Age,smoking habits,heat stress,and their interactive effects with carbon monoxide and peroxyacetylnitrate on man's aerobic power

Metabolic, body temperature, and cardiorespiratory responses of 16 healthy middle-aged (40–57 years) men, 9 nonsmokers and 7 smokers, were obtained during tests of maximal aerobic power at ambient environmental temperatures of 25 ± 0.5 and 35 ± 0.5°C and 20% relative humidity under four conditions: (a) filtered air, FA; (b) 50 ppm carbon monoxide in filtered air, CO; (c) 0.27 ppm peroxyacetylnitrate in filtered air, PAN; and (d) a combination of all three mixtures, PANCO. There was no significant change in maximum aerobic power \(\left( {\dot VO2max} \right)\) related to the presence of air pollutants, although total working time was lowered in the 25°C environment while breathing CO. Older nonsmokers did have a decrement in \(\left( {\dot VO2max} \right)\) while breathing 50 ppm CO, while older smokers failed to show any change. This difference was related to the initial COHb levels of the smokers, who, when breathing this level of ambient CO, had only a 14% increase in COHb over their initial levels in contrast to the 200% increase in the nonsmokers. Smoking habits were the most influential factor affecting the cardiorespiratory responses of these older men to maximal exercise. Regardless of ambient conditions, smokers had a significantly lower (27%) aerobic power than nonsmokers, were breathing closer to their maximal breathing capacities throughout the walk, and had a higher respiratory exchange ratio. While the \(\left( {\dot VO2max} \right)\) of nonsmokers was only 6% less than that of younger nonsmoking males ( \(\bar x\) age = 25 years) working under similar conditions, the aerobic power of the older smokers was 26% lower than that of young smokers ( \(\bar x\) age = 24 years).     

Temperature-dependent development of cardiac activity in unrestrained larvae of the minnow Phoxinus phoxinus

The minnow (Phoxinus phoxinus) was raised up to the stage of swim bladder inflation at temperatures between 10 degrees C and 25 degrees C, and the time of development significantly decreased at higher temperatures. Accordingly, initiation of cardiac activity was observed at day 2 in 25 degrees C animals and at day 4 in 12.5 degrees C animals. Only a minor increase in body mass was observed during the incubation period, and, at the end of the incubation period, animals raised at 25 degrees C did not have a significantly lower body mass compared with animals raised at 15 degrees C. Metabolic activity, determined as the rate of oxygen consumption of a larva, increased from 3.3 to 19.5 nmol/h during development at 15 degrees C and from 5.6 to 47.6 nmol/h during development at 25 degrees C. Heart rate showed a clear correlation to developmental stage as well as to developmental temperature, but at the onset of cardiac activity, diastolic ventricular volume and also stroke volume were higher at the lower temperatures. Furthermore, stroke volume increased with development, except for the group incubated at 12.5 degrees C, in which stroke volume decreased with development. Initial cardiac output showed no correlation to incubation temperature. Although metabolic activity increased severalfold during development from egg to the stage of swim bladder inflation at 15 degrees C and at 25 degrees C, weight-specific cardiac output increased only by approximately 40% with proceeding development. At 12.5 degrees C, cardiac output remained almost constant until opening of the swim bladder. The data support the notion that oxygen transport is not the major function of the circulatory system at this stage of development. The changes in heart rate with temperature appear to be due to the intrinsic properties of the pacemaker; there was no indication for a regulated response.     

Effect of hypercapnia on thermoregulation at high ambient temperature

The reported investigations were carried out on rabbits exposed for three hours to ambient temperature of 25 degrees C or 35 degrees breathing athmospheric air (controls) or gas mixtures containing 4% or 7% of CO2. During the exposure to 35 degrees C in rabbits breathing the gas mixture with 7% of CO2 the rise of rectal temperature was significantly greater, heat elimination from the auricular surface was increased, whereas the oxygen uptake was increased insignificantly. In tracheostomized rabbits breathing the gas mixture with 7% of CO2 at 32 degrees C the respiratory rate decreased but the respiration volume increased as compared with the animals breathing atmospheric air. It seems that the hyperthermic effect of hypercapnia demonstrated in this work can be attributed to the impairment of heat elimination through the upper airways due to an inhibition of thermal panting.     

