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PubMed1998

Does hearing aid benefit increase over time?

In a recent tutorial for the journal, Palmer et al. [J. Acoust. Soc. Am. 103, 1705-1721 (1998)] reviewed the literature on the potential for increases in hearing aid benefit over time (acclimatization). Their review might leave some readers with the impression that acclimatization has implications for the fitting and selection of hearing aids today. We (Turner and Bentler), along with two other researchers in the field (Humes and Cox), conducted a similar review of the literature a few years earlier [Turner et al., Ear and Hearing 17, 14S-28S (1996)] and found little evidence of a robust effect. The bulk of the existing evidence, including the most recent studies on this topic, support earlier conclusions, i.e., that there is no evidence for the existence of a strong acclimatization effect in current hearing aid use.

Hearing Aids↗
PubMed1986

Effect of salinity gradients and heterotrophic microbial activity on biodegradation of nitrilotriacetic acid in laboratory simulations of the estuarine environment.

The biodegradation of nitrilotriacetic acid (NTA), a synthetic replacement detergent builder, in the estuarine environment was examined by using a laboratory estuarine simulation. Two interdependent microcosms were used; each of five vessels was equilibrated with a saline gradient between 1.30 and 17.17%, with the final vessel subsequently being increased to a maximum salinity of 31.6%. Each microcosm was seeded simultaneously with heterotrophic bacteria from both fresh and saline sources. Viable counts demonstrated the ability of each microcosm to sustain a mixed heterotrophic bacterial community throughout the range of salinities for 183 days after a stabilization period. Isolation studies demonstrated that both systems contained four bacterial species, representatives of the genera Vibrio and Flavobacterium and members of the coryneform group and the family Enterobacteriaceae. Total bacterial numbers and species diversity decreased with increased salinity. NTA was administered at low and high concentrations, one concentration to each microcosm, initially with the least amount of saline. Removal of both concentrations of NTA occurred and was attributed to biodegradation after a period of bacterial acclimatization. Subsequent dosing of NTA to vessels of higher salinity demonstrated that biodegradation was incomplete at observed mean salinities of greater than 9.18% at low influent NTA concentrations and greater than 5.08% at high influent NTA concentrations. Therefore, acclimatization was dose dependent. It was concluded that NTA acclimatization at the higher salinities ceased because of salinity stress-induced failure of NTA catabolism and not the disappearance of a particular bacterial species.

Acetates↗
PubMed1993

Heterogeneous Distribution of Microbial Activity in Methanogenic Aggregates: pH and Glucose Microprofiles.

Methanogenic aggregates, harvested from an upflow anaerobic sludge blanket reactor treating potato starch wastewater, were acclimatized to either glucose or a mixture of sugars and organic nitrogen compounds (i.e., diluted molasses). Both types of granules exhibited internal pH and substrate concentration gradients in mineral medium (pH 7.0, 30 degrees C) as was measured with microelectrodes. Glucose-acclimatized granules suspended in a mineral medium lacking glucose exhibited a distinct internal pH decrease of about 1 U within the granule, suggesting strong metabolism by the acidogenic bacteria. Molasses-acclimatized and aged granules suspended in mineral medium did not exhibit such a pH decrease, suggesting the importance of the metabolic state of these acidogens. The pH gradient did not occur in deactivated granules and was not observable in strongly buffered media (mineral medium containing 33 mM phosphate or reactor liquid). When glucose (0.5 to 5.0 mM) was added to the mineral medium, granules exhibited a convex pH profile. Glucose consumption was located exclusively in the outer 200 to 300 mum of the aggregates (mean diameter = 1.5 mm). The addition of 20 mM 2-bromoethanesulfonic acid to the mineral medium indicated that the higher pH levels in the centre of the granule appeared to be related to the activity of methanogens. It is suggested that acidogenic activity occurs predominantly in the outer 200 to 300 mum of the aggregate and methanogenic activity occurs predominantly in the center of the investigated granules.

Journal Article↗
PubMed2001

Relationship of osmotic inhibition in thermoregulatory responses and sweat sodium concentration in humans.

