Influence of pregnancy on the febrile response to ICV administration of PGE1 in rats studied in a thermocline

Eliason, Heather L., and James E. Fewell. Influence ofpregnancy on the febrile response to ICV administration ofPGE₁ in rats studied in athermocline. J. Appl. Physiol. 82(5):1453-1458, 1997.Rats near term of pregnancy have an attenuatedfebrile response to intracerebroventricular (ICV) injection ofprostaglandin E₁ (PGE₁) when they are studied atan ambient temperature below their thermoneutral zone. Given thatnonshivering thermogenesis in brown adipose tissue is impaired inrodents near term of pregnancy, it is possible that the attenuatedfebrile response is forced by impairment of this component of theautonomic thermoregulatory response. If this were the case, thennear-term pregnant rats should develop a "normal" fever afterPGE₁ administration if they werestudied in a thermocline where they could utilize behavioral as well asautonomic thermoregulatory effectors to increase their body coretemperature (T_bc). Experimentswere, therefore, carried out on 13 nonpregnant and 14 pregnantchronically instrumented rats in a thermocline (temperature gradient10-40°C) to investigate theirT_bc responses to ICV injection ofPGE₁. ICV injection of 0.2 µgPGE₁ produced significantincreases in T_bc and fever index in both nonpregnant and pregnant animals (day19 of gestation); the increases, however, weresignificantly attenuated in the pregnant compared with the nonpregnantrats. Behavioral (e.g., selected ambient temperature) and autonomic(e.g., oxygen consumption) thermoregulatory effectors were activated toincrease T_bc after ICVPGE₁ in both groups of animals,but the duration of activation was shortened in pregnant compared withnonpregnant rats. The abbreviated thermoregulatory effector responsesand the resulting attenuated febrile response toPGE₁ in the pregnant rats may have resulted from a pregnancy-related activation of an endogenous antipyretic system.

     

Autonomic and behavioral thermoregulation in guinea pigs during postnatal maturation

Fewell, James E., Maria Kang, and Heather L. Eliason.Autonomic and behavioral thermoregulation in guinea pigs during postnatal maturation. J. Appl.Physiol. 83(3): 830-836, 1997.Serial experimentswere carried out on seven chronically instrumented Hartley-strainguinea pigs at 1, 3, and 5 wk of age to define their autonomic andbehavioral thermoregulatory profiles and to test the hypothesis thatthey have the mechanisms in place shortly after birth that allow themto optimize their energy expenditure for thermoregulation by selectinga thermal environment that requires the lowest metabolic oxygenrequirements. Each animal was studied in both a thermocline todetermine selected ambient temperature and in a metabolic chamberto determine the thermoregulatory response to forced changes in ambienttemperature. In the thermocline, the guinea pigs at all postnatal agesselected an ambient temperature that placed core temperature, oxygenconsumption, thermal conductance, heart rate, and respiratory rate atlevels comparable to those observed at ambient temperatures in whichminimal oxygen consumption occurred in the metabolic chamber. Thus ourexperiments provide evidence that guinea pigs have theneurophysiological mechanisms in place shortly after birth that allowthem to optimize their energy expenditure for thermoregulation byselecting a thermal environment that corresponds to the lowestmetabolic oxygen requirements.

     

A relationship between heat loss and sleepiness: effects of postural change and melatonin administration

Kräuchi, Kurt, Christian Cajochen, and AnnaWirz-Justice. A relationship between heat loss and sleepiness:effects of postural change and melatonin administration.J. Appl. Physiol. 83(1): 134-139, 1997.Both the pineal hormone melatonin (Mel) and postural changeshave thermoregulatory sequelae. The purpose of the study was toevaluate their relationship to subjective sleepiness. Eight healthyyoung men were investigated under the unmasking conditions of aconstant routine protocol. Heart rate, rectal temperature(T_re), skin temperatures (foot,T_fo; and stomach), and subjectivesleepiness ratings were continuously recorded from 1000 to 1700. Mel (5 mg po) was administered at 1300, a time when Mel should not phaseshift the circadian system. Both the postural change at1000 from upright to a supine position (lying down in bed) and Meladministration at 1300 reduced T_reand increased T_fo in parallel withincreased sleepiness. These findings suggest that under comfortableambient temperature conditions, heat loss via the distal skin regions(e.g., feet) is a key mechanism for induction of sleepiness as corebody temperature declines.

