant. Second, the effective thickness of the diffusion barrier that can be deduced from Fick’s law should correspond to the actual thickness. Results: First, normal rat ME gas volume variations exhibited a linear decrease ( = -0.130μL min-1 ± 0.03) which lasted 31.1min ± 8.5 SD. Second, the effective thickness Le of the diffusion barrier was 71.4 μm, which is in accordance with that of histologic studies reported in the literature for rats where the thickness of mucosa varies between 9 and 150 μm. Conclusion: Since both assumptions were checked for validity, it is now possible to estimate the variation of effective blood flow surrounding the ME in experimental conditions using this mathematical model and knowing the thickness. Significance: Further studies in inflamed ears may bring informative data on the ME circulation and the role of the ME mucosa in gas exchanges in pathologic conditions. Support: No support

Middle ear gas volume variations: Transmucosal exchanges in inflamed ears

Problem: Gas exchanges in the middle ear (ME) are thought to be the cornerstone in the development of atelectasis and cholesteatoma. The purpose of the current study was to evaluate the transmucosal gas exchanges in the ME in inflamed conditions. Methods: We have designed an experimental model in order to study transmucosal gas exchanges. Volume variations measurements of the gas content of the ME are recorded at constant pressure and temperature in rats under general anesthesia. Twenty-five rats were divided into 2 groups. In group 1 (n = 16), inflammation was induced by transtympanic injection of 25 μL of lipopolysaccharide (LPS) serotype 026:B6 from E coli (1 mg/ml) with vehicle (150 mM NaCl, 10 mM phosphate buffer, with similar pH and osmolarity). Group 2 (n = 9) served as control. Animals were studied for 3 days after the injection. Bullae were then harvested, fixed in 10% phosphate-buffered formalin, decalcified with 10% EDTA buffer, embedded in paraffin wax, cut, and stained with hematoxin-eosin. The mucosa thicknesses between the groups were compared using a 2-sided t test. Statistical significance was set at P = 0.05. Results: In group 1, the kinetics of the rat ME gas volume variations exhibited a linear decrease (-0.098 μL min-1 ± 0.031) which was significantly higher ( P = 0.01) than that observed in group 2 (-0.061 μL min-1 ± 0.033). The mucosa thickness was significantly higher in inflamed ears (group 1, Le = 48.4 μm ± 11) than in noninflamed ears (group 2, Le = 20.5 μm ± 10.1). Conclusion: Significant increases of transmucosal gas exchanges were associated with thicker mucosa in inflamed ears. Significance: Further studies using mathematical modeling will help evaluate the respective role of the ME circulation and the ME mucosa in this process. Support: None reported.