Biomedical subjects

C C Barney

Publications and source records attributed to C C Barney.

At least 19 recordsLinked to original sources

PubMed1999

Thermal dehydration-induced thirst in spontaneously hypertensive rats.

Spontaneously hypertensive (SH) rats and normotensive Wistar-Kyoto (WKY) rats were exposed to either 25 or 37.5 degrees C for 3.5 h, and their thermal and water balance responses were compared. After exposure, either a blood sample was obtained or the rats were allowed to rehydrate for 4 h. SH rats had both higher core temperatures and evaporative water losses during heat exposure. Measurements of hematocrit, hemoglobin concentration, plasma protein and sodium concentrations, and plasma osmolality indirectly showed that the SH rats were dehydrated relative to the WKY rats after exposure to either 25 or 37.5 degrees C. SH rats drank significantly more water but also had significantly higher urine volumes than the WKY rats and thus rehydrated only slightly better than the WKY rats. SH and WKY rats had similar levels of water intake and urine output after 24 h of water deprivation. The elevated thermal response of SH rats to heat exposure does not appear to lead to uncompensatable changes in body water status.

Animals↗

PubMed1997

Effects of preloads of water and saline on thermal dehydration-induced thirst.

The relative contribution of cellular and extracellular water deficits to the genesis of thirst due to thermal dehydration was studied in male Sprague-Dawley rats following exposure to a 40 degrees C environment for 4 h. Intragastric (I.G.) and intravenous (I.V.) preloads of water reduced the elevated plasma sodium and plasma osmolality of thermally dehydrated rats to control levels, but preloads of saline did not. I.G. and I.V. preloads of saline returned the hematocrit and plasma protein concentration of thermally dehydrated rats to control levels. Both the I.G. water preload and the I.G. saline preload reduced water intake, with the I.G. water preload having a greater effect. The I.V. water preload reduced water intake nearly to control levels, whereas the I.V. saline preload was without effect on water intake. These data indicate that the water intake of thermally dehydrated rats is primarily due to a cellular water deficit and that oral and gastric factors are also important in terminating water intake in thermally dehydrated rats.

Animals↗

PubMed1995

Nycthemeral variation in thermal dehydration-induced thirst.

Temporal variation in spontaneous water intake in rats is well established but little is known about temporal variation in water intake following dehydration. In the present study different male Sprague-Dawley strain rats were exposed without water for 3 h to either a 25 degrees C or a 40 degrees C environment every 4 h for 20 h. The rats were then allowed access to water in a 25 degrees C environment for 2 h. Rats exposed to 25 degrees C showed significant temporal variation in evaporative water loss, urine output, urine sodium and potassium excretion, water intake, and percent rehydration with higher values occurring during the night. Rats exposed to 40 degrees C had greater evaporative water loss, urine sodium excretion, feces output and water intake than the rats exposed to 25 degrees C and had temporal variations which were similar to those of the rats exposed to 25 degrees C. The robust effects of thermal-dehydration on water balance in rats are additive to rather than interactive with the effects of time of day.

Animals↗

PubMed1995

Thermal dehydration-induced thirst in rats: role of body temperature.

Male Sprague-Dawley rats were used to study the possible role of hyperthermia in the thirst associated with thermal dehydration. Rats were exposed to 40 degrees C for 4 h and then allowed access to water at different times after they were transferred to 25 degrees C. Delaying the time prior to allowing the rats to drink did not significantly alter either water intake or percent rehydration even though core temperature decreased during the first 1.5 h after removal from the heat. Exposing thermally dehydrated rats to 5 degrees C for 30 min prior to allowing them access to water also failed to significantly affect water intake or percent rehydration. Thermally dehydrated rats allowed to drink while remaining in the heat did not show a significant increase in water intake during the first hour or percent rehydration over rats drinking at 25 degrees C. Nondehydrated rats did show significant increases in water intake and percent rehydration when allowed to drink in the heat. Hyperthermia does not play a role in drinking in thermally dehydrated rats but can stimulate drinking in water-replete rats.

Animals↗

PubMed1995

Sympathetic nerve responses to hyperthermia in the anesthetized rat.

