Human auditory brain stem response during induced hyperthermia

A continuous monitoring of auditory brain stem response (ABR) and esophageal (Tes) and rectal temperatures (Tre) were recorded in male undergraduate subjects to investigate a relationship between the interpeak latencies (IPLs) and core temperature. The average change of Tes (36.8-39.5 degrees C) was achieved by immersing the subjects in a temperature-controlled water bath (30-42 degrees C). The IPLs became shorter with the rise in body temperature and were correlated with both Tes and Tre. The average slopes for IPL(I-III) and IPL(I-V) were significantly higher than those for IPL(III-V). The present study of humans indicated that changes of IPL(I-III) and IPL(I-V) were 0.11 and 0.16 ms, respectively, per 1 degree C change in core temperature during induced hyperthermia.     

No evidence for brain stem cooling during face fanning in humans.

The interpeak latencies (IPLs) of the acoustically evoked brain stem potentials depend on brain stem temperature. This was used to see whether face fanning during hyperthermia lowers brain stem temperature. In 15 subjects, three thermally stable conditions were maintained by a water bath. In each condition the IPLs were determined in 10 separate trials. In condition A esophageal temperature (Tes) was 36.9 +/- 0.3 degrees C and increased to 38.6 +/- 0.2 degrees C in condition B. In conditions A and B the head was enclosed in a ventilated hood (air temperature 38 degrees C, relative humidity 100%) to suppress any direct heat loss from the head. From conditions A to B the IPL at peaks I-V decreased by 0.146 ms/degrees C change in Tes, reflecting a change in brain stem temperature. In condition C the hood was removed and the face was fanned by a cold air-stream (8-15 degrees C, 4-10 m/s) to maximize direct heat loss from the head. Skin temperature at the sweating forehead decreased from 38 to 23 degrees C, whereas Tes in condition C was maintained at the same level as in condition B (38.5 +/- 0.2 degrees C). The IPL at peaks I-V showed no difference between conditions B and C. It is concluded that face fanning in hyperthermic subjects does not dissociate brain stem temperature from Tes.     

Auditory brain-stem responses in the fragile X syndrome.

Auditory brain-stem responses (ABRs) were recorded from a group of 12 mentally retarded males with the fragile X (fra[X]). The responses were analyzed in terms of ABR thresholds, absolute latencies, and interpeak latencies. One patient had increased ABR thresholds, indicating hearing impairment. Five fra(X) subjects had prolonged I-V interpeak latencies. Comparisons between the fra(X) group (excluding one possible hard-of-hearing subject) and a control group of age-matched males with normal intelligence showed that the fra(X) group's interpeak latencies were significantly prolonged for the III-V and I-V but not for the I-III. This pattern of prolongation of interpeak latencies suggests that central, as opposed to peripheral, nervous-system dysfunction predominates in many patients having this syndrome. In addition, frequently observed prolongation of the transmission time may indicate that brain-stem white-matter functioning is also apt to be involved in this syndrome.     

Effect of cold air inhalation on core temperature in exercising subjects under heat stress

Whether increasing respiratory heat loss (RHL) during exercise under heat stress can contain elevation of rectal temperature (Tre) was examined. Eight men cycled twice at 45-50% their maximum work rate until exhaustion at ambient temperature and relative humidity of 38 degrees C and 90-95%, respectively. They inspired either cold (3.6 degrees C) or ambient air in random sequence. When subjects breathed cold air during 23 min of exercise, a ninefold increase in RHL was observed vs. similar work during hot air inhalation (32.81 vs. 3.46 W). Respiratory frequency (f) and rate of rise in Tre decreased significantly (P less than or equal to 0.004 and P less than or equal to 0.002, respectively). The rise in skin temperature in each inhalant gas condition was accompanied by a parallel almost equal increase in core temperature above basal (delta Tre) for equivalent gains in skin temperature. The increase in tidal volume and decreased f in the cold condition allowed more effective physical conditioning of cold inspirate gas in the upper airways and aided RHL. Cold air inhalation also produced a significant (P less than or equal to 0.05) decrease in heart rate vs. hot air inhalation in the final stages of exercise. Insignificant changes in O2 consumption and total body fluid loss were found. These data show that cold air inhalation during exercise diminishes elevation of Tre and suggest that both the intensity and duration of work can thus be extended. The importance of the physical exchange of heat energy and any physiological mechanisms induced by the cold inspirate in producing the changes is undetermined.     