Heat acclimatization improves thermoregulatory responses to heat stress and decreases sweat sodium concentration ([Na(+)](sweat)). The reduced [Na(+)](sweat) results in a larger increase in plasma osmolality (P(osmol)) at a given amount of sweat output. The increase in P(osmol) inhibits thermoregulatory responses to increased body core temperature. Therefore, we hypothesized that the inhibitory effect of plasma hyperosmolality on the thermoregulatory responses to heat stress should be attenuated with the reduction of [Na(+)](sweat) due to heat acclimatization. Eleven subjects (9 male and 2 female) were passively heated by immersing their lower legs into water at 42 degrees C (room temperature 28 degrees C and relative humidity 30%) for 50 min following isotonic or hypertonic saline infusion. We determined the increase in the esophageal temperature (T(es)) required to elicit sweating and cutaneous vasodilation (CVD) (DeltaT(es) thresholds for sweating and CVD, respectively) in each condition and calculated the elevation of the T(es) thresholds per unit increase in P(osmol) as the osmotic inhibition of sweating and CVD. The osmotic shift in the DeltaT(es) thresholds for both sweating and CVD correlated linearly with [Na(+)](sweat) (r = 0.858 and r = 0.628, respectively). Thus subjects with a lower [Na(+)](sweat) showed a smaller osmotic elevation of the DeltaT(es) thresholds for sweating and CVD. These results suggest the possibility that heat acclimatization attenuates osmotic inhibition of thermoregulatory responses as well as reducing [Na(+)](sweat).

Adult↗
PubMed1984

Relationship of hypoxic ventilatory response to exercise performance on Mount Everest.

At very high altitude, exercise performance in the human sojourner may depend on a sufficient hypoxic ventilatory response (HVR). To study the relationship of HVR to exercise performance at high altitude, we studied HVR at sea level and 5,400 m and exercise ventilation at sea level, 5,400 m, and 6,300 m in nine members of the American Medical Research Expedition to Everest. The relationship of HVR between individuals was maintained when HVR was repeated after acclimatization to 5,400 m (P less than 0.05). There was a significant correlation in all subjects between HVR and ventilatory equivalent during exercise at sea level (r = 0.704, P less than 0.05). Subjects were then grouped into high (H) and low (L) HVR responders (ventilation increase to end-tidal PO2 of 40 Torr = 21.2 +/- 5.4 and 5.6 +/- 0.9 1 X min-1, respectively. At low and moderate levels of exercise, ventilation at sea level and after acclimatization to 6,300 m was higher in the high HVR group. At 6,300 m blood O2 saturation (Sao2%) decreased from rest to maximum exercise: H = 8.3 +/- 1.8%, L = 20.0 +/- 2.5% (P less than 0.01). HVR correlated inversely in all subjects with the decrease in Sao2 from rest to maximum exercise (P less than 0.05). Climbers with the highest HVR values reached and slept at higher altitudes. We conclude that the relative value of HVR in our group of climbers was not significantly altered after acclimatization; HVR predicts exercise ventilation at sea level and high altitude; the drop in Sao2% that occurs with exercise is inversely related to HVR; and sojourners with high HVR may perform better at extreme altitude.

Altitude↗
PubMed1988

Carotid chemoreceptor activity during acute and sustained hypoxia in goats.

The role of carotid body chemoreceptors in ventilatory acclimatization to hypoxia, i.e., the progressive, time-dependent increase in ventilation during the first several hours or days of hypoxic exposure, is not well understood. The purpose of this investigation was to characterize the effects of acute and prolonged (up to 4 h) hypoxia on carotid body chemoreceptor discharge frequency in anesthetized goats. The goat was chosen for study because of its well-documented and rapid acclimatization to hypoxia. The response of the goat carotid body to acute progressive isocapnic hypoxia was similar to other species, i.e., a hyperbolic increase in discharge as arterial PO2 (PaO2) decreased. The response of 35 single chemoreceptor fibers to an isocapnic [arterial PCO2 (PaCO2) 38-40 Torr)] decrease in PaO2 of from 100 +/- 1.7 to 40.7 +/- 0.5 (SE) Torr was an increase in mean discharge frequency from 1.7 +/- 0.2 to 5.8 +/- 0.4 impulses. During sustained isocapnic steady-state hypoxia (PaO2 39.8 +/- 0.5 Torr, PaCO2, 38.4 +/- 0.4 Torr) chemoreceptor afferent discharge frequency remained constant for the first hour of hypoxic exposure. Thereafter, single-fiber chemoreceptor afferents exhibited a progressive, time-related increase in discharge (1.3 +/- 0.2 impulses.s-1.h-1, P less than 0.01) during sustained hypoxia of up to 4-h duration. These data suggest that increased carotid chemoreceptor activity contributes to ventilatory acclimatization to hypoxia.

