Redistribution of cardiac output in anesthetized thermally dehydrated rats

Cardiac output (CO) and its distribution were studied in dehydrated (37 degrees C) anesthetized (Na thiopentone) rats prior to and following heat acclimation (at 34 degrees C), using 57Co 15 micron microspheres. In non-acclimated dehydrated rats, CO decreased while heart rate (HR) increased significantly. Following acclimation CO increased without any change in HR; during dehydration CO remained elevated together with a significant increase in HR. In non-acclimated rats at low dehydration blood perfusion to peripheral thermoregulatory areas increased while perfusion of splanchnic area decreased; at high dehydration level peripheral blood flow decreased whereas splanchnic blood flow was augmented. In acclimated dehydrated rats, CO distribution to thermoregulatory areas did not change while perfusion of the splanchnic area decreased. It is suggested that following acclimation, the increased CO contributes to maintenance of thermoregulatory peripheral blood flow; in non-acclimated rats severe dehydration leads to augmented blood flow in the permeable splanchnic vascular bed, increasing efflux of plasma protein and failure of plasma volume conservation.     

Plasma volume regulation during heat stress: albumin synthesis vs capillary permeability. A comparison between desert and non-desert species

1. Plasma albumin synthesis was measured in rats and sand rats (Psammomys obesus) during heat acclimation (34 degrees C) and following thermal dehydration (37 degrees C) using 3H 1-leucine as a tracer. 2. In rats, heat acclimation resulted in 48% reduction in albumin synthesis. In sand rats synthesis increased by 160%. Both species achieved a new stabilization of the albumin synthetic system on the 5th day of acclimation. 3. Following thermal dehydration albumin synthesis increased in rats and decreased in sand rats. Acclimation did not alter this response. 4. In our dehydrating system plasma volume was maintained via maintenance of adequate albumin mass. In rats, albumin synthesis apparently contributes to this process. In sand rat, vascular permeability rather than albumin synthesis plays this role.     

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

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

Thermoregulation in the meerkat (Suricata suricatta Schreber, 1776)

Tre of the suricates exhibits a marked diurnal rhythm (mean Tre at night 36.3 +/- 0.6 degrees C and 38.3 +/- 0.5 degrees C during the day). Oxygen consumption is lowest at Ta 30-32.5 degrees C (mean 0.365 +/- 0.022 ml O2 g-1 hr-1); this is 42% below the value expected from body mass. At Ta below the TNZ, oxygen uptake rises rapidly, minimal thermal conductance (0.040 ml O2 g-1 h-1 degrees C-1) being 18% above the mass-specific level. Lowest heart rates occur at Ta 30 degrees C (mean 109.6 +/- 9.8 beats min-1) and oxygen pulse is minimal at Ta 30-35 degrees C with 40-45 microliter O2 beat-1. At Ta 15-32.5 degrees C total evaporative water loss is between 0.46-0.63 ml H2O kg-1 hr-1 and increases markedly during heat stress (to a mean of 5.35 ml H2O kg-1 hr-1 at Ta 40 degrees C). This rise of TEWL is mainly attributable to the onset of panting at Ta above 35 degrees C.     

Synthesis of 70K stress protein by human leukocytes: effect of exercise in the heat

To determine whether reinduction of 70,000-Da (70K) stress protein synthesis could be used as an assay for thermal history and/or cellular levels of 70K stress protein in hyperthermic humans, leukocytes were obtained before and after 2 h of exercise and then incubated at 37 or 41 degrees C. Five healthy males completed 2 h of treadmill exercise consisting of running at 4-6 km/h for 30-45 min followed by 75-90 min of walking up a 2-10% grade. This exercise bout was performed by two subjects in hot (46 degrees C, 15% relative humidity) and by five subjects in cooler (30 degrees C, 40% relative humidity) environmental conditions. Exercise resulting in rectal temperature (Tre) less than 40 degrees C did not alter the amount of 70K stress protein synthesized by leukocytes incubated at 41 degrees C. In contrast, exercise resulting in Tre greater than 40 degrees C reduced the amount of 70K stress protein synthesized by leukocytes incubated at 41 degrees C. A protein immunoblot, probed with an antibody specific for the inducible 72K stress protein, showed that the reduction of 35S-labeled 70K stress protein in these postexercise leukocyte samples occurred without marked elevations of this protein. In vitro incubation of human leukocytes at 40 degrees C for 15-120 min reduced, in a time-dependent manner, the amount of 70K stress protein synthesized during a subsequent 41 degrees C heat stress. This reduction of 70K stress protein synthesis in 41 degrees C-treated leukocytes was abolished when cycloheximide was present during the 40 degrees C preincubation.(ABSTRACT TRUNCATED AT 250 WORDS)     

The physiological strain index applied to heat-stressed rats.