Cardiovascular reactions to cold exposures differ with age and gender

This study was conducted since virtually no information was available concerning age- and gender-related differences in cardiovascular adjustments to cold exposure. Men and women between the ages of 20 and 30 and 51 and 72 yr, wearing swim suits, rested for 2 h in 28, 20, 15, and 10 degrees C ambient temperatures (Ta), with 40% relative humidity. Cardiac output (Qc) and stroke volumes (Qs) were higher in younger than older subjects regardless of Ta. Cardiac output was not influenced by gender, but all cold exposures resulted in increased Qs and decreased heart rate in men but not women. Regardless of age or gender, Qc increased about 10% only during exposure to 10 degrees C. Cold exposure resulted in minimal increases in the mean systolic and diastolic pressures (Pa) of the younger subjects. The Pa of older subjects were higher than in the young during 28 degrees C exposures and increased during all cold exposures. Total peripheral resistance and forearm blood flows were higher in older than young subjects exposed to cold. Total peripheral resistance, systolic and diastolic Pa, and finger and forearm blood flows were not affected by gender, but hand plus forearm blood flows were higher in men than women exposed to 28 degrees C. Although Qc appeared adequate to meet increased oxygen demands of shivering in the older subjects, rising Pa may become limiting in extended exposures. A similar response in hypertensive or angina-prone individuals may result in some untoward responses.     

Combined effects of ozone exposure and ambient heat on exercising females

Ten aerobically trained young adult females exercised continuously at 66% of maximum O2 uptake for 1 h while exposed orally to filtered air and 0.15 and 0.30 parts per million (ppm) ozone (O3) in both moderate (24 degrees C) and hot (35 degrees C) ambient conditions. Exposure to 0.30 ppm O3 induced significant impairment in forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1.0), and other pulmonary function variables. Exercise respiratory frequency (fR) increased, whereas tidal volume and alveolar volume (VA) decreased with 0.30 ppm O3 exposure. Significant interactions of O3 and ambient heat were obtained for fR and VA, whereas FVC and FEV1.0 displayed a trend toward an O3-temperature interaction. Although expired ventilation increased, the interactions could not be ascribed to a greater O3 effective dose in the 35 degrees C exposures. However, subjective discomfort increased with both O3 and heat exposure such that three subjects ceased exercise prematurely when O3 and ambient heat were combined. We conclude that accentuation of subjective limitations and certain physiological alterations by ambient heat coinciding with photochemical oxidant episodes is likely to result in more severe impairment of exercise performance, although the mechanisms remain unclear.     

Aerobic power as a factor in women's response to work in hot environments.

Twelve young women, athletes (n = 6) and nonathletes (n = 6), walked on a treadmill at loads equivalent to approximately 30% Vo2 max for two 50-min periods in three environments: 1) 28 degrees C, 45% rh, 2) 35 degrees C, 65% rh, and 3) 48 degrees C, 10% rh. There were no differences between groups in rectal temperature, heart rate, evaporative heat loss, or mean skin temperature at 28 or 35 degrees C or during the first work period in the 48 degrees C environment. However, a significantly lower cardiac output (Q) and stroke volume (SV) observed for nonathletes by the 46th min of work at 48 degrees C may explain why no nonathletes were able to complete a 2nd h of work while four of six athletes successfully finished the period. It appears that in conditions of severe heat stress (48 degrees C) athletes were able to maintain a cardiac output sufficient to meet the metabolic requirements and the large increase in peripheral blood flow for a longer period of time than nonathletes.     

