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1. The effects of hypohydration produced by 48 hr water deprivation were examined in dogs during moderate treadmill exercise at an ambient temperature (Ta) of 21 degrees C. 2. Hypohydration caused a significant elevation in plasma levels of adrenaline (A), proteins (pp) and osmolality (pOsm). 3. During 1 hr of running, plasma concentrations of adrenaline (A) and noradrenaline (NA) rose significantly, whilst no change in these hormones occurred in dogs hydrated ad libitum. 4. The results suggest that hypovolemia in the dog may be a sufficient stimulus to intensify the sympatho-adrenal response to moderate exercise performed at a room Ta.

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To study physiological effects of restricted activity (RA) and subsequent retraining, 10 male mongrel dogs (1-5 years) performed a submaximal exercise endurance test on a treadmill (12 degrees slope, 1.6 m.s-1) during kennel control, after 8 weeks of cage (40 cm-w x 80 cm-h x 110 cm-l) confinement, and after 8 weeks of retraining using the same treadmill protocol 1 h/d for 6 d/week. Compared with control endurance (172 +/- 19 min), endurance decreased to 102 +/- 15 min (delta = -41%, p less than 0.05) after RA and increased to 223 +/- 24 min (delta = +30%, p less than 0.05) after training: the respective final levels and changes in rectal temperature were 41.25 and +2.15 degrees C, 41.60 and +2.70 degrees C (NS), and 41.35 and +2.40 degrees C (NS), respectively. Resting and post-exercise blood glucose and lactate concentrations were unchanged in the three experiments. After RA, resting muscle glycogen was reduced from a control level of 49.9 +/- 4.3 to 34.1 +/- 4.5 mmol.kg-1 (delta = 32%, p less than 0.05) which returned to the control level of 58.4 +/- 3.5 mmol.kg-1 after retraining. Resting plasma FFA levels were unchanged, but the RA post-exercise change was decreased from a control level of +0.400 +/- 0.099 to +0.226 +/- 0.039 mmol.L-1 (p less than 0.05). Neither restricted activity nor training affected glucose tolerance significantly. The results indicated that RA reduces exercise endurance, the effectiveness of exercise thermoregulation, muscle glycogen stores, and the lipolytic response to exercise and to noradrenaline stimulation. All these changes were reversed following 8 weeks of retraining.

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The purpose of these studies was to determine how plasma levels of arginine vasopressin (pAVP) are related to workload, plasma osmolality (pOsm), blood volume (BV) and plasma angiotensin II (pAII) in exercising dogs. Measurements were made in dogs running on a treadmill at 7.5 km. hr-1 at slopes of 0, 10% and 20% when they were hydrated ad lib and when they had been deprived of drinking water and also in dogs running on a 20% slope after an IV infusion of hypertonic NaCl. Dehydration increased pOsm by 6.6% and reduced BV by 10% in resting dogs. In dehydrated animals, pAVP, pAII and pOsm were elevated above hydrated levels at rest and during exercise at all three workloads. In hydrated dogs, pOsm rose during exercise at 10% and 20% slopes but pAVP rose above resting levels only at the highest workload and pAII was not affected by exercise. In dehydrated dogs, pOsm and pAVP rose during exercise at 10% and 20% slopes and pAII was elevated at the 20% slope. BV decreased during exercise at the highest workload in both hydrated and dehydrated animals. After hypertonic NaCl, pAVP rose during exercise but pOsm and pAII did not. The results suggest that both osmotic and nonosmotic factors contribute to the release of AVP in exercising dogs and that exercise leads to a leftward shift in the relationship of pAVP to pOSM which could be a result of reduced blood volume.

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Dehydrated mammals reduce thermoregulatory evaporation and regulate deep body temperature (Tb) at elevated levels when they are exposed to heat. These experiments were designed to study the effects of plasma volume (PV) replacement and the effects of drinking H2O or 0.9% NaCl on thermal panting in dehydrated dogs resting at Ta 40-41 degrees C. Five dogs were studied when they were hydrated (control) and in 4 different experiments when they had been dehydrated (D) by removal of drinking water: (1) D, no treatment; (2) D + intravenous dextran infusion; (3) D + drinking H2O; (4) D + drinking NaCl. Compared to controls, dehydrated dogs had lower respiratory frequency (f), higher Tb, lower PV and blood volume (BV) and higher plasma osmolality (pOsmol). Intravenous dextran infusion restored BV to the control level without reducing pOsmol; but f and Tb remained at dehydrated levels after the infusion. When the dogs drank either H2O or NaCl,f increased significantly during the first minute after drinking. pOsmol decreased by 6 min after drinking H2O but did not change after drinking NaCl. BV measured 5 min after the end of drinking H2O was not different from dehydrated BV. It is concluded that (1) Restoration of BV to hydrated levels in dehydrated, heat-exposed dogs with elevated pOsmol does not restore f or Tb to hydrated levels; (2) There is a rapid recovery of thermal panting after drinking which is not dependent on changes in pOsmol or in BV.