     

Ventilatory and metabolic responses to ambient hypoxia or hypercapnia in rats exposed to CO hypoxia

Gautier, Henry, Cristina Murariu, and Monique Bonora.Ventilatory and metabolic responses to ambient hypoxia orhypercapnia in rats exposed to CO hypoxia. J. Appl. Physiol.83(1): 253-261, 1997.We have investigated at ambienttemperatures (T_am) of 25 and5°C the effects of ambient hypoxia(Hx_am; fractional inspired O₂ = 0.14) and hypercapnia(fractional inspiredCO₂ = 0.04) on ventilation (),O₂ uptake(O₂), andcolonic temperature (T_c) in 12 conscious rats before and after carotid body denervation (CBD). Therats were concomitantly exposed to CO hypoxia (Hx_CO; fractional inspired CO = 0.03-0.05%), which decreases arterial O₂ saturation by ~25-40%.The results demonstrate the following. 1) AtT_am of 5°C, in both intact andCBD rats,/O₂ islarger when Hx_am orCO₂ is associated withHx_CO than with normoxia. At T_am of 25°C, this is also thecase except for CO₂ in CBD rats. 2) AtT_am of 5°C, the changes inO₂ andT_c seem to result from additiveeffects of the separate changes induced byHx_am,CO₂, andHx_CO. It is concluded that, inconscious rats, central hypoxia does not depress respiratory activity.On the contrary, particularly whenO₂ is augmented during acold stress, both/O₂during Hx_CO and the ventilatoryresponses to Hx_am andCO₂ are increased. The mechanismsinvolved in this relative hyperventilation are likely to involvediencephalic integrative structures.

     

Ozone toxicity in the rat. III. Effect of changes in ambient temperature on pulmonary parameters

Wiester, Mildred J., William P. Watkinson, Daniel L. Costa,Kay M. Crissman, Judy H. Richards, Darrell W. Winsett, and Jerry W. Highfill. Ozone toxicity in the rat. III. Effect of changes inambient temperature on pulmonary parameters. J. Appl.Physiol. 81(4): 1691-1700, 1996.Pulmonarytoxicity of ozone (O₃) wasexamined in adult male Fischer 344 rats exposed to 0.5 parts/millionO₃ for either 6 or 23 h/day over 5 days while maintained at an ambient temperature(T_a) of either 10, 22, or34°C. Toxicity was evaluated by using changes in lung volumes andthe concentrations of constituents of bronchoalveolar lavage fluid thatsignal lung injury and/or inflammation. Results indicated thattoxicity increased as T_adecreased. Exposures conducted at 10°C were associated with thegreatest decreases in body weight and total lung capacity and thegreatest increases in lavageable protein, lysozyme, alkaline phosphatase activity, and percent neutrophils.O₃ effects not modified byT_a included increases in residualvolume and lavageable potassium, glucose, urea, and ascorbic acid.There was a progressive decrease in lavageable uric acid with exposureat 34°C. Most effects were attenuated during the 5 exposure daysand/or returned to normal levels after 7 air recovery days,regardless of prior O₃ exposure orT_a. It is possible thatT_a-induced changes in metabolic rate may have altered ventilation and, therefore, theO₃ doses among rats exposed at thethree different T_a levels.

     

Chronic hormone replacement therapy alters thermoregulatory and vasomotor function in postmenopausal women