Adaptation, Physiological↗
PubMed1994

Comparison of ventilatory responses to sustained reduction in arterial oxygen tension vs. content in awake ponies.

To gain insight into central and peripheral contributions to changes in breathing during hypoxia, we compared effects on breathing of reducing inspired PO2 (hypoxic hypoxia) with reducing arterial O2 content (CaO2) through elevation of carboxy-hemoglobin (COHb) (CO hypoxia). Twelve awake ponies were studied during 1 h of breathing room air followed by 6 h when COHb was increased to 25% and CaO2 was decreased by 17%. When COHb was increased, arterial PCO2 (PaCO2) increased gradually to 1.3 Torr above (P < 0.05) control level between 30 and 45 min of CO exposure. Pulmonary ventilation (VE) decreased (P = 0.09) approximately 1 liter the first 30 min of CO exposure. After approximately 45 min, PaCO2 began to decrease, steadily reaching 1.5 Torr below (P < 0.05) control level by 4.5 h of CO hypoxia. VE did not change significantly after 30 min of elevated COHb. Eight ponies were also studied during 5 h of hypoxic hypoxia (arterial PO2 approximately 40 Torr). PaCO2 decreased 5 Torr (P < 0.05) within 5 min of hypoxia and decreased another 4 Torr (P < 0.05) between 30 min and 5 h of hypoxia consistent with hypoxic ventilatory acclimatization. VE increased (P < 0.05) within 3 min of hypoxic hypoxia but then decreased (P < 0.05; VE roll off) toward control and did not increase significantly with acclimatization. Because CO and hypoxic hypoxia both decrease brain oxygenation but only hypoxic hypoxia increases carotid chemoreceptor activity, we conclude that initial hypoventilation with CO hypoxia and VE roll off with hypoxic hypoxia are consistent with hypoxic ventilatory depression within the brain. In addition, hyperventilation with prolonged CO hypoxia is consistent with a central nervous system mechanism contributing to this phase of hypoxic ventilatory acclimatization in ponies.

Animals↗
PubMed2001

Living and training in moderate hypoxia does not improve VO2 max more than living and training in normoxia.

The objective of these experiments was to determine whether living and training in moderate hypoxia (MHx) confers an advantage on maximal normoxic exercise capacity compared with living and training in normoxia. Rats were acclimatized to and trained in MHx [inspired PO2 (PI(O2)) = 110 Torr] for 10 wk (HTH). Rats living in normoxia trained under normoxic conditions (NTN) at the same absolute work rate: 30 m/min on a 10 degrees incline, 1 h/day, 5 days/wk. At the end of training, rats exercised maximally in normoxia. Training increased maximal O2 consumption (VO2 max) in NTN and HTH above normoxic (NS) and hypoxic (HS) sedentary controls. However, VO2 max and O2 transport variables were not significantly different between NTN and HTH: VO2 max 86.6 +/- 1.5 vs. 86.8 +/- 1.1 ml x min(-1) x kg(-1); maximal cardiac output 456 +/- 7 vs. 443 +/- 12 ml x min(-1) x kg(-1); tissue blood O2 delivery (cardiac output x arterial O2 content) 95 +/- 2 vs. 96 +/- 2 ml x min(-1) x kg(-1); and O2 extraction ratio (arteriovenous O2 content difference/arterial O2 content) 0.91 +/- 0.01 vs. 0.90 +/- 0.01. Mean pulmonary arterial pressure (Ppa, mmHg) was significantly higher in HS vs. NS (P < 0.05) at rest (24.5 +/- 0.8 vs. 18.1 +/- 0.8) and during maximal exercise (32.0 +/- 0.9 vs. 23.8 +/- 0.6). Training in MHx significantly attenuated the degree of pulmonary hypertension, with Ppa being significantly lower at rest (19.3 +/- 0.8) and during maximal exercise (29.2 +/- 0.5) in HTH vs. HS. These data indicate that, despite maintaining equal absolute training intensity levels, acclimatization to and training in MHx does not confer significant advantages over normoxic training. On the other hand, the pulmonary hypertension associated with acclimatization to hypoxia is reduced with hypoxic exercise training.