A physiological strain index (PSI) based on heart rate (HR) and rectal temperature (Tre) was recently suggested to evaluate exercise-heat stress in humans. The purpose of this study was to adjust PSI for rats and to evaluate this index at different levels of heat acclimation and training. The corrections of HR and Tre to modify the index for rats are as follows: PSI = 5 (Tre t - Tre 0). (41.5 - Tre 0)-1 + 5 (HRt - HR0). (550 - HR0)-1, where HRt and Tre t are simultaneous measurements taken at any time during the exposure and HR0 and Tre 0 are the initial measurements. The adjusted PSI was applied to five groups (n = 11-14 per group) of acclimated rats (control and 2, 5, 10, and 30 days) exposed for 70 min to a hot climate [40 degrees C, 20% relative humidity (RH)]. A separate database representing two groups of acclimated or trained rats was also used and involved 20 min of low-intensity exercise (O2 consumption approximately 50 ml. min-1. kg-1) at three different climates: normothermic (24 degrees C, 40% RH), hot-wet (35 degrees C, 70% RH), and hot-dry (40 degrees C, 20% RH). In normothermia, rats also performed moderate exercise (O2 consumption approximately 60 ml. min-1. kg-1). The adjusted PSI differentiated among acclimation levels and significantly discriminated among all exposures during low-intensity exercise (P < 0.05). Furthermore, this index was able to assess the individual roles played by heat acclimation and exercise training.     

Effects of short-term exercise in the heat on thermoregulation, blood parameters, sweat secretion and sweat composition of tropic-dwelling subjects

This study investigates the effects of a short-term aerobic training program in a hot environment on thermoregulation, blood parameters, sweat secretion and composition in tropic-dwellers who have been exposed to passive heat. Sixteen healthy Malaysian-Malay male volunteers underwent heat acclimation (HA) by exercising on a bicycle ergometer at 60% of VO2max for 60 min each day in a hot environment (Ta: 31.1+/-0.1 degrees C, rh: 70.0+/-4.4%) for 14 days. All parameters mentioned above were recorded on Day 1 and at the end of HA (Day 16). On these two days, subjects rested for 10 min, then cycled at 60% of VO2max for 60 min and rested again for 20 min (recovery) in an improvised heat chamber. Rectal temperature (Tre), mean skin temperature (Tsk) heart rate (HR), ratings of perceived exertion (RPE), thermal sensation (TS), local sweat rate and percent dehydration were recorded during the test. Sweat concentration was analysed for sodium [Na+]sweat and potassium. Blood samples were analysed for biochemical changes, electrolytes and hematologic indices. Urine samples were collected before and after each test and analysed for electrolytes.After the period of acclimation the percent dehydration during exercise significantly increased from 1.77+/-0.09% (Day 1) to 2.14+/-0.07% (Day 16). Resting levels of hemoglobin, hematocrit and red blood cells decreased significantly while [Na+]sweat increased significantly. For Tre and Tsk there were no differences at rest. Tre, HR, RPE, TS, plasma lactate concentration, hemoglobin and hematocrit at the 40th min of exercise were significantly lower after the period of acclimation but mean corpuscular hemoglobin and serum osmolality were significantly higher while no difference was seen in [Na+]sweat and Tsk. It can be concluded that tropic-dwelling subjects, although exposed to prolonged passive heat exposure, were not fully heat acclimatized. To achieve further HA, they should gradually expose themselves to exercise-heat stress in a hot environment.     

Effect of thermal stress and dehydration on plasma levels of glucose, free fatty acids and growth hormone in the pigeon.