Energetic responses to cold temperatures in rats lacking forebrain-caudal brain stem connections

Hypothalamic neurons are regarded as essential for integrating thermal afferent information from skin and core and issuing commands to autonomic and behavioral effectors that maintain core temperature (T(c)) during cold exposure and for the control of energy expenditure more generally. Caudal brain stem neurons are necessary elements of the hypothalamic effector pathway and also are directly driven by skin and brain cooling. To assess whether caudal brain stem processing of thermal afferent signals is sufficient to drive endemic effectors for thermogenesis, heart rate (HR), T(c), and activity responses of chronic decerebrate (CD) and control rats adapted to 23 degrees C were compared during cold exposure (4, 8, or 12 degrees C) for 6 h. Other CDs and controls were exposed to 4 or 23 degrees C for 2 h, and tissues were processed for norepinephrine turnover (NETO), a neurochemical measure of sympathetic drive. Controls maintained T(c) for all temperatures. CDs maintained T(c) for the 8 and 12 degrees C exposures, but T(c) declined 2 degrees C during the 4 degrees C exposure. Cold exposure elevated HR in CDs and controls alike. Tachycardia magnitude correlated with decreases in environmental temperature for controls, but not CDs. Cold increased NETO in brown adipose tissue, heart, and some white adipose tissue pads in CDs and controls compared with their respective room temperature controls. These data demonstrate that, in neural isolation from the hypothalamus, cold exposure drives caudal brain stem neuronal activity and engages local effectors that trigger sympathetic energetic and cardiac responses that are comparable in many, but not in all, respects to those seen in neurologically intact rats.     

Mechanism of afterdrop after cold water immersion

It was hypothesized that if afterdrop is a purely conductive phenomenon, the afterdrop during rewarming should proceed initially at a rate equal to the rate of cooling. Eight male subjects were cooled on three occasions in 22 degrees C water and rewarmed once by each of three procedures: spontaneous shivering, inhalation of heated (45 degrees C) and humidified air, and immersion up to the neck in 40 degrees C water. Deep body temperature was recorded at three sites: esophagus, auditory canal, and rectum. During spontaneous and inhalation rewarming, there were no significant differences between the cooling (final 30 min) and afterdrop (initial 10 min) rates as calculated for each deep body temperature site, thus supporting the hypothesis. During rapid rewarming, the afterdrop rate was significantly greater than during the preceding cooling, suggesting a convective component contributing to the increased rate of fall. The rapid reversal of the afterdrop also indicates that a convective component contributes to the rewarming process as well.     

Peripheral blood flow during rewarming from mild hypothermia in humans

During the initial stages of rewarming from hypothermia, there is a continued cooling of the core, or after-drop in temperature, that has been attributed to the return of cold blood due to peripheral vasodilatation, thus causing a further decrease of deep body temperature. To examine this possibility more carefully, subjects were immersed in cold water (17 degrees C), and then rewarmed from a mildly hypothermic state in a warm bath (40 degrees C). Measurements of hand blood flow were made by calorimetry and of forearm, calf, and foot blood flows by straingauge venous occlusion plethysmography at rest (Ta = 22 degrees C) and during rewarming. There was a small increase in skin blood flow during the falling phase of core temperature upon rewarming in the warm bath, but none in foot blood flow upon rewarming at room air, suggesting that skin blood flow seems to contribute to the after-drop, but only minimally. Limb blood flow changes during this phase suggest that a small muscle blood flow could also have contributed to the after-drop. It was concluded that the after-drop of core temperature during rewarming from mild hypothermia does not result from a large vasodilatation in the superficial parts of the periphery, as postulated. The possible contribution of mechanisms of heat conduction, heat convection, and cessation of shivering thermogenesis were discussed.     