Altitude↗
PubMed1991

Effect of cold exposure on the hypothalamic release of thyrotropin-releasing hormone and catecholamines.

The effects of cold exposure on the release of thyrotropin-releasing hormone (TRH) and catecholamines as estimated by push-pull perfusion of the mediobasal hypothalamus were studied. Before cold exposure, the male rats had been kept at room temperature or at 30 degrees C for 3 weeks. Transfer to 4 degrees C increased plasma levels of thyroid-stimulating hormone (TSH), but this cold-induced TSH response was more pronounced in animals which had been acclimatized to 30 degrees C. Exposure to 4 degrees C also increased plasma thyroid hormone levels, but had no effect on plasma prolactin. The hypothalamic content of TRH and dopamine remained similar after transfer to 4 degrees C, but after 6 h of cold, the content of noradrenaline and adrenaline had increased 1.6-fold and 3-fold, respectively. In vivo hypothalamic release of TRH, adrenaline and dopamine remained similar during a 2-hour period in control rats kept at room temperature or 30 degrees C. The hypothalamic release of TRH, dopamine and adrenaline did not change in rats transferred from room temperature to 4 degrees C. The amount of dopamine and adrenaline in push-pull perfusate also remained similar in rats acclimatized to 30 degrees C after transfer to low temperatures. However, in these rats kept at 30 degrees C for 3 weeks, exposure to 4 degrees C increased TRH release in perfusate from the mediobasal hypothalamus in the first 15 min of cold exposure (2-fold increase). Thus, exposure to cold stimulates the hypothalamo-pituitary-thyroid axis and increases the hypothalamic release of TRH in rats which had been acclimatized to 30 degrees C.

Animals↗
PubMed2006

Changes in ventilatory threshold at high altitude: effect of antioxidants.

PURPOSE: To investigate the effects of prolonged hypoxia and antioxidant supplementation on ventilatory threshold (VT) during high-altitude (HA) exposure (4300 m). METHODS: Sixteen physically fit males (25 +/- 5 yr; 77.8 +/- 8.5 kg) performed an incremental test to maximal exertion on a cycle ergometer at sea level (SL). Subjects were then matched on VO2peak, ventilatory chemosensitivity, and body mass and assigned to either a placebo (PL) or antioxidant (AO) supplement group in a randomized, double-blind manner. PL or AO (12 mg of beta-carotene, 180 mg of alpha-tocopherol acetate, 500 mg of ascorbic acid, 100 mug of selenium, and 30 mg of zinc daily) were taken 21 d prior to and for 14 d at HA. During HA, subjects participated in an exercise program designed to achieve an energy deficit of approximately 1400 kcal.d(-1). VT was reassessed on the second and ninth days at HA (HA2, HA9). RESULTS: Peak power output (Wpeak) and VO2peak decreased (28%) in both groups upon acute altitude exposure (HA2) and were unchanged with acclimatization and exercise (HA9). Power output at VT (WVT) decreased from SL to HA2 by 41% in PL, but only 32% in AO (P < 0.05). WVT increased in PL only during acclimatization (P < 0.05) and matched AO at HA9. Similar results were found when VT was expressed in terms of % Wpeak and % VO2peak. CONCLUSIONS: VT decreases upon acute HA exposure but improves with acclimatization. Prior AO supplementation improves VT upon acute, but not chronic altitude exposure.

Adult↗
PubMed2006

Prevention of acute mountain sickness by acetazolamide in Nepali porters: a double-blind controlled trial.