Pigeons were subjected to high ambient temperature and water deprivation for 3 days (28 degrees C, 31 degrees C and 36.5 degrees C respectively). After 3 days of heat stress and dehydration, the plasma levels of glucose, free fatty acids (FFA) and growth hormone (GH) were measured. Although the level of plasma glucose was not significantly altered, FFA and GH were found to be significantly increased. The possible mediation of the neurohypophysial hormone, vasotocin, in the syndhronous rise in plasma GH and FFA, is suggested.     

Interrelationships between heat acclimation and salivary cooling mechanism in conscious rats

1. Adaptation of salivary cooling mechanism during acclimation to heat (34 degrees C) and its role in thermoregulation of the rats was studied on conscious rats with either one submaxillary gland chronically cannulated or both submaxillaries ligated. 2. During heat stress (40 degrees C) acclimated rats showed a decrease both in rectal temperature threshold for salivation (Tre-TS), in salivary flow rate and in Tre (hyperthermic plateau). Animals survived for extended periods and rats with ligated glands survived 40% less than non-ligated rats. 3. For both cannulated and ligated rats short term acclimation (5 days) was the most effective. 4. It is suggested that earlier activation of salivation mechanism is associated with the decreased hyperthermic plateau and that the decreased salivary flow rate allows better control of water balance of the animals. Consequently, survival period during heat stress is extended.     

Control of panting in the desert iguana: roles for peripheral temperatures and the effect of dehydration

Although it is generally held that panting is a physiological mechanism for the regulation of brain temperature during heat stress, a number of studies have pointed to the importance of peripheral input for the initiation of the panting response in a variety of animals. By presenting ambient heat loads of 47 degrees, 54 degrees, 58 degrees, and 65 degrees C, and measuring skin, ear and core temperatures of the desert iguana, Dipsosaurus dorsalis, at the onset of panting, we found that the skin temperature at panting onset was independent of ambient heat load. This suggests that skin (peripheral) temperature is the body temperature on which the central thermoregulatory center cues to initiate thermal panting. Peripheral temperature control of panting was retained when the plasma osmolality of the desert iguana was increased by 100 mOsm/kg H2O to simulate dehydration. Dehydration to 80% initial body weight (IBW) resulted in a progressive increase in panting threshold (skin) from 42 degrees C for untreated lizards to 42.5 degrees C at 90% IBW to 43.3 degrees C at 80% IBW. Injection of 80% IBW lizards with a volume of 10 mM NaCl equivalent to weight loss resulted in a decrease in panting threshold to 40.8 degrees C. Injection with 1% body weight 3000 mM NaCl produced a dramatic increase in panting threshold to 45.9 degrees C. These data suggest that the desert iguana responds to dehydration by elevating panting threshold, thus promoting water conservation. These data also suggest that changes in plasma osmolality may be involved in the "setting" of panting threshold.     

Lipids of plasma membranes prepared from oat root cells : effects of induced water-deficit tolerance

Plasma membranes were isolated from oat (Avena sativa) roots by the phase-partitioning method. The membranes were exposed to repeated periods of moderate water-deficit stress, and a water-deficit tolerance was induced (acclimated plants). The plasma membranes of the controls (nonacclimated plants) were characterized by a high phospholipid content, 79% of total lipids, cerebrosides (9%) containing hydroxy fatty acids (>90% 24:1-OH) and free sterols, acylated sterylglucosides, sterylglucosides, and steryl esters, together amounting to 12%. Major phospholipids were phosphatidylcholine and phosphatidylethanolamine with lesser amounts of phosphatidylglycerol, phosphatidylinositol, and phosphatidic acid. After the membranes were acclimated to dehydration, the lipid to protein ratio decreased from 1.3 to 0.7 micromoles per milligram. Furthermore, the cerebrosides decreased to 5% and free sterols increased from 9% (nonacclimated plants) to 14%. Because the total phospholipids did not change significantly, the free sterol to phospholipid ratio increased from 0.12 to 0.19. There was no change in the relative distribution of sterols after acclimation. The ratio of phosphatidylcholine to phosphatidylethanolamine changed from 1.1 in the nonacclimated plants to 0.69 in the acclimated plants. The results show that acclimation to dehydration implies substantial alterations in the lipid composition of the plasma membrane.     

Effect of propranolol on thyroxine-induced changes in body temperature and metabolism during exercise in dogs.