Brooks, E. M., A. L. Morgan, J. M. Pierzga, S. L. Wladkowski, J. T. O'Gorman, J. A. Derr, and W. L. Kenney. Chronic hormone replacement therapy alters thermoregulatory and vasomotor function in postmenopausal women. J. Appl.Physiol. 83(2): 477-484, 1997.This investigationexamined effects of chronic (2 yr) hormone replacement therapy (HRT),both estrogen replacement therapy (ERT) and estrogen plus progesteronetherapy (E+P), on core temperature and skin blood flow responses ofpostmenopausal women. Twenty-five postmenopausal women [9 not onHRT (NO), 8 on ERT, 8 on E+P] exercised on a cycle ergometer for1 h at an ambient temperature of 36°C. Cutaneous vascularconductance (CVC) was monitored by laser-Doppler flowmetry, and forearmvascular conductance (FVC) was measured by using venous occlusionplethysmography. Iontophoresis of bretylium tosylate was performedbefore exercise to block local vasoconstrictor (VC) activity at oneskin site on the forearm. Rectal temperature (T_re) was ~0.5°C lower forthe ERT group (P < 0.01) comparedwith E+P and NO groups at rest and throughout exercise. FVC: mean body temperature (T_b) and CVC:T_b curves were shifted~0.5°C leftward for the ERT group(P < 0.0001). Baseline CVC wassignificantly higher in the ERT group(P < 0.05), but there was nointeraction between bretylium treatment and groups once exercise wasinitiated. These results suggest that1) chronic ERT likely acts centrally to decrease T_re,2) ERT lowers theT_re at which heat-loss effector mechanisms are initiated, primarily by actions on active cutaneous vasodilation, and 3) addition ofexogenous progestins in HRT effectively blocks these effects.

     

Pregnancy alters body-core temperature response to a simulated open field in rats

Fewell, James E., and Patricia A. Tang. Pregnancyalters body-core temperature response to a simulated open field in rats. J. Appl. Physiol. 82(4):1406-1410, 1997.Exposure of a rat to a novel environment (e.g.,a simulated open field) induces a transient increase in body-coretemperature, which is often called stress-induced hyperthermia.Although pregnancy is known to influence thermoregulatory control, itseffect on stress-induced hyperthermia is unknown. Therefore, 24 Sprague-Dawley rats (8 nonpregnant and 16 pregnant) were studied totest the hypothesis that pregnancy would alter the development ofstress-induced hyperthermia after exposure to a simulated open field.Body-core temperature index increased significantly after exposure to asimulated open field in nonpregnant and gestationday-10 rats but not in gestation day-15 andday-20 rats. Thus our data provideevidence that pregnancy influences the body-core temperature responseof rats exposed to a simulated open field in a gestation-dependentfashion. The functional consequences as well as the mechanisms involvedremain to be determined.

     

Heat stroke: opioid-mediated mechanisms

Romanovsky, Andrej A., and Clark M. Blatteis. Heatstroke: opioid-mediated mechanisms. J. Appl.Physiol. 81(6): 2565-2570, 1996.In our previousstudy in guinea pigs, intensive and prolonged intraperitoneal heating(IPH) caused heat stroke characterized by high mortality andaccompanied by two paradoxical phenomena: ear skin vasoconstriction ata high body temperature (T_b)(hyperthermia-induced vasoconstriction) and a post-IPHT_b fall at an ambient temperature (T_a) below thermoneutrality(hyperthermia-induced hypothermia). In this study, we tested thehypothesis that the mechanisms of the two phenomena involve endogenousopioid agonists. Experiments were conducted in 24 unanesthetized,lightly restrained guinea pigs, each chronically implanted with anintraperitoneal thermode and intrahypothalamic thermocouple. Thethermoregulatory effects of a wide-spectrum opioid-receptor antagonist,naltrexone (NTX; 50 or 0 µmol/kg sc), were studied in IPH-inducedheat stroke and under normal conditions. IPH was accomplished byperfusing (50 ml/min; 80 min) water (45°C) through the thermode.T_a was maintained at ~24°C.Skin vasodilation occurred at the onset of IPH but later changed tovasoconstriction despite high T_band continuing IPH. IPH-induced hyperthermia (1.8 ± 0.1°C) was followed by a post-IPH T_b fall (5.1 ± 0.7°C; calculated for the survivors only). The 48-h mortality ratewas 50%. NTX prevented the hyperthermia-induced vasoconstriction andattenuated the hyperthermia-induced hypothermia (1.8 ± 0.4°C). None of the NTX-treated animals died. The effects of NTX onT_b regulation under normalconditions were minor. These results indicate that the phenomena ofboth hyperthermia-induced vasoconstriction and hyperthermia-inducedhypothermia are opioid dependent. The latter is speculated to reflectopioid-mediated inhibition of metabolism; the former is thought toresult from opioid-induced hemodynamic alterations. Because bothphenomena did not occur in the NTX-treated survivors, the skinvasoconstriction at high T_b andthe posthyperthermia T_b fall maybe viewed as markers of the severity of heat stroke. It is suggestedthat opioid antagonists may have therapeutic potential in heat-induceddisorders.