OBJECTIVE: This study aimed to determine the efficacy, tolerability, and practicality of acetazolamide for the prevention of acute mountain sickness (AMS) in Nepali trekking porters early in the trekking season. METHODS: This study was a randomized, double-blind controlled trial with 400 male Nepali porters in the Mount Everest region of Nepal, trekking from Namche Bazaar (3440 m) to Lobuche (4930 m), the study endpoint. Participants were randomized to receive 250 mg acetazolamide daily or placebo, and AMS symptom scores (Lake Louise) were compared in highlanders vs lowlanders. RESULTS: Only 109 (27.2%) of the 400 porters completed the trial (28 highlanders, 81 lowlanders). The rest either dropped out (275/400 porters, 68.8%) or were excluded (16/400 porters, 4%). Acute mountain sickness occurred in 13 (11.9%) of 109 porters; all were lowlanders; 7 were taking acetazolamide, 6 taking placebo. Birthplace, acclimatization in the week before the trial, ascent rate, and rest days were the most important variables affecting the incidence of AMS. No highlanders, but 13 (16.1%) of 81 lowlanders had AMS (P = .016). Acclimatization in the pretrial week reduced AMS incidence (P = .013), as did a slower ascent rate (P = .0126), but rest days were the most potent prophylactic variable (P = .0001). Side effects were more frequent in porters taking acetazolamide than in the placebo group (P = .0001), but there were no serious side effects. CONCLUSIONS: Acetazolamide was tolerable, but impractical for the routine prevention of AMS in Nepali porters. A good trekking schedule and adequate acclimatization remain the most effective preventive measures. This study identified lowland porters as a high-risk group for developing AMS.

Acetazolamide↗
PubMed2001

Evaluation of hoof wall surface temperature as an index of digital vascular perfusion during the prodromal and acute phases of carbohydrate-induced laminitis in horses.

OBJECTIVE: To evaluate the use of hoof wall surface temperature (HWST) as an indirect indicator of digital perfusion and to describe HWST patterns during the prodromal and acute phases of carbohydrate-induced laminitis in horses. ANIMALS: 30 adult horses without foot abnormalities. PROCEDURES: Three experiments were performed. In the first, HWST was measured in 2 groups of horses acclimatized to hot (n = 6), or cold (6) environments and exposed to cold (15 C) ambient temperature. In the second experiment, HWST were measured in both forefeet of 6 horses before and after application of a tourniquet to 1 forefoot to induce vascular occlusion. In the third experiment, HWST were recorded in 12 horses before and during the prodromal and acute phases of carbohydrate-induced laminitis. RESULTS: Mean HWST of hot-acclimatized cold-challenged horses was significantly less than that of cold-acclimatized cold-challenged horses at all times. Transient episodes of high HWST were observed during prolonged cold-induced vasoconstriction. Hoof wall surface temperature significantly decreased during arterial occlusion and increased during reperfusion. Digital hypothermia was observed during the prodromal phase of carbohydrate-induced laminitis. CONCLUSIONS AND CLINICAL RELEVANCE: Determination of HWST is a valid technique to evaluate digital perfusion under appropriate controlled conditions in horses. Digital hypothermia detected during the prodromal phase of laminitis is consistent with decreased digital vascular perfusion or metabolic activity. If administered to horses during the prodromal phase, agents that enhance digital perfusion may prevent development of laminitis.

Animals↗
PubMed1994

Diurnal variations in total forearm and skin microcirculatory blood flow in man.

