Hypoxia, temperature, and pH/CO2 effects on respiratory discharge from a turtle brain stem preparation

Johnson, Stephen M., Rebecca A. Johnson, and Gordon S. Mitchell. Hypoxia, temperature, andpH/CO₂ effects on respiratory discharge from a turtle brain stem preparation. J. Appl. Physiol. 84(2): 649-660, 1998.An in vitrobrain stem preparation from adult turtles (Chrysemyspicta) was used to examine the effects of anoxia andincreased temperature and pH/CO₂on respiration-related motor output. At pH ~7.45, hypoglossal (XII)nerve roots produced patterns of rhythmic bursts (peaks) of discharge(0.74 ± 0.07 peaks/min, 10.0 ± 0.6 s duration) that werequantitatively similar to literature reports of respiratory activity inconscious, vagotomized turtles. Respiratory discharge was stable for 6 h at 22°C; at 32°C, peak amplitude and frequency progressivelyand reversibly decreased with time. Two hours of hypoxia had no effecton respiratory discharge. Acutely increasing bath temperature from 22 to 32°C decreased episode and peak duration and increased peakfrequency. Changes in pH/CO₂increased peak frequency from zero at pH 8.00-8.10 to maxima of0.81 ± 0.01 and 1.44 ± 0.02 peaks/min at 22°C (pH 7.32) and32°C (pH 7.46), respectively;pH/CO₂ sensitivity was similar atboth temperatures. We conclude that1) insensitivity to hypoxiaindicates that rhythmic discharge does not reflect gasping behavior,2) increased temperature altersrespiratory discharge, and 3)central pH/CO₂ sensitivity isunaffected by temperature in this preparation (i.e.,Q₁₀ ~1.0).

     

Alterations in the surface properties of lung surfactant in the torpid marsupial Sminthopsis crassicaudata

Lopatko, Olga V., Sandra Orgeig, Christopher B. Daniels, andDavid Palmer. Alterations in the surface propertiesof lung surfactant in the torpid marsupial Sminthopsiscrassicaudata. J. Appl.Physiol. 84(1): 146-156, 1998.Torpor changes thecomposition of pulmonary surfactant (PS) in the dunnartSminthopsis crassicaudata [C.Langman, S. Orgeig, and C. B. Daniels. Am. J. Physiol. 271 (Regulatory IntegrativeComp. Physiol. 40): R437-R445, 1996]. Herewe investigated the surface activity of PS in vitro. Five micrograms ofphospholipid per centimeter squared surface area of whole lavage (frommice or from warm-active, 4-, or 8-h torpid dunnarts) were applieddropwise onto the subphase of a Wilhelmy-Langmuir balance at 20°Cand stabilized for 20 min. After 4 h of torpor, the adsorption rateincreased, and equilibrium surface tension (ST_eq), minimal surface tension(ST_min), and the %areacompression required to achieveST_min decreased, compared with thewarm-active group. After 8 h of torpor,ST_min decreased [from 5.2 ± 0.3 to 4.1 ± 0.3 (SE) mN/m]; %area compressionrequired to achieve ST_min decreased (from 43.4 ± 1.0 to 27.4 ± 0.8); the rate ofadsorption decreased; and ST_eqincreased (from 26.3 ± 0.5 to 38.6 ± 1.3 mN/m). ST-areaisotherms of warm-active dunnarts and mice at 20°C had a shoulderon compression and a plateau on expansion. These disappeared on theisotherms of torpid dunnarts. Samples of whole lavage (from warm-activeand 8-h torpor groups) containing 100 µg phospholipid/ml were studiedby using a captive-bubble surfactometer at 37°C. After 8 h oftorpor, ST_min increased (from 6.4 ± 0.3 to 9.1 ± 0.3 mN/m) and %area compressiondecreased in the 2nd (from 88.6 ± 1.7 to 82.1 ± 2.0) and 3rd(from 89.1 ± 0.8 to 84.9 ± 1.8) compression-expansion cycles, compared with warm-active dunnarts. ST-area isotherms ofwarm-active dunnarts at 37°C did not have a shoulder oncompression. This shoulder appeared on the isotherms of torpiddunnarts. In conclusion, there is a strong correlation between in vitrochanges in surface activity and in vivo changes in lipid composition of PS during torpor, although static lung compliance remained unchanged (see Langman et al. cited above). Surfactant from torpid animals ismore active at 20°C and less active at 37°C than that ofwarm-active animals, which may represent a respiratory adaptation tolow body temperatures of torpid dunnarts.