Effects of thyroxine on temperature and metabolism during exercise were studied in dogs after beta-adrenergic blockade. Dogs performed 60 min treadmill exercise of moderate intensity 5 and 72 h following thyroxine injected s.c. in a single dose of 0.1 mg/kg b.w. Thyroxine increased significantly the lipolytic response to exercise as well as blood lactate (LA) concentrations and rectal temperature (Tre) during exercise as early as 5h following the hormone administration. The changes became more pronounced 72 h after the injection. At rest Tre, blood FFA and LA levels in the thyroxine-treated dogs did not differ from the control values, and blood glucose was slightly, but significantly higher. Propranolol given intravenously in a dose of 0.25 mg/kg at 30 min of the exercise performed 72 h following thyroxine injection abolished the plasma FFA rise, and inhibited to a certain extent increases in Tre and blood LA concentrations during the next 30 min of exercise.     

Pre-existing inflammatory state compromises heat tolerance in rats exposed to heat stress

This study investigated the roles of endotoxemia and heat-induced tissue damage in the pathology of heat stroke. In groups of eight, male Wistar rats were treated with heat exposure only (HE), or heat exposure with turpentine (T+HE), dexamethasone (D+HE), and turpentine and dexamethasone combined (TD+HE). The rats remained sedated for 2 h after receiving the respective treatments, followed by heat exposure until the core temperature (T(c)) was 42 degrees C for 15 min; control rats received turpentine (T), dexamethasone (D), and turpentine and dexamethasone (TD) without heat stress. Blood samples were collected before treatment (baseline I), after 2 h of passive rest (baseline II), at T(c) 40 degrees C (T40), and 15 min after achieving T(c) 42 degrees C (T42). No rats died in the nonheat-stressed groups. Survival rate was lowest in the TD+HE rats (37.5%), followed by the HE (62.5%), T+HE (75%), and D+HE (100%) rats (P < 0.05). The duration of survival at T42 degrees C was shortest in the TD+HE rats (9.9 +/- 6.2 min) (P < 0.01), followed by the T+HE (11.3 +/- 6.1 min) and the HE (12.2 +/- 4 min) (P < 0.05) rats. The increase in plasma IL-6 concentrations was highest in the T+HE (352%) and HE (178%) rats (P < 0.05). D+HE treatment suppressed the increases in plasma aspartate transaminase, alanine aminotransferase, and IL-6 and LPS concentrations during severe heat stress. Heat stroke can be triggered by endotoxemia or heat-induced tissue damage, and preexisting inflammation compromises heat tolerance, whereas blocking endotoxemia increases heat tolerance.     

Seasonal changes in circadian rhythms of body temperatures in humans living in a dry tropical climate

Seven volunteers (3 females and 4 males; 3 Caucasians and 4 Africans) participated in two 24 h sessions during the cool dry (CD) and the hot dry (HD) seasons of the sahelian tropical climate. Body temperatures were taken on portable cassette recorders for 24 h. Rectal (Tre) and mean skin (Tsk) temperatures decreased in the HD compared to the CD conditions, meeting one of the criteria for adaptation to heat. No ethnic differences in thermal responses were found. Males and females differed in their body temperature rhythms and in their reactions to heat. Body temperatures were higher in females than in males. Males reacted to heat with a decrease in Tre, without change in the Tre-Tsk gradient. Females showed a decrease in both Tre and Tsk, more marked for Tsk, with an increase in the Tre-Tsk gradient. It was concluded that males showed seasonal acclimatization to heat via a decrease in metabolism confirmed by a decrease in plasma levels of thyroid stimulating hormone (TSH) in the HD condition. Females showed a mixed metabolic and thermolytic type of acclimatization, with an absence of variation in plasma TSH levels. In conclusion, the steady rise in temperature between the CD and HD conditions was sufficient to trigger an acclimatization to heat similar in Caucasian and African subjects, although exposure to the external climate differed widely.     