The influence of hyperventilation on the measurement of stroke volume using a CO2 rebreathing method

The influence of different degrees of hyperventilation on stroke volume measured with a CO2 rebreathing method was studied in seven normal subjects and seven patients with aortic regurgitation. Hyperventilation was initially performed with a rebreathing rate of 30 min-1 and a tidal volume corresponding to 60% of the subject's vital capacity. The tidal volume was then randomly decreased or increased by 0.5 and 1.01 and the procedure was repeated with rebreathing rates of 25 and 35 min-1. The possible influence of habituation to repeated measurements was tested in seven of the subjects. No significant differences in response to hyperventilation of stroke volume, cardiac output or heart rate were found between normal subjects and patients. When the tidal volume was increased, there was a significant increase in heart rate and also an increase in cardiac output, which was significant when comparing measurements performed with the lowest and highest tidal volumes. When comparing initial and final measurements, there was a significant decrease in heart rate and a tendency to decrease in cardiac output. Stroke volume was not affected by variations in rebreathing rate from 25 to 35 min-1 or tidal volume changes of +/- 0.51 and was also unaffected by repeated measurements.     

Thermal, metabolic, and cardiovascular responses to various degrees of cold stress.

The metabolic, thermal, and cardiovascular responses of two male Caucasians to 1 2 h exposure to ambient temperature ranging between 28 degrees C and 5 degrees C were studied and related to the respective ambient temperatures. The metabolic heat production increased linearly with decreasing ambient temperature, where heat production (kcal times m- minus 2 times h- minus 1) = minus 2.79 Ta degrees C + 103.4, r = -0.97, P smaller than 0.001. During all exposures below 28 degrees C, the rate of decrease in mean skin temperature (Tsk) was found to be an exponential function dependent upon the ambient temperature (Ta) and the time of exposure. Reestablishment of Tsk steady state occurred at 90-120 min of exposure, and the time needed to attain steady state was linearly related to decreasing Ta. The net result was that a constant ratio of 1.5 of the external thermal gradient to the internal thermal gradient was obtained, and at all experimental temperatures, the whole body heat transfer coefficient remained constant. Cardiac output was inversely related to decreasing Ta, where cardiac output (Q) = minus 0.25 Ta degrees C + 14.0, r = minus 0.92, P smaller than 0.01. However, the primary reason for the increased Q, the stroke output, was also described as a third-order polynomial, although the increasing stroke volume throughout the Ta range (28-5 degrees C) was linearly related to decreasing ambients. The non-linear response of this parameter which occurred at 20 degrees C larger than or equal to Ta larger than or equal to 10 degrees C suggested that the organism's cardiac output response was an integration of the depressed heart rate response and the increasing stroke output at these temperatures.     

An inquiry into the role of cardiac filling pressure in acclimatization to heat

During the first exposure of exercising subjects to hot environments (30-50 degrees C), cardiac output, heart rate, and body temperature increase over that seen in cool environments, while stroke volume decreases. If daily heat exposures occur, during the second heat exposure, heart rates and rectal temperatures are decreased from day 1 while cardiac output is maintained. This decrease in physiological strain occurs with little or no increase in evaporative heat loss. The alleviating agent appears to be an expansion of plasma volume. Several brief studies have indicated decreases in cardiac filling pressure during exercise in heat, and though inferential, it appears that the progressive increase in plasma volume during the first five to six days of heat exposure assists in maintaining cardiac filling pressure. Later, with increased evaporative heat loss due to increased sweat secretion, the mechanism of supplying increased volume to maintain cardiac filling is changed; fluid is transferred from extravascular to intravascular compartment, thus protecting venous return and cardiac filling pressure. These statements are based on limited data, and there is need of experiments designed to confirm or deny certain conclusions as to the role of cardiac filling pressure in acclimatization to heat.     

Decrease in heart rates by artificial CO2 hot spring bathing is inhibited by beta1-adrenoceptor blockade in anesthetized rats.