     

Thermal and metabolic responses to cold-water immersion at knee, hip, and shoulder levels

Lee, Dae T., Michael M. Toner, William D. McArdle, IoannisS. Vrabas, and Kent B. Pandolf. Thermal and metabolic responses tocold-water immersion at knee, hip, and shoulder levels.J. Appl. Physiol. 82(5):1523-1530, 1997.To examine the effect of cold-water immersion atdifferent depths on thermal and metabolic responses, eight men (25 yrold, 16% body fat) attempted 12 tests: immersed to the knee (K), hip(H), and shoulder (Sh) in 15 and 25°C water during both rest (R) orleg cycling [35% peak oxygen uptake; (E)] for up to 135 min. At 15°C, rectal (T_re)and esophageal temperatures(T_es) between R and E were notdifferent in Sh and H groups (P > 0.05), whereas both in K group were higher during E than R(P < 0.05). At 25°C,T_re was higher(P < 0.05) during E than R at alldepths, whereas T_es during E washigher than during R in H and K groups.T_re remained at control levels inK-E at 15°C, K-E at 25°C, and in H-E groups at 25°C,whereas T_es remained unchanged inK-E at 15°C, in K-R at 15°C, and in all 25°C conditions (P > 0.05). During R and E, themagnitude of T_re change wasgreater (P < 0.05) than themagnitude of T_es change in Sh andH groups, whereas it was not different in the K group(P > 0.05). Total heat flow wasprogressive with water depth. During R at 15 and 25°C, heatproduction was not increased in K and H groups from control level(P > 0.05) but it did increase in Shgroup (P < 0.05). The increase inheat production during E compared with R was smaller(P < 0.05) in Sh (121 ± 7 W/m² at 15°C and 97 ± 6 W/m² at 25°C) than in H (156 ± 6 and 126 ± 5 W/m²,respectively) and K groups (155 ± 4 and 165 ± 6 W/m², respectively). These datasuggest that T_re andT_es respond differently duringpartial cold-water immersion. In addition, water levels above knee in15°C and above hip in 25°C cause depression of internal temperatures mainly due to insufficient heat production offsetting heatloss even during light exercise.

     

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.

     

A role for gastrointestinal endotoxins in enhancement of heat tolerance by physical fitness