The aim of the present study was to determine diurnal variations in total forearm and skin microcirculatory blood flow in healthy man. At six time points between 08.00 and 18.00 hours was measured: blood pressure, forearm blood flow (FBF; strain gauge plethysmography), skin thermoregulatory blood flow (LDF; laser-Doppler fluxmetry), and skin nutritive blood flow (CBV: Capillary Blood Cell Velocity; intravital capillary microscopy) in 15 healthy, fasting, and resting men. FBF increased gradually from 2.8 in the morning to 4.3 ml 100 ml min-1 in the afternoon (p < 0.001). In contrast, LDF decreased, predominantly in the morning, from 18.3 at 09.00 hours to 13.1 at 12.00 hours and to 12.1 perfusion units at 17.30 hours (p < 0.001). However, performing the same protocol starting in the afternoon resulted in a similar initial decrease in LDF, suggesting an acclimatization phenomenon. Although not statistically significant, the decrease in CBV showed a similar pattern as compared to LDF. Blood pressure did not change. In conclusion, forearm blood flow increased during the day, probably due to diurnal variation in muscle flow. The initial decrease we observed in skin thermoregulatory blood flow is probably not related to diurnal variation but due to long-term acclimatization to the experimental conditions. These data suggest different regulatory mechanisms for the different vascular beds studied. Measurements of forearm blood flow should preferably be performed at the same time of day, and skin microcirculatory haemodynamic measurements should be performed after a standard period of acclimatization.

Adult↗
PubMedDate not supplied

[Estimation of gasometric values at different altitudes above sea level in Mexico].

We calculated reference values for arterial blood gases at different altitudes in Mexico assuming that sea level PaCO2 is 40 Torr, and in Mexico City (2.24 km. above the sea level) is 31.13 Torr, average of reported reference values. With the previous two points, it is possible to calculate a linear regression: PaCO2 = 40-3.96(altitude in km.). The equation is very similar to that calculated from reports in alveolar gas in North-Americans (Fitzgerald < 5 km): PACO2 = 39.3-3.11(altitude in km), and from subjects acclimatized to acute altitude exposure (< 5 km): PACO2 = 38.3-2.5 (altitude in km). It is also similar to a alinear equation that can be calculated assuming that hyperventilation in permanent habitants of moderate altitudes is inversely proportional to inspired molar concentration of O2: PaCO2 = PIO2/3.74. On the other hand, the equation is very different than that obtained from Andean natives (Hurtado): PaCO2 = 40.4-1.35(altitude in km). The proposed linear equation for Mexico gives very similar results (< 2 Torr difference) than a complex curvilinear equation by Morris et al. appropriate only up to 2.3 km. Evidence from acute exposure to altitude (acclimatized) and in North-Americans (alveolar gas) supports a reasonably accurate linear relationship up to 4 km. and also that the increase in ventilation in response to moderate altitudes in adult permanent residents is inversely proportional to molar concentration of O2. PAO2 was calculated with alveolar gas equation and resting the P(A-a)O2 we obtained PaO2. In conclusion, according to reference values in Mexico City, PaCO2 decreases about 4 Torr per km of altitude above the sea level. The decrease is similar to that reported in North-Americans and in acute exposure to altitude (acclimatized), but much less than that reported in native Peruvians. Ventilation is inversely proportional to the molar concentration of O2 at least up to an altitude where SaO2 is at or above 90%.

Altitude↗
PubMed2003

Health outcome following multi-day occupational air diving.

Acclimatization to decompression stress has been reported in caisson workers and helium-oxygen divers; however the alternative notion that the risk of decompression sickness increases with successive days of diving is widespread. We examined 201 multi-day series of 2 to 29 diving days identified retrospectively in a database of occupational air dives for evidence of acclimatization or sensitization. Decompression related health status was measured using a self-administered diver health survey; resulting scores were analyzed by linear modelling. Daily diving consisted of 1-3 dives each to mean maximum depth of 17.2 (SD 3.9) meters seawater for a mean duration of 23 (SD 17) min. Daily diver health scores increased with calculated daily risk of decompression sickness but were not influenced by the order of dives in multi-day series. Poor health outcome indicated by treated decompression sickness and diver health scores > 8 occurred early in multi-day series. There was no evidence of sensitization to decompression stress whereas the timing of poor health outcomes suggests an element of acclimatization.

Analysis of Variance↗
PubMed2004

[Chronic intermittent hypoxia decreases acute hypoxic inhibition of voltage-gated potassium channel in rat pulmonary arterial smooth muscle cells].