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The effect of acetysalicylic acid (aspirin) on thermoregulation in a warm environment was studied in hydrated and dehydrated adult rats to test the hypothesis that dehydration hyperthermia can be modified by an antipyretic drug. Metabolic rate (MR), evaporative water loss (EWL), and deep body temperature (Tb) were measured during 2 h of exposure to an ambient temperature of 36 degrees C after the rats had received an oral pellet of aspirin (100 mg.kg-1) or placebo. The dehydrated placebo group had a higher Tb and lower EWL than the hydrated placebo group. Aspirin increased MR and EWL in both hydrated and dehydrated animals. Aspirin did not affect Tb in hydrated rats, but reduced Tb by 0.2 degree C in dehydrated rats during the heat exposure. The elevation in EWL appears to be a thermoregulatory response to increased heat production in both hydrated and dehydrated animals after aspirin treatment. The possibility that aspirin may act in dehydrated animals to restore central thermosensitivity toward hydrated levels needs to be tested further.

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The effect of intracerebroventricular (icv) infusions of hypertonic NaCl or sucrose on thermoregulatory responses to heat was studied in conscious rabbits to test the idea that brain osmoreceptors are involved in the inhibition of evaporative heat loss and elevation of body temperature in dehydrated mammals at high ambient temperature (Ta). In rabbits hydrated ad lib and resting at a Ta of 33 degrees C, icv infusion (3.4 microliter/min) of hypertonic (1,500 mosm) NaCl or sucrose in artificial cerebrospinal fluid (ACSF) produced a significant reduction in respiratory frequency (f) and in ear skin temperature (Te) and a rise in brain temperature (preoptic area, Tpoa). icv infusion of ACSF alone or ACSF + NaCl at 500 and at 750 mosm had no effect on f or on Te or Tpoa. Infusion of NaCl + ACSF at 1,000 mosm reduced f but did not affect Te or Tpoa. In hydrated rabbits, icv infusion of 1,500 mosm NaCl abolished the rise in f and in Te elicited by POA heating at Ta of 25 degrees C. In dehydrated rabbits at 33 degrees C, f was below hydrated levels and icv infusion of water (6.8 microliter/min) produced a reversible elevation in f. These findings suggest that brain osmoreceptors can influence thermoregulation in hot environments.

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The highest ambient temperature tolerated by rabbits was 30 degrees C at the relative humidity of air 80-95%. During the exposure to these environmental conditions the vasomotor thermoregulatory response developed fully, while the respiratory frequency did not attain the maximum level, i.e. the rabbit's potential ability for thermal panting. Prolonged heat exposure (approx. 4 hours) had a depressive effect on the respiratory frequency. Increased concentration of carbon dioxide (3, 6 and 9%) in the inspired gas mixture did not disturb the thermoregulatory mechanisms at 30 degrees C in the rabbits.

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Panting response and a fall in rectal temperature following intraventricular injection of 5-hydroxytryptamine (5-HT) were significantly reduced in dehydrated rabbits as compared with normally hydrated animals. The vasomotor heat loss response to 5-HT was essentially similar in both groups. These as well as earlier findings suggest that dehydration may modify signals generated in brain thermoregulatory centers controlling evaporative but not the vasomotor heat loss.

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The purpose of this study was to test the hypothesis that thermoregulation during exercise can be affected by extracellular fluid hyperosmolality [Osm] without changing the plasma Na+ concentration. The effects of preexercise venous infusions of hypertonic mannitol and NaCl solutions on rectal temperature (Tre) responses were compared in dogs running at moderate intensity for 60 min on a treadmill. Plasma E1Na+] was increased by 12 meq/l (P less than 0.05) after NaCl infusion, and decreased by 9 meq/l (P less than 0.05) after mannitol infusion. Both infusions increased plasma [Osm] by 15 mosmol/kg (P less than 0.05). After both infusions, Tre was essentially constant during 60 min rest. However, compared with the noninfusion exercise increase in Tre of 1.3 degrees C, Tre increased by 1.9 degrees C (delta delta Tre = 0.5 degrees C, P less than 0.05) after both postinfusion exercise experiments. It was concluded that inducing extracellular hyperosmolality, without elevating plasma [Na+], can induce excessive increases in Tre during exercise but not at rest.

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