脑干听觉诱发电位与后循环TIA及脑干梗死的相关性研究

目的:研究脑干听觉诱发电位(BAEP)与后循环短暂性脑缺血发作(TIA)及脑干梗死的相关性。方法:选取我院收治的后循环TIA患者46例作为TIA组,选取同期收治的脑干梗死患者44例作为脑干梗死组,选取同期健康体检者49例作为健康组,TIA组和脑干梗死组均在发病后1周内进行BAEP检查,健康体检者在体检时进行BAEP检查,比较3组的Ⅰ、Ⅲ、Ⅴ波的潜伏期(PL)及Ⅰ-Ⅲ、Ⅲ-Ⅴ、Ⅰ-Ⅴ波峰间的潜伏期(IPL)。结果:TIA组BAEP异常率71.74%,脑干梗死组BAEP异常率56.82%,健康组BAEP异常率24.49%,TIA组患者BAEP异常率高于健康组,差异有统计学意义(P0.05)。脑干梗死组BAEP异常率高于健康组,差异有统计学意义(P0.05)。TIA组患者PL的Ⅰ、Ⅲ、Ⅴ水平均高于健康组,差异有统计学意义(P0.05)。TIA组患者IPL的Ⅰ-Ⅲ、Ⅲ-Ⅴ、Ⅰ-Ⅴ水平均高于健康组,差异有统计学意义(P0.05)。脑干梗死组患者PL的Ⅰ、Ⅲ、Ⅴ水平均高于健康组,差异有统计学意义(P0.05)。脑干梗死组患者IPL的Ⅰ-Ⅲ、Ⅲ-Ⅴ、Ⅰ-Ⅴ水平均高于健康组,差异有统计学意义(P0.05)。脑干梗死组患者IPL与PL均明显高于TIA组(P0.05)。结论:BAEP与后循环TIA及脑干梗死存在相关性,并且较为敏感,是优秀的诊断方法之一。     

Lead-Induced Hearing Loss in Rats and the Protective Effect of Copper

Lead is a common environmental pollutant which can induce various toxic effects to humans and/or animals. This work aimed to study the hearing loss in rats induced by lead and the protective effect of copper. The auditory brainstem response (ABR) was used to study the hearing loss in rats. The results showed that lead prolonged the latencies of wave I to V of ABRs of the rats but did not affect the interpeak latencies of waves I-III, III-V, and I-V, indicating that lead could cause hearing loss in rats by impairing the cochlea. After receiving copper, the quality and the wave latencies of the ABR of the rats were restored to a certain extent, indicating that copper played a protective role in lead-induced hearing impairment. The mechanisms were also proposed that lead could cause hearing loss in rats mainly through damaging the cochlea component, and copper might antagonize the toxicity of lead in three primary ways.     

Effect of alcohol on thermal balance of man in cold water.

The effects of alcohol on core cooling rates (rectal and tympanic), skin temperatures, and metabolic rate were determined for 10 subjects rendered hypothermic by immersion for 45 min in 10 degrees C water. Experiments were duplicated with and without a 20-min period of exercise at the beginning of cold water immersion. Measurements were continued during rewarming in a hot bath. With blood alcohol concentrations averaging 82 mg 100 mL-1, core cooling rates and changes in skin temperatures were insignificantly different from controls, even if the exercise period was imposed. Alcohol reduced shivering metabolic rate by an overall mean of 13%, insufficient to affect cooling rate. Alcohol had no effect on metabolic rate during exercise. During rewarming by hot bath, the amount of 'afterdrop' and rate of increase in core temperature were unaffected by alcohol. It was concluded that alcohol in a moderate dosage does not influence the rate of progress into hypothermia or subsequent, efficient rewarming. This emphasizes that the high incidence of alcohol involvement in water-related fatalities is due to alcohol potentiation of accidents rather than any direct effects on cold water survival, although very high doses of alcohol leading to unconsciousness would increase rate of progress into hypothermia.     