Effect of thermal history on the rat's response to varying environmental temperature

After acclimating individually housed male rats to temperatures of either 24.5 +/- 0.1 or 29.2 +/- 0.1 degrees C for 14 days, randomly paired animals from each group were acutely exposed (3 h) in series to experimental temperatures between 18.0 and 34.5 degrees C in a controlled environment room. Relative humidity of 50 +/- 0.3% and a 12-h light-dark photoperiod (light from 0900 to 2100 h) were maintained. Metabolic rate (MR) and evaporative water loss (EWL) were-measured using an open-flow system; thermistors were used to measure the rectal (Tre) and tail skin (Tts) temperatures. MR was relatively constant over a temperature range of 22.2 to 27.0 degrees C for rats acclimated to 24.5 degrees C and 20.0 to 29.2 degrees C for rats acclimated to 29.2 degrees C. Above and below these ranges, MR for both groups was significantly (P less than 0.05) elevated. At their respective acclimation temperatures, the absolute Tre and Tts of 29.2 degrees C rats were maintained at an elevated level compared with 24.5 degrees C rats. Although EWL for both groups was relatively constant between 18.0 and 27.0 degrees C, 24.5 degrees C rats displayed higher EWL changes at most environmental temperatures above 27.0 degrees C. At 34.5 degrees C, 29.2 degrees C rats dissipated 26% more metabolic heat by evaporation compared with 24.5 degrees C rats. These data suggest that acclimation temperatures of rats affected the thermoneutral zone and alter the set-point temperature around which thermal responses are regulated.     

The myocardial heat shock response following sodium salicylate treatment

In cultured cells, salicylate has been shown to potentiate the induction of Hsp72 so that a mild heat stress (40 degrees C) in the presence of salicylate induces an Hsp72 response that is similar to a severe heat stress (42 degrees C). To determine whether salicylate can potentiate the myocardial Hsp70 response in vivo and confer protection from an ischemic stress, male Sprague-Dawley rats (250-300 g) were placed into 5 groups: (1) control, (2) salicylate only (400 mg/kg), (3) mild heat stress (40 degrees C for 15 minutes), (4) mild heat stress plus salicylate, and (5) severe heat stress (42 degrees C for 15 minutes). Twenty-four hours following salicylate treatment and/or heat stress, animals were anesthetized, their hearts rapidly isolated, and hemodynamic function evaluated using the Langendorff technique. Hsp72 content was subsequently assessed by Western blotting. Although salicylate in combination with a mild heat stress induced heat shock factor activation, only the hearts from severely heat-stressed animals (42 degrees C) demonstrated a significantly elevated myocardial Hsp72 content and a significantly enhanced postischemic recovery of left ventricular developed pressure and rates of contraction and relaxation. These results support the role for Hsp72 as a protective protein and suggest that neither salicylate treatment alone nor salicylate in combination with a mild heat stress potentiates the myocardial Hsp72 response.     

Effects of estrus cycle on thermoregulatory responses during exercise in rats

In female rats, rectal temperature (Tre), tail vasomotor response, oxygen uptake (VO2), and carbon dioxide production (VCO2) were measured in proestrus and estrus stages during treadmill running at two different speeds at an ambient temperature (Ta) of 24 degrees C. Experiments were performed at 2.00-6.00 a.m., when the difference in Tre was greatest between the two stages; Tre at rest in the estrus stage was 0.54 degrees C higher than in the proestrus stage. In a mild warm environment, threshold Tre for a rise in tail skin temperature (Ttail) was also higher in the estrus stage than in the proestrus stage. In contrast, no difference was seen in the threshold Tre and steady state Tre at the end of exercise between proestrus and estrus stages. These values were higher at the higher work intensity. VO2 was also similar between the two stages, except in the second 5 min after the beginning of exercise, when VO2 was greater and Tre rose more steeply in the proestrus stage. These data indicate that deep body temperature during exercise is regulated at a certain level depending on the work intensity and is not influenced by the estrus cycle.     