To investigate the effects of carbon dioxide (CO2) hot spring baths on physiological functions, head-out immersion of urethane-anesthetized, fursheared male Wistar rats was performed. Animals were immersed in water (30 or 35 degrees C) with high-CO2 content ( approximately 1,000 parts/million; CO2-water). CO2-water for bathing was made by using an artificial spa maker with normal tap water and high-pressure CO2 from a gas cylinder. When a human foot was immersed for 10 min in the CO2-water at 35 degrees C, the immersed skin reddened, whereas skin color did not change in normal tap water at the same temperature. Arterial blood pressure, heart rate (HR), underwater skin tissue blood flow, and temperatures of the colon and immersed skin were continuously measured while animals were immersed in a bathtub of water for approximately 30 min at room temperature (26 degrees C). Immersed skin vascular resistance, computed from blood pressure and tissue blood flow, was significantly lower in the CO2-water bath than in tap water at 30 degrees C, but no differences were apparent at 35 degrees C. HR of rats in CO2-water was significantly slower than in tap water at 35 degrees C. Decreased HR in CO2-water was inhibited by infusion of atenolol (beta1-adrenoceptor blocker), but it was unaffected by atropine (muscarinic cholinoceptor blocker). Theses results suggest that bradycardia in CO2 hot spring bathing is caused by inhibition of the cardiac sympathetic innervation. This CO2-water maker should prove a useful device for acquiring physiological evidence of balneotherapy.     

Role of tracheal and bronchial circulation in respiratory heat exchange

Due to their anatomic configuration, the vessels supplying the central airways may be ideally suited for regulation of respiratory heat loss. We have measured blood flow to the trachea, bronchi, and lung parenchyma in 10 anesthetized supine open-chest dogs. They were hyperventilated (frequency, 40; tidal volume 30-35 ml/kg) for 30 min or 1) warm humidified air, 2) cold (-20 degrees C dry air, and 3) warm humidified air. End-tidal CO2 was kept constant by adding CO2 to the inspired ventilator line. Five minutes before the end of each period of hyperventilation, measurements of vascular pressures (pulmonary arterial, left atrial, and systemic), cardiac output (CO), arterial blood gases, and inspired, expired, and tracheal gas temperatures were made. Then, using a modification of the reference flow technique, 113Sn-, 153Gd-, and 103Ru-labeled microspheres were injected into the left atrium to make separate measurements of airway blood flow at each intervention. After the last measurements had been made, the dogs were killed and the lungs, including the trachea, were excised. Blood flow to the trachea, bronchi, and lung parenchyma was calculated. Results showed that there was no change in parenchymal blood flow, but there was an increase in tracheal and bronchial blood flow in all dogs (P less than 0.01) from 4.48 +/- 0.69 ml/min (0.22 +/- 0.01% CO) during warm air hyperventilation to 7.06 +/- 0.97 ml/min (0.37 +/- 0.05% CO) during cold air hyperventilation.     

Physiological responses of aged men to head-up tilt during heat exposure

The effects of age on cardiovascular and thermoregulatory responses to passive tilting were investigated using six old (61-73 yr) and 10 young (21-39 yr) unacclimatized men. Experiments were carried out at 26 degrees C and after exposure to 40 degrees C and 40% relative humidity for 105 min. Continuous measurements of esophageal (Tes) and mean skin (Tsk) temperatures and heart rate (HR) were recorded. Other variables studied included blood pressure (BP), forearm blood flow (FBF), and cardiac output (CO), which were measured at 4- to 5-min intervals. Measurements were made in the supine position and after 70 degrees head-up tilt for 15 min. Cardioacceleration during the tilt test was greater in the young men than in the old. Other cardiovascular responses of the old men to orthostatism were qualitatively similar to that of the young except for FBF and forearm vascular conductance. The old men did not show significant changes in FBF during tilting, suggesting a deterioration in the sympathetic nervous reflex in the aged. However, other circulatory adaptations seemed to overcome this deficiency resulting in orthostatic tolerance similar to that of the young. During head-up tilt at 26 and 40 degrees C, Tes of both age groups increased. This may reflect a decrease in conductive heat transfer presumably due to diminished blood flow to the periphery.     