Sakurada, Sotaro, and J. Robert S. Hales. A role forgastrointestinal endotoxins in enhancement of heat tolerance by physical fitness. J. Appl. Physiol.84(1): 207-214, 1998.To further elucidate mechanisms underlyingthe higher heat tolerance of physically fit compared with sedentarypeople, we have investigated the possibility that endotoxins (ofgastrointestinal origin) act, as in the normal development of fever, toraise body temperature and therefore reduce heat tolerance. In aninitial series of experiments, five physically fit and four sedentarysheep were exposed twice at rest to an environment of 42/35°C(dry/wet bulb temperature). When animals were given normal saline iv,rectal temperature (T_re) rose at a significantly higherrate in sedentary than in fit animals; this confirms that heattolerance is improved by physical fitness. Treatment withiv indomethacin did not affect the rate of rise of T_re infit animals. In sedentary animals, however, T_re was loweredto approximate that of fit animals. Because indomethacin blocksprostaglandin pathways involved in endotoxin-induced fever, theindomethacin-induced improvement of heat tolerance of sedentary but notfit animals supports the contention that endotoxins play a role indetermining that difference in heat tolerance. In a second series ofexperiments, quantitative cardiovascular measurements were made byusing radioactive microspheres. Under normothermic conditions, bloodflows in the brain, ileum, and diaphragm were higher in fit than insedentary animals. During hyperthermia up to T_re of42°C (in a 42/39°C environment), fit compared with sedentary animals exhibited 1) a greaterincrease in cardiac output, 2) anincrease in blood flow through arteriovenous anastomoses to higher andbetter maintained levels, 3) lessreduction in blood flow to the ileum, and4) greater increase in blood flowsto the myocardium, turbinates, nasal mucosa, and respiratorymuscles. Endotoxins are likely to come from the gut lumen,because reduction of gut blood flow forms part of the normal responseto heat stress. We suggest that improvement of heat tolerance byphysical fitness is caused by a greater cardiovascular capacity thatpermits not only greater perfusion of heat-loss tissues but themaintenance of a better gastrointestinal tract blood supply, therebybetter maintaining the normal barrier to movement of endotoxins from gut lumen to plasma. Sedentary people, with their lower cardiovascular capacity, redistribute more blood flow away from the gut during environmentally induced hyperthermia, thus allowing endotoxin-induced fever to aggravate hyperthermia.

     

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.

     

Enhancement of signal quality in esophageal recordings of diaphragm EMG

Sinderby, Christer A., Jennifer C. Beck, Lars H. Lindström, and Alejandro E. Grassino. Enhancement of signalquality in esophageal recordings of diaphragm EMG. J. Appl. Physiol. 82(4): 1370-1377, 1997.The cruraldiaphragm electromyogram (EMGdi) is recorded from a sheet of muscle,the fiber direction of which is mostly perpendicular to an esophagealbipolar electrode. The region from which the action potentials areelicited, the electrically active region of the diaphragm(EAR_di) and the center of this region (EAR_{di ctr}) mayvary during voluntary contractions in terms of their position withrespect to an esophageal electrode. Depending on the bipolarelectrode's position with respect to theEAR_{di ctr}, the EMGdi isfiltered to different degrees. The objectives of the present study wereto reduce these filtering effects on the EMGdi by developing ananalysis algorithm referred to as the "double-subtraction technique." The results showed that changes in the position of theEAR_{di ctr} by ±5 mm withrespect to the electrode pairs located 10 mm caudal and 10 mm cephaladprovided a systematic variation in the EMG power spectrumcenter-frequency values by ±10%. The double-subtraction techniquereduced the influence of movement of theEAR_{di ctr} relative to theelectrode array on EMG power spectrum center frequency and root meansquare values, increased the signal-to-noise ratio by 2 dB, andincreased the number of EMG samples that were accepted by the signalquality indexes by 50%.

     

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.

     

Ultrasound evaluation of piglet diaphragm function before and after fatigue

Kocis, Keith C., Peter J. Radell, Wayne I. Sternberger, JaneE. Benson, Richard J. Traystman, and David G. Nichols. Ultrasound evaluation of piglet diaphragm function before and after fatigue. J. Appl. Physiol. 83(5):1654-1659, 1997.Clinically, a noninvasive measure of diaphragmfunction is needed. The purpose of this study is to determine whetherultrasonography can be used to 1)quantify diaphragm function and 2)identify fatigue in a piglet model. Five piglets were anesthetized withpentobarbital sodium and halothane and studied during the followingconditions: 1) baseline (spontaneous breathing); 2) baseline + CO₂ [inhaledCO₂ to increase arterial PCO₂ to 50-60 Torr (6.6-8kPa)]; 3) fatigue + CO₂ (fatigue induced with 30 minof phrenic nerve pacing); and 4)recovery + CO₂ (recovery after 1 hof mechanical ventilation). Ultrasound measurements of the posteriordiaphragm were made (inspiratory mean velocity) in the transverseplane. Images were obtained from the midline, just inferior to thexiphoid process, and perpendicular to the abdomen. M-mode measures weremade of the right posterior hemidiaphragm in the plane just lateral tothe inferior vena cava. Abdominal and esophageal pressures weremeasured and transdiaphragmatic pressure (Pdi) was calculated duringspontaneous (Sp) and paced (Pace) breaths. Arterial blood gases werealso measured. Pdi(Sp) and Pdi(Pace)during baseline + CO₂ were 8 ± 0.7 and 49 ± 11 cmH₂O, respectively, anddecreased to 6 ± 1.0 and 27 ± 7 cmH₂O,respectively, during fatigue + CO₂. Mean inspiratory velocityalso decreased from 13 ± 2 to 8 ± 1 cm/s during theseconditions. All variables returned to baseline during recovery + CO₂. Ultrasonography can beused to quantify diaphragm function and identify piglet diaphragm fatigue.