Radio frequency (13.56 MHz) energy enhances recovery from mild hypothermia

The rate of warming after hypothermia depends on the method of rewarming. This study compared the effectiveness of radio frequency (RF) energy against hot (41 degrees C) water immersion (HW) and an insulated cocoon (IC) for rewarming hypothermic men. Six men fasted overnight and were rewarmed for 1 h after attaining a 0.5 degree C reduction in rectal temperature (Tre). Tre and esophageal (Tes) temperature were recorded every 5 min with nonmetallic thermal probes. The base-line value for Tre and Tes just before rewarming was subtracted from each 5 min Tre and Tes during rewarming to give delta Tre and delta Tes. The 12 delta Tes values were averaged for each individual and were compared using analysis of variance. The average delta Tes for RF (1.15 +/- 0.22 degrees C/h) was faster (P less than 0.001) than either IC (0.37 +/- 0.16 degrees C/h) or HW (0.18 +/- 0.09 degree C/h). The present study shows the superiority of RF energy for rewarming mildly hypothermic men.     

Iron chelation or anti-oxidants prevent renal cell damage in the rewarming phase after normoxic, but not hypoxic cold incubation

It has now been firmly established that, not only ischemia/reperfusion, but also cold itself causes damage during kidney transplantation. Iron chelators or anti-oxidants applied during the cold plus rewarming phase are able to prevent this damage. At present, it is unknown if these measures act only during the cold, or whether application during the rewarming phase also prevents damage. We aimed to study this after cold normoxic and hypoxic conditions. LLC-PK1 cells were incubated at 4 degrees C in Krebs-Henseleit buffer for 6 or 24h, followed by 18 or 6h rewarming, respectively. Cold preservation was performed under both normoxic (95% air/5% CO2) and hypoxic (95% N2/5% CO2) conditions. The iron chelator 2,2'-DPD (100 microM), anti-oxidants BHT (20 microM) or sibilinin (200 microM), and xanthine oxidase inhibitor allopurinol (100 microM) were added during either cold preservation plus rewarming, or rewarming alone. Cell damage was assessed by LDH release (n=3-9). Addition of 2,2'-DPD and BHT during cold hypoxia plus rewarming did, but during rewarming alone did not prevent cell damage. When added during rewarming after 6h cold normoxic incubation, BHT and 2,2'-DPD inhibited rewarming injury compared to control (p<0.05). Allopurinol did not prevent cell damage in any experimental set-up. Our data show that application of iron chelators or anti-oxidants during the rewarming phase protects cells after normoxic but not hypoxic incubation. Allopurinol had no effect. Since kidneys are hypoxic during transplantation, measures aimed at preventing cold-induced and rewarming injury should be taken during the cold.     

A second postcooling afterdrop: more evidence for a convective mechanism.

An attempt was made to demonstrate the importance of increased perfusion of cold tissue in core temperature afterdrop. Five male subjects were cooled twice in water (8 degrees C) for 53-80 min. They were then rewarmed by one of two methods (shivering thermogenesis or treadmill exercise) for another 40-65 min, after which they entered a warm bath (40 degrees C). Esophageal temperature (Tes) as well as thigh and calf muscle temperatures at three depths (1.5, 3.0, and 4.5 cm) were measured. Cold water immersion was terminated at Tes varying between 33.0 and 34.5 degrees C. For each subject this temperature was similar in both trials. The initial core temperature afterdrop was 58% greater during exercise (mean +/- SE, 0.65 +/- 0.10 degrees C) than shivering (0.41 +/- 0.06 degrees C) (P < 0.005). Within the first 5 min after subjects entered the warm bath the initial rate of rewarming (previously established during shivering or exercise, approximately 0.07 degrees C/min) decreased. The attenuation was 0.088 +/- 0.03 degrees C/min (P < 0.025) after shivering and 0.062 +/- 0.022 degrees C/min (P < 0.025) after exercise. In 4 of 10 trials (2 after shivering and 2 after exercise) a second afterdrop occurred during this period. We suggest that increased perfusion of cold tissue is one probable mechanism responsible for attenuation or reversal of the initial rewarming rate. These results have important implications for treatment of hypothermia victims, even when treatment commences long after removal from cold water.     