For determination the ionic mechanisms of the hypoxic acclimatization at the level of channels, male Spradue-Dawley rats were divided into two groups: control normoxic group and chronic intermittent hypoxic group [O2 concentration: (10 +/-0.5)%, hypoxia 8 h a day]. Using whole cell patch-clamp technique, voltage-gated potassium channel currents (IK(V)) were recorded in freshly isolated pulmonary arterial smooth muscle cells (PASMCs) of rat with acute isolated method. The effect of acute hypoxia on IK(V) of PASMCs from chronic intermittent hypoxia group was investigated to offer some basic data for clarifying the ionic mechanisms of the hypoxic acclimatization. The results showed: (1) In control normoxic group, after acute hypoxia free-Ca(2+) solution, the resting membrane potential (Em) of PASMCs was depolarized significantly from -47.2+/-2.6 mV to -26.7+/-1.2 mV, and the IK(V) of PASMCs was decreased significantly from 153.4+/-9.5 pA/pF to 70.1+/-0.6 pA/pF, the peak current percent inhibition was up to (57.6+/-3.3)% at +60 mV, and current-voltage relationship curve shifted to the right. (2) In chronic intermittent hypoxic group, the IK(V) of PASMCs was decreased significantly by exposure to intermittent hypoxia in a time-dependent manner, appeared to start on day 10 and continued to day 30 (the longest time tested) of hypoxia, and current-voltage relationship curve shifted to the right in a time-dependent manner. (3) Compared with the control normoxic group, the percent IK(V) inhibition by acute hypoxia was significantly attenuated in the chronic intermittent hypoxia group and this inhibition effect declined with time exposure to hypoxia. The results suggest that K(V) inhibition was significantly attenuated by chronic intermittent hypoxia, and this effect may be a critical mechanism of the body hypoxic acclimatization.

Animals↗
PubMed1996

Acinetobacter radioresistens metabolizing aromatic compounds. 1. Optimization of the operative conditions for phenol degradation.

A strain of Acinetobacter radioresistens was able to utilize phenol as the only carbon and energy source, after an acclimatization period of 3 days in which increasing phenol concentrations from 50 to 200 mg/l were supplied. At 30 degrees C, the complete phenol utilization in batch degradation tests occurred in 2.5-3 h at pH 7 and 8, but it increased strongly at pH 6 (over 40 h). No microbial growth was detected at 40 degrees C, while at 20 degrees C (pH 7-8) the time necessary for complete phenol degradation was about twofold longer than that at 30 degrees C (pH 7-8) revealing a good capability of the strain as a seed-micro-organism for enhancing phenol degradation. The bacterial growth in acclimatized cultures, evaluated with the viable cell count, always displayed a trend consistent with the use of phenol as a substrate with an eventual lag phase and then an exponential phase, while in the non-acclimatized cultures an initial stage of cellular death was observed.

Acinetobacter↗
PubMed1998

Word recognition score changes after stapedectomy for far advanced otosclerosis.

OBJECTIVE: This study aimed to examine word recognition score (WRS) changes after stapedectomy for far-advanced otosclerosis (FAO). The WRS changes were examined to determine whether they were consistent with acclimatization or recovery from auditory deprivation changes that have been seen after the restoration of sound by amplification. STUDY DESIGN: Retrospective. SETTING: Private otology practice. PATIENTS: A total of 24 patients were selected by including all the case in which a stapedectomy was performed within the past 10 years to improve the hearing of a severe or profoundly hearing-impaired patient with otosclerosis. INTERVENTION: Diagnostic. MAIN OUTCOME MEASURE: Changes in WRSs. RESULTS: One month after surgery, the mean WRS had improved 16.5%. The WRSs continued to improve an additional 12% or more for 17 (71%) of 24 patients within 2 years after their initial postoperative hearing test. The mean WRS improvement within 2 years of the initial postoperative test was 16.2%. CONCLUSIONS: Initial WRS changes were attributed to hearing thresholds no longer being at or beyond audiometric limits. Additional WRS changes were consistent with reports of acclimatization or recovery from auditory deprivation that have been seen after hearing aid use. The authors believe these additional WRS changes illustrate that at least some improvement in WRSs from acclimatization or auditory recovery may be fairly common after the restoration of sound. Finally, the authors believe the overall WRS improvement (32.7%) should be taken into account when considering stapedectomy for patients with FAO.

Audiometry, Pure-Tone↗