正常人左心室功能指标的参考值及其预计公式的初步研究报告*

目的: 当前评估左心室容量和功能仍常用正常值范围,个体化分析也仅使用体表面积进行校正。尚缺少个体化因素相关的大样本参考值和预计公式。方法: 本研究纳入美国加州洛杉矶县南湾地区1200名健康志愿者,其中男807女393,年龄20岁-94岁,心脏CT造影（CTA）,经过高精度三维成像技术处理,计算左心室容积在收缩和舒张过程中的连续动态变化,测定左心室（LV）容量和功能指标：舒张末期容积（EDV)、收缩末期容积(ESV)、每搏输出量(SV)、射血分数(EF)和心输出量(CO)。将以上指标与一般特征指标进行多因素相关分析,以探索正常人预计值计算公式。结果: 男性除LVEF小于女性外（P<0.001）,其余各指标均大于女性（P<0.001）。多元线性回归分析提示, 性别、年龄、身高和体质量均为EDV、ESV、SV的独立影响因子(P<0.001); 而CO仅受年龄、性别、体质量显著影响(P<0.001),但与身高无关(P>0.05)。CO的预测公式CO (L·min^-1)= 6.963+0.446(Male) -0.037×年龄(yr)+0.013×体质量(kg)。结论: 性别、年龄、身高、体质量均影响左心室容量和功能,建立预测值计算公式,对心血管疾病的无创评估和个体化精准医疗具有重要参考价值。     

Effects of phosphine on the neural regulation of gas exchange in Periplaneta americana

Phosphine is used for fumigating stored commodities, however an understanding of the physiological response to phosphine in insects is limited. Here we show how the central pattern generator for ventilation in the central nervous system (CNS) responds to phosphine and influences normal resting gas exchange. Using the American cockroach, Periplaneta americana, that perform discontinuous gas exchange (DGE) at rest, we simultaneously measure ventilatory nervous output from the intact CNS, VCO(2) and water loss from live specimens. Exposure to 800 ppm phosphine at 25 degrees C for 2 h (n=13) during recording did not cause any mortality or obvious sub-lethal effects. Within 60 s of introducing phosphine into the air flow, all animals showed a distinct CNS response accompanied by a burst release of CO(2). The initial ventilatory response to phosphine displaced DGE and was typically followed by low, stable and continuous CO(2) output. CNS output was highest and most orderly under normoxic conditions during DGE. Phosphine caused a series of ventilatory CNS spikes preceding almost complete cessation of CNS output. Minimal CNS output was maintained during the 2 h normoxic recovery period and DGE was not reinstated. VCO(2) was slightly reduced and water loss significantly lower during the recovery period compared with those rates prior to phosphine exposure. A phosphine narcosis effect is rejected based on animals remaining alert at all times during exposure.     

The effect of progressive hypoxia on respiration in the dogfish (scyliorhinus canicula) at different seasonal temperatures.

1. Dogfish were acclimated to 7, 12 or 17 degrees C and exposed to progressive hypoxia at the temperature to which they had been acclimated. During normoxia, the Q10 values for oxygen uptake, heart rate, cardiac output and respiratory frequency over the full 10 degrees C range were: 2.1, 2.1, 2.1 and 2.5 respectively. Increased acclimation temperature had no effect on cardiac stroke volume or systemic vascular resistance, although there was a decrease in branchial vascular resistance, pHa and pHv. 2. Progressive hypoxia had no effect on heart rate or oxygen uptake at 7 degrees C, whereas at 12 degrees C and 17 degrees C there was bradycardia, and a reduction in O2 uptake, with the critical oxygen tension for both variables being higher at the higher temperature. Cardiac stroke volume increased during hypoxia at each temperature, such that cardiac output did not change significantly at 12 and 17 degrees C. Neither pHa nor pHv changed significantly during hypoxia at any of the three temperatures. 3. The influence of acclimation temperatures on experimental results from poikilotherms is pointed out. Previously-published results show quantitative differences. 4. The significance of the present results with respect to the functioning and location of oxygen receptors is discussed. It is argued that as the metabolic demand and critical oxygen tension of the whole animal are increased at high acclimation temperatures the same must be the case with the oxygen receptor. This would raise the stimulation threshold and could account for the bradycardia seen during hypoxia becoming manifest at higher values of PI,O2, Pa,O2 and Pv,O2 as the acclimation temperature is raised.     