Effects of estrogen on thermoregulatory tail vasomotion and heat-escape behavior in freely moving female rats

Effects of estrogen on thermoregulatory vasomotion and heat-escape behavior were investigated in ovariectomized female rats supplemented with estrogen (replaced estrogen rats) or control saline (low estrogen rats). First, we measured tail temperature of freely moving rats at ambient temperatures (T(a)) between 13 and 31 degrees C. Tail temperature of the low estrogen rats was higher than that of the replaced estrogen rats at T(a) between 19 and 25 degrees C, indicating that the low estrogen rats exhibit more skin vasodilation than the replaced estrogen rats. There was no significant difference in oxygen consumption and core temperature between the two groups. Second, we analyzed heat-escape behaviors in a hot chamber where rats could obtain cold air by moving in and out of a reward area. The low estrogen rats kept T(a) at a lower level than did the replaced estrogen rats. These results imply that the lack of estrogen facilitates heat dissipation both by skin vasodilation and by heat-escape behavior. Ovariectomized rats may mimic climacteric hot flushes not only for autonomic skin vasomotor activity but also for thermoregulatory behavior.     

Tau binds and organizes Escherichia coli replication proteins through distinct domains. Domain III, shared by gamma and tau, binds delta delta ' and chi psi

The DnaX complex of the DNA polymerase holoenzyme assembles the beta(2) processivity factor onto the primed template enabling highly processive replication. The key ATPases within this complex are tau and gamma, alternative frameshift products of the dnaX gene. Of the five domains of tau, I-III are shared with gamma In vivo, gamma binds the auxiliary subunits deltadelta' and chipsi (Glover, B. P., and McHenry, C. S. (2000) J. Biol. Chem. 275, 3017-3020). To localize deltadelta' and chipsi binding domains within gamma domains I-III, we measured the binding of purified biotin-tagged DnaX proteins lacking specific domains to deltadelta' and chipsi by surface plasmon resonance. Fusion proteins containing either DnaX domains I-III or domains III-V bound deltadelta' and chipsi subunits. A DnaX protein only containing domains I and II did not bind deltadelta' or chipsi. The binding affinity of chipsi for DnaX domains I-III and domains III-V was the same as that of chipsi for full-length tau, indicating that domain III contained all structural elements required for chipsi binding. Domain III of tau also contained deltadelta' binding sites, although the interaction between deltadelta' and domains III-V of tau was 10-fold weaker than the interaction between deltadelta' and full length tau. The presence of both delta and chipsi strengthened the delta'-C(0)tau interaction by at least 15-fold. Domain III was the only domain common to all of tau fusion proteins whose interaction with delta' was enhanced in the presence of delta and chipsi. Thus, domain III of the DnaX proteins not only contains the deltadelta' and chipsi binding sites but also contains the elements required for the positive cooperative assembly of the DnaX complex.     

Influence of skeletal muscle glycogen on passive rewarming after hypothermia

To examine the influence of muscle glycogen on the thermal responses to passive rewarming subsequent to mild hypothermia, eight subjects completed two cold-water immersions (18 degrees C), followed by 75 min of passive rewarming (24 degrees C air, resting in blanket). The experiments followed several days of different exercise-diet regimens eliciting either low (LMG; 141.0 +/- 10.5 mmol.kg.dry wt-1) or normal (NMG; 526.2 +/- 44.2 mmol.kg.dry wt-1) prewarming muscle glycogen levels. Cold-water immersion was performed for 180 min or to a rectal temperature (Tre) of 35.5 degrees C. In four subjects (group A, body fat = 20 +/- 1%), postimmersion Tre was similar to preimmersion Tre for both trials (36.73 +/- 0.18 vs. 37.26 +/- 0.18 degrees C, respectively). Passive rewarming in group A resulted in an increase in Tre of only 0.13 +/- 0.08 degrees C. Conversely, initial rewarming Tre for the other four subjects (group B, body fat = 12 +/- 1%) averaged 35.50 +/- 0.05 degrees C for both trials. Rewarming increased Tre similarly in group B during both LMG (0.76 +/- 0.25 degrees C) and NMG (0.89 +/- 0.13 degrees C). Afterdrop responses, evident only in those individuals whose body core cooled during immersion (group B), were not different between LMG and NMG. These data support the contention that Tre responses during passive rewarming are related to body insulation. Furthermore these results indicate that low muscle glycogen levels do not impair rewarming time nor alter after-drop responses during passive rewarming after mild-to-moderate hypothermia.     