     

Windchill and the risk of tissue freezing

Danielsson, Ulf. Windchill and the risk of tissuefreezing. J. Appl. Physiol. 81(6): 2666-2673, 1996.Low air temperatures and high wind speeds are associated with anincreased risk of freezing of the exposed skin. P. A. Siple and C. F. Passel (Proc. Am. Phil. Soc. 89: 177-199, 1945) derivedtheir windchill index from cooling experiments on a water-filledcylinder to quantify the risk of frostbite. Their results arereexamined here. It is found that their windchill index does notcorrectly describe the convective heat transfer coefficient(h_c) for such a cylinder; theeffect of the airspeed (v) isunderestimated. New risk curves have been developed, based on theconvection equations valid for cylinders in a cross flow,h_c  v^0.62, and tissuefreezing data from the literature. An analysis of the data reveals alinear relationship between the frequency of finger frostbite and thesurface temperature. This relation closely follows a normaldistribution of finger-freezing temperatures, with an SD of 1°C. Asthe skin surface temperature falls from 4.8 to 7.8°C,the risk of frostbite increases from 5 to 95%. These data indicatethat the risk of finger frostbite is minor above an air temperature of10°C, irrespective of v,but below 25°C there is a pronounced risk, even at lowv.

     

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.

     

Inferior pharyngeal constrictor electromyographic activity during permeability pulmonary edema in lambs

Diaz, Véronique, Irenej Kianicka, PatrickLetourneau, and Jean-Paul Praud. Inferior pharyngealconstrictor electromyographic activity during permeability pulmonaryedema in lambs. J. Appl. Physiol. 81(4): 1598-1604, 1996.Newborn mammals exhibit an active expiratory upper airwayclosure during the first hours of extrauterine life. We have recentlyshown that permeability pulmonary edema led to active expiratoryglottic closure in awake newborn lambs while hypoxia (inspiredO₂ fraction 8%; 15 min) did not. In the presentstudy, we tested the hypothesis that expiratory glottic closure wasaccompanied by an increase in pharyngeal constrictor muscle expiratoryelectromyographic (EMG) activity. We studied seven awake nonsedatedlambs aged 8-20 days. Airflow (facial mask + pneumotachograph),blood gases (arterial catheter), and EMG activity of both thethyroarytenoid muscle (a glottic adductor) and the inferior pharyngealconstrictor muscle were recorded before and after intravenous injectionof halothane (0.05 ml/kg) to induce a permeability pulmonary edema. Acentral apnea (duration 15 s to 5 min) with continuous thyroarytenoidand inferior pharyngeal constrictor activity was observed withinseconds after halothane injection. One lamb died despite rescuingmaneuvers. An expiratory phasic thyroarytenoid and inferior pharyngealconstrictor muscle activity with simultaneous zero airflow graduallytook place and, by 30 min after halothane injection, was present ateach expiration in the six remaining lambs. Expiratory glottic andpharyngeal constrictor muscle EMG activity was subsequently presentduring the whole study period (1.5-5 h), even after correction ofthe initial hypoxia. Permeability lung edema was present at postmortem examination in all seven lambs. We conclude that a permeability pulmonary edema induced by intravenous halothane in nonsedated lambsenhances both glottic and pharyngeal constrictor muscle expiratory EMG.We hypothesize that expiratory contraction of the inferior pharyngealconstrictor muscle could participate in the active expiratory upperairway closure; this, in turn, might improve alveolocapillary gasexchange by increasing the end-expiratory lung volume.