     

Hyperhydration: thermoregulatory effects during compensable exercise-heat stress

Latzka, William A., Michael N. Sawka, Scott J. Montain, GaryS. Skrinar, Roger A. Fielding, Ralph P. Matott, and Kent B. Pandolf.Hyperhydration: thermoregulatory effects during compensable exercise-heat stress. J. Appl.Physiol. 83(3): 860-866, 1997.This studyexamined the effects of hyperhydration on thermoregulatory responsesduring compensable exercise-heat stress. The general approach was todetermine whether 1-h preexercise hyperhydration [29.1 ml/kg leanbody mass; with or without glycerol (1.2 g/kg lean body mass)]would improve sweating responses and reduce core temperature duringexercise. During these experiments, the evaporative heat loss required(E_req = 293 W/m²) to maintain steady-statecore temperature was less than the maximal capacity(E_max = 462 W/m²) of the climate forevaporative heat loss(E_req/E_max = 63%). Eight heat-acclimated men completed five trials: euhydration, glycerol hyperhydration, and water hyperhydration both with and withoutrehydration (replace sweat loss during exercise). During exercise inthe heat (35°C, 45% relative humidity), there was no differencebetween hyperhydration methods for increasing total body water (~1.5liters). Compared with euhydration, hyperhydration did not alter coretemperature, skin temperature, whole body sweating rate, local sweatingrate, sweating threshold temperature, sweating sensitivity, or heartrate responses. Similarly, no difference was found between water andglycerol hyperhydration for these physiological responses. These datademonstrate that hyperhydration provides no thermoregulatory advantageover the maintenance of euhydration during compensable exercise-heatstress.

     

Modification of active cutaneous vasodilation by oral contraceptive hormones

Charkoudian, Nisha, and John M. Johnson. Modificationof active cutaneous vasodilation by oral contraceptive hormones. J. Appl. Physiol. 83(6):2012-2018, 1997.It is not clear whether the alteredthermoregulatory reflex control of the cutaneous circulation seen amongphases of the menstrual cycle also occurs with the synthetic estrogenand progesterone in oral contraceptive pills and whether any suchmodifications include altered control of the cutaneous activevasodilator system. To address these questions, we conducted controlledwhole body heating experiments in seven women at the end of the thirdweek of hormone pills (HH) and at the end of the week of placebo/nopills (LH). A water-perfused suit was used to control body temperature.Laser Doppler flowmetry was used to monitor cutaneous blood flow at acontrol site and at a site at which noradrenergic vasoconstrictorcontrol had been eliminated by iontophoresis of bretylium (BT),isolating the active cutaneous vasodilator system. The oral temperature(T_or) thresholds for cutaneousvasodilation were higher in HH at both control [37.09 ± 0.12 vs. 36.83 ± 0.07°C (LH), P < 0.01] and BT-treated [37.19 ± 0.05 vs. 36.88 ± 0.12°C (LH), P < 0.01]sites. The T_or threshold forsweating was similarly shifted (HH: 37.15 ± 0.11°C vs. LH: 36.94 ± 0.11°C, P < 0.01). Arightward shift in the relationship of heart rate toT_or was seen in HH. Thesensitivities (slopes of the responses vs.T_or) did not differstatistically between phases. The similar threshold shifts at controland BT-treated sites suggest that the hormones shift the function ofthe active vasodilator system to higher internal temperatures. Thesimilarity of the shifts among thermoregulatory effectors suggests acentrally mediated action of these hormones.