The aim of the present study was to characterize the sympathetic nerve responses to hyperthermia in chloralose-anesthetized rats. Discharges were recorded from the renal, lumbar, and splanchnic sympathetic nerves. Mean arterial pressure, heart rate, and sympathetic nerve discharge (SND) were recorded continuously during progressive increases in core body temperature (Tc) from 38.0 to 41.0 degrees C. The following observations were made: 1) significant increases in renal, lumbar, and splanchnic SND were observed during hyperthermia; 2) autospectral analysis of renal and lumbar SND revealed that the frequency distribution of SND can be altered during progressive increases in Tc; and 3) increases in splanchnic SND to acute heating were similar in baroreceptor-innervated and -denervated rats. We conclude that 1) hyperthermia is a potent stimulus to the sympathetic nervous system and increases the activity in three sympathetic nerves that innervate different regional arterial beds, 2) acute heating influences the neural circuits involved in generating SND as evidenced by changes in the basic pattern of renal and lumbar SND, and 3) the increase in splanchnic SND during hyperthermia is not opposed by the arterial and cardiopulmonary baroreceptors.

Animals↗

PubMed1992

Opioid modulation of thermal dehydration-induced thirst in rats.

Male Sprague-Dawley rats were utilized to study the effects of the opioid receptor antagonists, naloxone and naltrexone, on thirst induced by thermal dehydration. In an initial experiment, the depressant effect of naloxone (1.0 mg/kg, IP) on the water intake of rats deprived of water for 24 h was confirmed. In subsequent experiments, rats were thermally dehydrated by exposing them without water to a 40 degrees C environment for 1-4 h. Following heat exposure, rats were injected with either naloxone or naltrexone either IP or ICV. Fifteen minutes later, rats were provided with water and water intake was measured for 2 h. Both naloxone and naltrexone had dose (0.1-5.0 mg/kg, IP)-dependent effects of reducing water intake of rats thermally dehydrated for 3 h. Water intake of rats thermally dehydrated for 2 or 4 h was also attenuated by pretreatment with naloxone. Rats thermally dehydrated for 3 h exhibited decreases in water intake following ICV injection of either naloxone or naltrexone at a dose of 50 micrograms. Neither naloxone nor naltrexone had an effect on urine output in any experiment. The water intake data support the hypothesis that thirst induced by thermal dehydration in rats is modulated by an opioid mechanism.

Animals↗

PubMed1991

Thermal dehydration-induced thirst in rats: role of angiotensin II.

Dehydration can be brought about by either water deprivation or by heat exposure (thermal dehydration). Angiotensin II has been shown to have a role in water deprivation-induced thirst. The current study was designed to determine whether angiotensin II is involved in thirst caused by thermal dehydration. Male Sprague-Dawley strain rats were dehydrated by exposure to a 40 degree C environment for 2-4 h or by water deprivation for 44 h. Water deprivation but not heat exposure significantly increased plasma renin activity. Neither ureteric ligation nor nephrectomy significantly altered water intake after thermal dehydration. Captopril, an inhibitor of angiotensin converting enzyme, given at a dose of 100 mg/kg ip, significantly decreased water intake in water-deprived rats but not in thermally dehydrated rats. Angiotensin II therefore does not appear to play a role in the control of water intake of thermally dehydrated rats. The physiological responses to dehydration in rats are dependent on the way in which the dehydration is brought about.

Angiotensin II↗

PubMed1990

Control of water intake in thermally dehydrated rats.

Male rats were thermally dehydrated by exposure without water to an environmental temperature of 40 degrees C for 0-4 hr or to environmental temperatures of 25-40 degrees C for 4 hr. Water intake was then measured for 2 hr or a blood sample was taken to determine the effect of heat exposure on body water status. Evaporative water loss and water intake increased with increased duration and severity of heat exposure. Heat exposure significantly increased plasma osmolality and plasma sodium concentration and significantly decreased plasma potassium concentration. Hematocrit and plasma protein concentration increased slightly but not significantly with heat exposure. The increases in water intake in association with increases in evaporative water loss, plasma osmolality and plasma sodium concentration with no significant increases in hematocrit or plasma protein concentration indicates that the thirst induced by thermal dehydration is primarily osmotic in nature. Water intake equal to about 50% of the evaporative plus urinary water loss reduced plasma osmolality and sodium concentration to control levels, removing the stimulus to drink before the water loss was replaced.

Animals↗

PubMed1990

Measurements of core temperature in spontaneously hypertensive rats by radiotelemetry.