Cardiovascular response to acute hypoxemia induced by prolonged breath holding in air

Prolonged breath hold (BH) represents a valid model for studying the cardiac adaptation to acute hypoxemia in humans. Cardiac magnetic resonance (CMR) allows a three-dimensional, high-resolution, noninvasive, and nonionizing anatomical and functional evaluation of the heart. The aim of the study was to assess the adaptation of the cardiovascular system to prolonged BH in air. Ten male volunteer diving athletes (age 30 +/- 6 yr) were studied during maximal BH duration with CMR. Four epochs were studied: I, rest; II and III, intermediate BH; and IV, peak BH. Oxygen saturation (So(2)), heart rate (HR), blood pressure (BP), systemic vascular resistance (VR), end-diastolic (EDV) and end-systolic volumes (ESV), stroke volume (SV), cardiac output (CO), ejection fraction (EF), maximal elastance index (EL), systolic wall thickening (SWT), and end-systolic wall stress (ESWS) of the left ventricle (LV) were measured in all four BH epochs. Average BH duration was 3.7 +/- 0.3 min. So(2) was reduced (I: 97 +/- 0.2%, range 96-98%, vs. IV: 84 +/- 2.0%, range 76-92%; P < 0.00001). BP, EDV, ESV, SV, CO, and ESWS linearly increased from epochs I to IV, whereas EF, EL, and SWT showed an opposite behavior, decreasing from resting to epoch IV (all trends are P < 0.01). During prolonged BH in air, a marked enlargement of the LV chamber occurs in healthy diving athletes. This response to acute hypoxemia allows SV,CO, and arterial pressure to be maintained despite the severe reduction in LV contractile function.     

The effect of modified atmospheres on the survival of the eggs of four storage mite species

The results of a laboratory investigation into the effects of modified atmospheres (MA) on the eggs of mite pests of grain and cheese are presented. Four species of astigmatid mite were tested; Acarus farris (Oudemans). A. siro L., Lepidoglyphus destructor (Schrank) and Tyrophagus longior (Gervais). All are found in many habitats including grain and cheese stores. Three low oxygen (O2) MA mixtures were used, based on carbon dioxide (CO2), nitrogen (N2) or simulated burner gas (0.5 or 2% O2, 10% CO2, balance N2) plus 60% CO2 in air (8% O2). The mites were exposed at 15 degrees C and 80% r.h., a combination of conditions that occurs at the surface of stored grain during the autumn which promotes mite population growth. The exposure periods required to prevent egg hatch for each species in every mixture are given. Tyrophagus longior was the most tolerant species, followed by A. siro and A. farris, with L. destructor the most susceptible. Burner gas was the most effective mixture overall with 0.5% O2 but with an increase in the O2 level to 2% for all the mixtures, CO2 became the more effective control agent. With 60% CO2 in air some loss of efficacy was observed against the three most tolerant species and even more so for L. destructor. Sublethal exposures to MAs for at least 4 days in L. destructor, 6 days in A. farris and A. siro and 8 days for T. longior caused a delay in egg hatch.     

Ventilatory baroreflex sensitivity in humans is not modulated by chemoreflex activation