A technique to measure the ability of the human nose to warm and humidify air.

To assess the ability of the nose to warm and humidify inhaled air, we developed a nasopharyngeal probe and measured the temperature and humidity of air exiting the nasal cavity. We delivered cold, dry air (19-1 degrees C, <10% relative humidity) or hot, humid air (37 degrees C, >90% relative humidity) to the nose via a nasal mask at flow rates of 5, 10, and 20 l/min. We used a water gradient across the nose (water content in nasopharynx minus water content of delivered air) to assess nasal function. We studied the characteristics of nasal air conditioning in 22 asymptomatic, seasonally allergic subjects (out of their allergy season) and 11 nonallergic normal subjects. Inhalation of hot, humid air at increasingly higher flow rates had little effect on both the relative humidity and the temperature of air in the nasopharynx. In both groups, increasing the flow of cold, dry air lowered both the temperature and the water content of the inspired air measured in the nasopharynx, although the relative humidity remained at 100%. Water gradient values obtained during cold dry air challenges on separate days showed reproducibility in both allergic and nonallergic subjects. After exposure to cold, dry air, the water gradient was significantly lower in allergic than in nonallergic subjects (1,430 +/- 45 vs. 1,718 +/- 141 mg; P = 0.02), suggesting an impairment in their ability to warm and humidify inhaled air.     

Cold acclimation can induce microtubular cold stability in a manner distinct from abscisic acid

The response of cortical microtubules to low temperature was investigated for the Chinese winter wheat (Triticum aestivum L.) cultivar Jing Nong 934. Microtubules in the cortex of the root elongation zone disassembled rapidly in response to a cold shock of -7 degrees C and reassembled upon rewarming to 25 degrees C. The microtubules acquired resistance against this cold shock in response to cold acclimation in chilling, but non-freezing, temperature or after a treatment with abscisic acid (ABA). Cold acclimation and ABA differed with respect to the appearance of microtubules: fine, transverse strands were observed after cold acclimation, whereas ABA produced steeply oblique microtubule bundles. The findings are discussed in terms of an ABA-independent pathway for acquired cold stability of microtubules.     

Depression of sublingual temperature by cold saliva.

Sublingual and oesophageal temperatures were compared at various air temperatures in 16 subjects. In warm air (25-44 degrees C) sublingual temperatures stabilized within plus or minus 0-45 degrees C of oesophageal temperatures, but in air at room temperature (18-24 degrees C) they were sometimes as much as 1-1 degrees C below and in cold air (5-10 degrees C) as much as 4-4 degrees C below oesophageal readings. The sublingual-oesophageal temperature difference in cold air was greatly reduced by keeping the face warm, but it was not reduced in two patients breathing through tracheostomies and thereby eliminating cold air flow from the nose and pharynx. Parotid saliva temperature was low and saliva flow high during exposure, and cold saliva seemed to be mainly responsible for the erratic depression of sublingual temperature in the cold. These results indicate hazards in the casual use of sublingual temperatures, and indicate that external heat may have to be supplied to enable them to give reliable clinical assessments of body temperature.     

模拟冬季低温和夜间退潮对无瓣海桑幼苗的协同作用

利用人工控制手段,模拟冬季低温和夜间低潮对无瓣海桑幼苗的影响,分析气温-水温协同作用下无瓣海桑幼苗的低温适应机制.结果表明:低温显著抑制了无瓣海桑幼苗株高和基径的增长,而提高水温5℃对其的缓解作用分别达41.2％和44.6％;低气温(15℃)显著降低了叶片的最大光化学效率(Fv/Fm)值,进而影响叶片的光合能力,而提高水温未能显著缓解其损伤;低气温时,提高水温能促进幼苗叶片脯氨酸的积累,增加可溶性糖含量,缓解低温对叶片的伤害.极端低温发生时,夜间高潮对幼苗起到较好的保温作用,缓解了低温对幼苗生长和叶片的生理伤害,提高了无瓣海桑幼苗的成活率.