     

Oxygen pulse in guinea pigs in hyperbaric helium and hydrogen

Kayar, Susan R., and Erich C. Parker. Oxygen pulse inguinea pigs in hyperbaric helium and hydrogen. J. Appl. Physiol. 82(3): 988-997, 1997.We analyzedO₂ pulse, the total volume of O₂ consumed per heart beat, inguinea pigs at pressures from 10 to 60 atmospheres. Animals were placedin a hyperbaric chamber and breathed 2%O₂ in either helium (heliox) orhydrogen (hydrox). Oxygen consumption rate(O₂) was measured by gaschromatographic analysis. Core temperature and heart rate were measuredby using surgically implanted radiotelemeters. TheO₂ was modulated over afourfold range by varying chamber temperature from 25 to 36°C. There was a direct correlation betweenO₂ and heartrate, which was significantly different for animals in heliox vs.hydrox (P = 0.003). By usingmultivariate regression analysis, we identified variables that weresignificant to O₂ pulse: bodysurface area, chamber temperature, core temperature, and pressure.After normalizing for all nonpressure variables, the residualO₂ pulse was found to decreasesignificantly (P = 0.02) with pressurefor animals in heliox but did not decrease significantly(P = 0.38) with pressure for animalsin hydrox over the range of pressures studied. This amounted to aroughly 25% lower O₂ pulse fornormothermic animals in 60 atmospheres heliox vs. hydrox. These resultssuggest that reduction of cardiovascular efficiency in a hyperbaricenvironment can be mitigated by the choice of breathing gas.

     

Appropriate thermal manipulations eliminate tremors in rats recovering from halothane anesthesia

Grahn, D. A., M. C. Heller, J. E. Larkin, and H. C. Heller.Appropriate thermal manipulations eliminate tremors in ratsrecovering from halothane anesthesia. J. Appl.Physiol. 81(6): 2547-2554, 1996.Tremors arecommon in mammals emerging from anesthesia. To determine whetherappropriate thermal manipulations immediately before emergence fromanesthesia are sufficient to eliminate these tremors,electroencephalographic (EEG) and electromyographic (EMG) activities,hypothalamic temperature (T_hy),and O₂ consumption were monitoredin 12 rats recovering from halothane anesthesia under three thermalregimes. EEG and EMG activities were recorded throughout anesthesia andserved as feedback signals for controlling anesthetic depth. Duringanesthesia, T_hy was either1) allowed to fall to32-34°C, 2) maintained at37-39°C, or 3) allowed to fall to 32-34°C and then raised to 37-39°C. Whenhypothermic on emergence from anesthesia, all of the animals exhibitedpostanesthetic tremors that persisted untilT_hy values returned tonormothermia. None of the animals expressed postanesthetic tremors whennormothermic on emergence from anesthesia. In addition, the timebetween emergence from anesthesia (as determined by EEG/EMG parameters)and the initiation of coordinated motor activities was significantlydecreased in the normothermic animals.

     

Behaviorally mediated,warm adaptation: A physiological strategy when mice behaviorally thermoregulate

Laboratory mice housed under standard vivarium conditions with an ambient temperature (T_a) of ~22 °C are likely to be cold stressed because this T_a is below their thermoneutral zone (TNZ). Mice raised at T_as within the TNZ adapt to the warmer temperatures, developing smaller internal organs and longer tails compared to mice raised at 22 °C. Since mice prefer T_as equal to their TNZ when housed in a thermocline, we hypothesized that mice reared for long periods (e.g., months) in a thermocline would undergo significant changes in organ development and tail length as a result of their thermoregulatory behavior. Groups of three female BALB/c mice at an age of 37 days were housed together in a thermocline consisting of a 90 cm long aluminum runway with a floor temperature ranging from 23 to 39 °C. Two side-by-side thermoclines allowed for a total of 6 mice to be tested simultaneously. Control mice were tested in isothermal runways maintained at a T_a of 22 °C. All groups were given cotton pads for bedding/nest building. Mass of heart, lung, liver, kidney, brain, and tail length were assessed after 73 days of treatment. Mice in the thermocline and control (isothermal) runways were compared to cage control mice housed 3/cage with bedding under standard vivarium conditions. Mice in the thermocline generally remained in the warm end throughout the daytime with little evidence of nest building, suggesting a state of thermal comfort. Mice in the isothermal runway built elaborate nests and huddled together in the daytime. Mice housed in the thermocline had significantly smaller livers and kidneys and an increase in tail length compared to mice in the isothermal runway as well as when compared to the cage controls. These patterns of organ growth and tail length of mice in the thermocline are akin to warm adaptation. Thus, thermoregulatory behavior altered organ development, a process we term behaviorally mediated, warm adaptation. Moreover, the data suggest that the standard vivarium conditions are likely a cold stress that alters normal organ development relative to mice allowed to select their thermal preferendum.     