     

Recovery from mild hypothermia can be accelerated by mechanically distending blood vessels in the hand

Peripheral vasoconstriction decreases thermalconductance of hypothermic individuals, making it difficult to transferexternally applied heat to the body core. We hypothesizedthat increasing blood flow to the skin of a hypothermic individualwould enhance the transfer of exogenous heat to the body core, therebyincreasing the rate of rewarming. External auditory meatus temperature(T_EAM) was monitored inhypothermic subjects during recovery from general anesthesia. In 10 subjects, heat (45-46°C, water-perfused blanket) was appliedto a single forearm and hand that had been placed in a subatmosphericpressure environment (30 to 40 mmHg) to distend the bloodvessels. Heat alone was applied to control subjects (n = 6). The application ofsubatmospheric pressure resulted in a 10-fold increase in rewarmingrates as determined by changes inT_EAM [13.6 ± 2.1 (SE)°C/h in the experimental group vs. 1.4 ± 0.1°C/h in thecontrol group; P < 0.001]. Inthe experimental subjects, the rate of change ofT_EAM decreased sharply asT_EAM neared the normothermic range.

     

Myoglobin oxygen dissociation by multiwavelength spectroscopy

Schenkman, Kenneth A., David R. Marble, David H. Burns, andEric O. Feigl. Myoglobin oxygen dissociation by multiwavelength spectroscopy. J. Appl. Physiol. 82(1):86-92, 1997.Multiwavelength optical spectroscopy was used todetermine the oxygen-binding characteristics for equine myoglobin.Oxygen-binding relationships as a function of oxygen tension weredetermined for temperatures of 10, 25, 35, 37, and 40°C, at pH 7.0. In addition, dissociation curves were determined at 37°C for pH6.5, 7.0, and 7.5. Equilibration was achieved with a myoglobinsolution, at the desired temperature and pH, and 16 oxygen-nitrogen gasmixtures of known oxygen fraction. Correction for the inevitablepresence of metmyoglobin was made by using a three-component leastsquares analysis and by correcting the end point oxymyoglobin spectrafor the presence of metmyoglobin. ThePO₂ at which myoglobin ishalf-saturated with O₂ (P₅₀) was determined to be 2.39 Torr at pH 7.0 and 37°C. The myoglobin dissociationcurve was well fit by the Hill equation [saturation = PO₂/(PO₂ + P₅₀)].

     

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.

     

Hypothyroidism alters diaphragm muscle development

Sieck, Gary C., Louise E. Wilson, Bruce D. Johnson, andWen-Zhi Zhan. Hypothyroidism alters diaphragm muscle development. J. Appl. Physiol. 81(5):1965-1972, 1996.The impact of hypothyroidism (Hyp) onmyosin heavy chain (MHC) isoform expression, maximum specific force(P_o), fatigability, and maximumunloaded shortening velocity(V_o) wasdetermined in the rat diaphragm muscle (Dia) at 0, 7, 14, 21, and 28 days of age. Hyp was induced by treating pregnant rats with6-n-propyl-2-thiouracil (0.05% indrinking water) beginning at gestational day10 and was confirmed by reduced plasma levels of3,5,3-triiodothyronine and thyroxine. MHC isoforms wereseparated on sodium dodecyl sulfate-polyacrylamide gel electrophoresis gels and analyzed by densitometry. IsometricP_o and fatigue resistance of theDia were measured in vitro at 26°C, andV_o was determined at 15°C with the slack test. Compared with control muscles,expression of MHC-slow was higher and expression of adult fast MHCisoforms was lower in Hyp Dia at all ages. The neonatal isoform of MHC continued to be expressed in the Hyp Dia until day28. At each age,P_o and fatigability were reducedand V_o was slowerin the Hyp Dia. We conclude that Hyp-induced alterations in MHC isoform expression do not fully predict the changes in Dia contractile properties.