Effect of temperature and duration of hyperthermia on HSP72 induction in rat tissues

The aim of the present study was to determine whether heat shock protein 72 (HSP72) is induced in a heated rat model at rectal temperatures below 42 degrees C. Rats were divided into a control group and six groups (n = 6) heated to different rectal temperatures: 39 degrees C for 1 h (39), 40.0 degrees C for either 15 min (40S) or 1 h (40L), 41.0 degrees C for either 15 min (41S) or 1 h (41L) and 42.0 degrees C for 15 min (42). Tissues were sampled 4 h after heating. Following 1 h at 40.0 degrees C, HSP72 was significantly elevated in heart (p < 0.005), but not in gut or liver tissue. In all three tissues, HSP72 was significantly elevated under the conditions 41L and 42 compared to control tissue (p < 0.005). Marked differences were found in the amount of HSP72 induced in different tissues in response to the same heat stress. Duration of heating was important in modulating HSP72 induction, with a significantly greater induction of HSP72 following 1 h compared to 15 min at 41 degrees C in all three tissues (p < 0.02). A correlation was found between thermal load and HSP72 content in liver, heart (both p < 0.01) and gut (p < 0.001) for the rats heated to 41 and 42 degrees C. These data show that HSP72 is induced at temperatures below 42 degrees C, with striking differences between tissues.     

Arterial vs. rectal temperature in ponies: rest, exercise, CO2 inhalation, and thermal stresses

We assessed in ponies the adequacy of using rectal (Tre) rather than arterial temperature (Tar) under conditions common to ventilatory control experiments, i.e., CO2 breathing, thermal stress, and particularly exercise. We were interested in whether, and to what extent, Tar-Tre differences could lead to errors in arterial blood gas corrections. At control environmental temperatures (Ta) of 5 degrees C in the winter and 21 degrees C in the summer, Tar and Tre (37.1 degrees C) did not differ (P greater than 0.05). Elevating winter or summer Ta by 10-18 degrees C for 2-days or lowering summer Ta by 9 degrees C (2-days) did not change Tar or Tre (P greater than 0.05). Furthermore, elevating inspired PCO2 to 42 Torr for 15 min did not alter Tar or Tre from control (P greater than 0.05). During treadmill exercise, at 1.8 mph 5% grade, Tar and Tre did not change significantly (P greater than 0.05) from rest by 11 min of work. At 3 mph 5% grade, Tar increased progressively by 0.3 degrees C (P less than 0.05) while Tre tended to increase 0.1 degree C by 11 min. During moderate exercise at 6 mph 5% grade, Tar increased 0.9 degree C (P less than 0.05) while Tre increased 0.25 degree C (P less than 0.05). Finally, by 6 min of heavy exercise at 8 mph 20% grade, Tar increased 2 degrees C (P less than 0.05) while Tre increased 0.5 degree C (P less than 0.05). The Tar-Tre differences during the latter three work loads were statistically significant (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Physiological effects of dietary cadmium acclimation and waterborne cadmium challenge in rainbow trout: respiratory, ionoregulatory, and stress parameters

A suite of respiratory, acid-base, ionoregulatory, hematological, and stress parameters were examined in adult rainbow trout (Oncorhynchus mykiss) after chronic exposure to a sublethal level of dietary Cd (500 mg/kg diet) for 45 days and during a subsequent challenge to waterborne Cd (10 microg/L) for 72 h. Blood sampling via an indwelling arterial catheter revealed that dietary Cd had no major effects on blood gases, acid-base balance, and plasma ions (Ca(2+), Mg(2+), K(+), Na(+), and Cl(-)) in trout. The most notable effects were an increase in hematocrit (49%) and hemoglobin (74%), and a decrease in the plasma total ammonia (43%) and glucose (49%) of the dietary Cd-exposed fish relative to the nonexposed controls. Dietary Cd resulted in a 26-fold increase of plasma Cd level over 45 days (approximately 24 ng/mL). The fish exposed to dietary Cd showed acclimation with increased protection against the effects of waterborne Cd on arterial blood P(aCO2) and pH, plasma ions, and stress indices. After waterborne Cd challenge, nonacclimated fish, but not Cd-acclimated fish, exhibited respiratory acidosis. Plasma Ca(2+) levels declined from the prechallenge level, but the effect was more pronounced in nonacclimated fish (44%) than in Cd-acclimated fish (14%) by 72 h. Plasma K(+) was elevated only in the nonacclimated fish. Similarly, waterborne Cd caused an elevation of all four traditional stress parameters (plasma total ammonia, cortisol, glucose, and lactate) only in the nonacclimated fish. Thus, chronic exposure to dietary Cd protects rainbow trout against physiological stress caused by waterborne Cd and both dietary and waterborne Cd should be considered in determining the extent of Cd toxicity to fish.