Reduction in open field-induced hyperthermia in the rat exposed to chlorpyrifos,an anticholinesterase pesticide

Rodents develop a marked elevation in core temperature (T_c) when they are placed in an open field environment (OFE). Open field-induced hyperthermia (OFH) involves activation of thermoregulatory systems that are quiescent under baseline conditions. Cholinergic stimulation arising from exposure to organophosphates (OP) is expected to modulate OFH; subtle effects of OPs may be observed during OFH that would not occur in the absence of stress. We have found that methyl scopolamine (MS), a peripheral muscarinic antagonist, attenuates stress-induced hyperthermia. To this end, we assessed if a low dose of the OP pesticide chlorpyrifos (CHP) would alter OFH with and without administration of MS. T_c and motor activity (MA) of male, Sprague-Dawley rats were monitored by telemetry while housed in their home cage at an ambient temperature of 22°C. At 9 AM the rats were gavaged with corn oil or 10 mg/kg CHP that resulted in a ∼40% inhibition in plasma cholinesterase activity. T_c and MA were the same in the control and CHP groups prior to OFE. The rats were then dosed IP with saline or 1.0 mg/kg MS at 12 noon and subjected to OFE (61×61×61 cm box) for 1 h while T_c and MA were monitored every 2 min. T_c of the corn oil/saline group increased by 1.2°C during OFE, whereas T_c of the CHP/saline group was significantly attenuated. Administration of MS attenuated the OFH in rats treated with corn oil and CHP. Overall, exposure to OFE exacerbated the effects of a relatively low dose of CHP that had no effect in the unstressed animal. In addition, the OFH response to MS suggests a peripheral (i.e., outside of CNS) cholinergic pathway is operative in the control of OFH.     

Effect of triiodothyronine augmentation on rat lung surfactant phospholipids during sepsis

Ksenzenko, Sergey M., Scott B. Davidson, Amer A. Saba,Alexander P. Franko, Aml M. Raafat, Lawrence N. Diebel, and Scott A. Dulchavsky. Effect of triiodothyronine augmentation on rat lungsurfactant phospholipids during sepsis. J. Appl.Physiol. 82(6): 2020-2027, 1997.Surfactantfunctional effectiveness is dependent on phospholipid compositionalintegrity; sepsis decreases this through an undefined mechanism.Sepsis-induced hypothyroidism is commensurate and may be related. Thisstudy examines the effect of3,3,5-triiodo-L-thyronine(T₃) supplementation onsurfactant composition and function during sepsis. Male Sprague-Dawleyrats underwent sham laparotomy (Sham) or cecal ligation and puncture (CLP) with or without T₃supplementation [CLP/T₃ (3 ng/h)]. After 6, 12, or 24 h, surfactant was obtained by lavage.Function was assessed by a pulsating bubble surfactometer and in vivocompliance studies. Sepsis produced a decrease in surfactantphosphatidylglycerol and phosphatidic acid, with an increase in lessersurface-active lipids phosphatidylserine and phosphatidylinositol.Phosphatidylcholine content was not significantly changed. Sepsiscaused an alteration in the fatty acid composition and an increase insaturation in most phospholipids. Hormonal replacement attenuated thesechanges. Lung compliance and surfactant adsorption were reduced bysepsis and maintained by T₃treatment. Thyroid hormone may have an active role in lung functionalpreservation through maintenance of surfactant homeostasis duringsepsis.