Increasing arterial blood pressure (AP) decreases ventilation, whereas decreasing AP increases ventilation in experimental animals. To determine whether a "ventilatory baroreflex" exists in humans, we studied 12 healthy subjects aged 18-26 yr. Subjects underwent baroreflex unloading and reloading using intravenous bolus sodium nitroprusside (SNP) followed by phenylephrine ("Oxford maneuver") during the following "gas conditions:" room air, hypoxia (10% oxygen)-eucapnia, and 30% oxygen-hypercapnia to 55-60 Torr. Mean AP (MAP), heart rate (HR), cardiac output (CO), total peripheral resistance (TPR), expiratory minute ventilation (V(E)), respiratory rate (RR), and tidal volume were measured. After achieving a stable baseline for gas conditions, we performed the Oxford maneuver. V(E) increased from 8.8 ± 1.3 l/min in room air to 14.6 ± 0.8 l/min during hypoxia and to 20.1 ± 2.4 l/min during hypercapnia, primarily by increasing tidal volume. V(E) doubled during SNP. CO increased from 4.9 ± .3 l/min in room air to 6.1 ± .6 l/min during hypoxia and 6.4 ± .4 l/min during hypercapnia with decreased TPR. HR increased for hypoxia and hypercapnia. Sigmoidal ventilatory baroreflex curves of V(E) versus MAP were prepared for each subject and each gas condition. Averaged curves for a given gas condition were obtained by averaging fits over all subjects. There were no significant differences in the average fitted slopes for different gas conditions, although the operating point varied with gas conditions. We conclude that rapid baroreflex unloading during the Oxford maneuver is a potent ventilatory stimulus in healthy volunteers. Tidal volume is primarily increased. Ventilatory baroreflex sensitivity is unaffected by chemoreflex activation, although the operating point is shifted with hypoxia and hypercapnia.     

Respiratory and behavioral effects of ozone on a lizard and a frog

Ozone at concentrations found in urban air pollution is known to have significant physiological effects on humans and other mammals. Exposure of the lizard, Sceloporus occidentalis, to 0.6 ppm ozone for 4 h at 25 degrees C induced 1.6 degrees C of behavioral hypothermia immediately following exposure, but selected body temperature recovered to control 35.3 degrees C the next day. Lizards exposed at 35 degrees C to 0.6 ppm ozone for 4 h selected body temperatures 1.9 degrees C below controls after exposure, and the behavioral hypothermic response persisted and increased to 3.3 degrees C the following day. Four-hour exposures of the frog, Pseudacris cadaverina, to 0.2 to 0.8 ppm ozone resulted in concentration-dependent alterations of respiration including depression of lung ventilation and oxygen consumption and the adoption of a low profile posture that reduced the exposed body surface. Ozone levels in wilderness habitats downwind of urban sources can potentially have stressful physiological effects on wildlife. Defensive physiological and behavioral reactions to ozone exposure may interfere with routine activities, and oxidant air pollution may be in part responsible for observed wildlife population declines.     

Cold tolerance and the regulation of cardiac performance and hemolymph distribution in Maja squinado (Crustacea: decapoda)

Elevated Mg(2+) levels in the hemolymph ([Mg(2+)](HL)) of brachyuran crabs have recently been demonstrated to limit cold tolerance by reducing motor and circulatory activity. Therefore, the limiting function of elevated [Mg(2+)](HL) on circulatory performance and arterial hemolymph flow was investigated by the pulsed-Doppler technique in the spider crab Maja squinado during progressive cooling from 12 degrees to 0 degrees C. [Mg(2+)](HL) were reduced from control levels of 39.9 mmol L(-1) to levels of 6.1 mmol L(-1) by incubation in magnesium reduced seawater. At 12 degrees C cardiac output was 13.9+/-2.4 mL kg(-1) min(-1) and stroke volume 0.2+/-0.04 mL kg(-1) min(-1) in control animals. In [Mg(2+)](HL)-reduced animals cardiac output increased to 43.6+/-5.0 mL kg(-1) min(-1) and stroke volume rose to 0.6+/-0.1 mL kg(-1) min(-1). Temperature reduction in control animals revealed a break point at 8 degrees C linked to a major redirection of hemolymph flow from lateral to sternal and hepatic arteries. Cardiac output and heart rate dropped sharply during cooling until transiently constant values were reached. Further heart rate reduction occurred below 4.5 degrees C. Such a plateau was not detected in [Mg(2+)](HL)-reduced animals where the break point decreased to 6 degrees C, also indicated by a sharp drop in heart rate and cardiac output and the redirection of hemolymph flow. It is concluded that progressive cooling brings the animals from a temperature range of optimum cardiac performance into a deleterious range when aerobic scope for activity falls before critical temperatures are reached. Reduction of [Mg(2+)](HL) shifts this transition to lower temperatures. These findings support a limiting role for [Mg(2+)](HL) in thermal tolerance.