     

Effects of Temperature and Water Potential on Germination, Radicle Elongation and Emergence of Mungbean

Controlled environment experiments were performed to determinethe effects of temperature and water potential on germination,radicle elongation and emergence of mungbean (Vigna radiata(L.) Wilczek cv. IPB-M79-17-79). The effects of a range of constant temperatures (15–45°C) and water potentials (0 to –2.2 MPa) on germinationand radicle elongation rates were studied using an osmoticumtechnique, in which seeds were held against a semi-permeablemembrane sac containing a polyethylene glycol solution. Linearrelationships were established between median germination time(Gt₅₀) and water potential at different temperatures, and betweenreciprocal Gt₅₀ (germination rate) and temperature at differentwater potentials. Germination occurred at potentials as lowas –2.2 MPa at favourable temperatures (30–40 °C),but was fastest at 40 °C when water was not limiting, withan estimated base temperature (T_b) of about 10 °C. Subsequentradicle elongation, however, was restricted to a slightly narrowertemperature range and was fastest at 35 °C. The conceptof thermal time was used to develop an equation to model thecombined effects of water potential and temperature on germination.Predictions made using this model were compared with the actualgermination obtained in a related series of experiments in columnsof soil. Some differences observed suggested the additionalimportance of the seed/soil/water contact zone in influencingseed germination in soil. Seedling emergence appeared to reflectfurther the radicle elongation results by occurring within anarrower range of temperatures and water potentials than germination.Emergence had an estimated T_b of 12.6 °C and was fastestat 35 °C. A soil matric potential of not less than about–0.5 MPa at sowing was required to obtain 50% or moreseedling emergence. Key words: Germination, temperature, water potential     

Thermodormancy Release of Celery Seed by Gibberellins, 6-Benzylaminopurine, and Ethephon Applied in Organic Solvent to Dry Seeds

The emergence of celery (Apium graveolens L. cv. Utah 52–70)seeds was promoted by growth regulators when exposed to hightemperatures during the germination period. The growth regulatorswere applied to dry seeds prior to sowing, by means of the organicsolvent dichloromethane (DCM). A mixture of gibberellins A₄and A₇ (GA_4/7) strongly enhanced emergence at a high day-timetemperature of 35°C alternating with night temperaturesof 20°C and 25°C; however, emergence was very poor whenthe night temperature was raised to 30°C. Under the latterregime, only mixtures of GA_4/7 with 6-benzylaminopurine (BA)or with 2-chlorophosphonic acid (ethephon) promoted seed emergence.However, BA and ethephon applied separately or in combinationwere much less effective in enhancing seed emergence withoutthe addition of GA_4/7, under all the temperature regimes.     

Endogenous vasopressin does not mediate hypoxia-induced anapyrexia in rats

The present study was designed to test the hypothesis thatarginine vasopressin (AVP) mediates hypoxia-induced anapyrexia. Therectal temperature of awake, unrestrained rats was measured before andafter hypoxic hypoxia, AVP-blocker injection, or a combination of thetwo. Control animals received saline injections of the same volume.Basal body temperature was 36.52 ± 0.29°C. We observed asignificant (P < 0.05) reduction inbody temperature of 1.45 ± 0.33°C after hypoxia (7% inspiredO₂), whereas systemic andcentral injections of AVP V₁- andAVP V₂-receptor blockers caused nochange in body temperature. When intravenous injection of AVP blockerswas combined with hypoxia, we observed a reduction in body temperatureof 1.49 ± 0.41°C(V₁-receptor blocker) and of 1.30 ± 0.13°C (V₂-receptorblocker), similar to that obtained by application of hypoxia only.Similar results were observed when the blockers were injectedintracerebroventricularly. The data indicate that endogenous AVP doesnot mediate hypoxia-induced anapyrexia in rats.     

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.