     

Letters to the Editor

The following is the abstract of the article discussed in thesubsequent letter:

Koga, Shunsaku, Tomoyuki Shiojiri, Narihiko Kondo,and Thomas J. Barstow. Effect of increased muscle temperature on oxygen uptake kinetics during exercise. J. Appl. Physiol.83(4): 1333-1338, 1997.To test whether increased muscletemperature (T_m) would improve O₂ uptake(O₂) kinetics, seven menperformed transitions from rest to a moderate work rate [below theestimated lactate threshold (LT_est)] and a heavy workrate (O₂ = 50% of thedifference between LT_est and peakO₂) under conditions of normal T_m (N) and increased T_m (H), produced bywearing hot water-perfused pants before exercise. QuadricepsT_m was significantly higher in H, but rectal temperaturewas similar for the two conditions. There were no significantdifferences in the amplitudes of the fast component ofO₂ or in the time constantsof the on and off transients for moderate and heavy exercise betweenthe two conditions. The increment inO₂ between the 3rd and 6thmin of heavy exercise was slightly but significantly smaller for H thanfor N. These data suggest that elevated T_m before exercise onset, which would have been expected to increase O₂delivery and off-loading to the muscle, had no appreciable effect onthe fast exponential component ofO₂ kinetics (invariant timeconstant). These data further suggest that elevated T_m doesnot contribute to the slow component ofO₂ during heavy exercise.

     

Posthemorrhagic antipyresis: what stage of fever genesis is affected?

Romanovsky, Andrej A., and Yelena K. Karman.Posthemorrhagic antipyresis: what stage of fever genesis isaffected? J. Appl. Physiol. 83(2):359-365, 1997.It has been shown that hemorrhage leads to adecreased thermal responsiveness to lipopolysaccharide (LPS). The aimof this study was to clarify what stage of fever genesis[production of endogenous pyrogens such as interleukin-1 (IL-1),increase of the prostaglandin E₂(PGE₂) concentration in braintissue, activation of cold-defense effectors] is deficient inposthemorrhagic antipyresis. In adult rabbits, we evaluated the effectof acute hemorrhage (15 ml/kg) on the rectal temperature (T_re) responses to LPS fromSalmonella typhi (200 ng/kg iv),ethanol-purified preparation of homologous IL-1 (1 ml from 3.5 × 10⁷ cells, 1.5 ml/kg iv), andPGE₂ (1 µg,intracisternal injection). The effect of hemorrhage onT_re was also studied in afebrilerabbits, both at thermoneutrality (23°C) and during ramp cooling(to 7°C). The hemorrhage strongly attenuated the biphasicLPS-induced fever (a T_re rise of0.4 ± 0.1 instead of 1.2 ± 0.2°C at the time of the secondpeak), the monophasic T_re responseto IL-1 (by ~0.5°C for over 1-5 h postinjection), and thePGE₂-induced hyperthermia (0.4 ± 0.1 vs. 0.9 ± 0.1°C, maxima). In afebrileanimals, the hemorrhage neither affectedT_re at thermoneutrality norchanged the T_re response to coldexposure. The data suggest that neither insufficiency of cold-defenseeffectors nor lack of endogenous mediators of fever (IL-1,PGE₂) can be the only or eventhe major cause of posthemorrhagic antipyresis. Wespeculate that fever genesis is altered at a stage occurring after theintrabrain PGE₂ level is increasedbut before thermoeffectors are activated.

     

Dehydration markedly impairs cardiovascular function in hyperthermic endurance athletes during exercise

González-Alonso, José, RicardoMora-Rodríguez, Paul R. Below, and Edward F. Coyle.Dehydration markedly impairs cardiovascular function inhyperthermic endurance athletes during exercise. J. Appl. Physiol. 82(4): 1229-1236, 1997.Weidentified the cardiovascular stress encountered by superimposingdehydration on hyperthermia during exercise in the heat and themechanisms contributing to the dehydration-mediated stroke volume (SV)reduction. Fifteen endurance-trained cyclists [maximalO₂ consumption(O_{2 max}) = 4.5 l/min] exercised in the heat for 100-120 min and either became dehydrated by 4% body weight or remained euhydrated by drinkingfluids. Measurements were made after they continued exercise at 71%O_{2 max} for 30 minwhile 1) euhydrated with anesophageal temperature (T_es) of38.1-38.3°C (control); 2)euhydrated and hyperthermic (39.3°C);3) dehydrated and hyperthermic withskin temperature (T_sk) of34°C; 4) dehydrated withT_es of 38.1°C and T_sk of 21°C; and5) condition4 followed by restored blood volume. Compared withcontrol, hyperthermia (1°C T_esincrease) and dehydration (4% body weight loss) each separatelylowered SV 7-8% (11 ± 3 ml/beat;P < 0.05) and increased heart ratesufficiently to prevent significant declines in cardiac output.However, when dehydration was superimposed on hyperthermia, thereductions in SV were significantly (P < 0.05) greater (26 ± 3 ml/beat), and cardiac output declined 13% (2.8 ± 0.3 l/min). Furthermore, mean arterialpressure declined 5 ± 2%, and systemic vascular resistanceincreased 10 ± 3% (both P < 0.05). When hyperthermia wasprevented, all of the decline in SV with dehydration was due to reducedblood volume (~200 ml). These results demonstrate that thesuperimposition of dehydration on hyperthermia during exercise in theheat causes an inability to maintain cardiac output and blood pressurethat makes the dehydrated athlete less able to cope with hyperthermia.

     

Diaphragm thickening during inspiration

Cohn, David, Joshua O. Benditt, Scott Eveloff, and F. DennisMcCool. Diaphragm thickening during inspiration.J. Appl. Physiol. 83(1): 291-296, 1997.Ultrasound has been used to measure diaphragm thickness(T_di) in thearea where the diaphragm abuts the rib cage (zone of apposition).However, the degree of diaphragm thickening during inspiration reportedas obtained by one-dimensional M-mode ultrasound was greater than thatpredicted by using other radiographic techniques. Becausetwo-dimensional (2-D) ultrasound provides greater anatomic definitionof the diaphragm and neighboring structures, we used this technique toreevaluate the relationship between lung volume andT_di. We firstestablished the accuracy and reproducibility of 2-D ultrasound bymeasuring T_diwith a 7.5-MHz transducer in 26 cadavers. We found thatT_di measured byultrasound correlated significantly with that measured by ruler (R² = 0.89), withthe slope of this relationship approximating a line of identity(y = 0.89x + 0.04 mm). The relationship between lung volume andT_di was thenstudied in nine subjects by obtaining diaphragm images at the fivetarget lung volumes [25% increments from residual volume (RV) tototal lung capacity (TLC)]. Plots ofT_di vs. lungvolume demonstrated that the diaphragm thickened as lung volumeincreased, with a more rapid rate of thickening at the higher lungvolumes[T_di = 1.74 vital capacity (VC)² + 0.26 VC + 2.7 mm] (R² = 0.99; P < 0.001) where lung volumeis expressed as a fraction of VC. The mean increase inT_di between RVand TLC for the group was 54% (range 42-78%). We conclude that2-D ultrasound can accurately measureT_di and that theaverage thickening of the diaphragm when a subject is inhaling from RVto TLC using this technique is in the range of what would be predictedfrom a 35% shortening of the diaphragm.

     

Responses in rectal and skin temperatures to centrifugal forces in rats of different ambient temperatures

Effects of centrifugation upon rectal (T_re) and tail skin temperatures (T_s) were studied in male Wistar rats at varying ambient temperature (T_a) using a centrifuge which was placed in a climatic chamber. Centrifugal forces of Gz of 3.0 were imposed on rats which were suspended at horizontal body position using a newly developed mesh suits holding method in the animal box placed on the rotating arm of the centrifuge. Headwards or tailwards forces were applied according to the experimental design. No significant difference of the responses was observed between the two force directions.Centrifugations imposed at different T_a of 15, 20, 25, 30 and 32.5C resulted in falls in T_re accompanied by rises in tail T_s at the cooler environments, while rises in T_re accompanied by falls in T_s in the warmer environments. The T_a at which the response pattern of T_re and T_s was reversed (critical ambient temperature) was 26.8±2.3 (mean and SE) and 27.9±2.8C, respectively. Tolerance to centrifugation was markedly increased in cooler environments than in wanner ones. It was suggested that the increased skin pressure due to centrifugation exerted some inhibitory effects upon central thermoregulatory ability.