Spontaneously hypertensive (SH) rats have been shown to have elevated colonic temperatures when compared with normotensive Wistar-Kyoto (WKY) rats. In the present study, core temperatures of SH and WKY rats were compared using radiotelemetry temperature sensors implanted in the abdominal cavity. At an ambient temperature (Ta) of 25 degrees C, SH and WKY rats showed no significant difference in core temperature over a 24-h period. After 1 h exposures to Ta values of 5, 15, 25, or 35 degrees C, there were no significant differences between core temperatures of SH and WKY rats, but at 40 degrees C the SH rats had a significantly higher core temperature than the WKY rats. Handling and moderate restraint also led to significantly higher core temperatures in the SH rats. Core temperature was also significantly increased in the SH rats compared with the WKY rats when a temperature probe was either inserted intermittently or inserted and left in place. The results of this study indicate that nonstressed SH rats do not have an elevated core temperature but that stress such as heat exposure, handling, restraint, or even the presence of a colonic temperature probe can cause significant increases in core temperature in these rats.

Animals↗

PubMed1990

Effects of peripheral administration of naloxone on beta-adrenergic mediated responses.

A possible interaction between the opiate and beta-adrenergic systems in controlling body temperature, heart rate and water intake was investigated using adult male Sprague-Dawley rats. Peripheral administration of isoproterenol (8 and 50 micrograms/kg, s.c.) produced significant elevations of heart rate and tail skin and colonic temperatures, respectively. Peripheral pretreatment with naloxone (1 mg/kg, s.c.) was without effect on these beta-adrenergic responses. Administration of isoproterenol (25 micrograms/kg, s.c.) produced a significant increase in water intake which was abolished by peripheral pretreatment with naloxone (1 mg/kg, s.c.). Previous studies have suggested that the dipsogenic response to isoproterenol is mediated through angiotensin II. In the present study the angiotensin II-induced (200 micrograms/kg, s.c.) dipsogenic response was abolished by naloxone pretreatment. However, pretreatment with an equimolar dose of naloxone methobromide, an opiate antagonist which does not cross the blood-brain barrier, was ineffective in altering the dipsogenic response produced by peripheral administration of either angiotensin II or isoproterenol. Collectively, the data suggest that opiates do not alter peripheral beta-adrenergic responses and that the blocking effects of naloxone on the isoproterenol-induced drinking response is mediated centrally and may be due to blocking angiotensin II dipsogenesis.

Angiotensin II↗

PubMed1990

Mechanisms mediating the thermal response to morphine withdrawal in rats.

Studies were undertaken to evaluate the role of peripheral adrenergic mechanisms and the adrenal gland in the thermal responses which accompany morphine withdrawal in the rat. Ovariectomized rats were addicted to morphine and subsequently withdrawn by administration of naloxone. This treatment resulted in a significant rise (5-6 degrees C) in tail skin temperature (TST) and fall in colonic temperature (2-4 degrees C). Systemic administration of clonidine (0.5 mg/kg) completely suppressed this surge in TST and significantly attenuated the fall in core temperature. Similar results were observed following the systemic administration of ST-91, another alpha 2-adrenergic agonist which does not cross the blood-brain barrier. Central administration of ST-91 (50 micrograms/5 microliters, icv) was also successful in attenuating these temperature changes in the morphine-dependent rat. Adrenalectomy and peripheral administration of propranolol (10 mg/kg sc) both resulted in a significant attenuation of the surge in TST and the fall in core temperature in the morphine-dependent rat which suggest some peripherally mediated event is necessary to produce the full skin temperature surge. Collectively, the data suggest a role for the adrenal gland and adrenergic receptors in producing the surge in TST in morphine-dependent rats. It also suggests that the blocking effects of the alpha 2-adrenergic agonist can be mediated both centrally and peripherally.

Adrenal Glands↗

PubMed1989

Development of hypertension in rats during chronic exposure to cold.

Resting systolic, diastolic, and mean blood pressures (MBP), as well as heart rates, of unanesthetized, unrestrained, cold-acclimated (CA, 4 wk, 6 degrees C) rats were measured by direct arterial cannula and compared with those of controls maintained at 25 degrees C. Exposure to cold increased all these measurements significantly. Mean heart weight of CA rats was also increased significantly above that of controls. The responsiveness of MBP and heart rate to administration of the beta-adrenergic agonist, isoproterenol (3, 5, and 8 micrograms/kg ip), to unanesthetized, unrestrained, CA rats during exposure to air at 6 degrees C was similar to, and possibly less than, that of warm-acclimated (WA) rats measured at 25 degrees C. Acute administration of the alpha-adrenergic agonist, phenylephrine (100 micrograms/kg ip), to CA rats while in air at 6 degrees C induced less of a change in MBP from pretreatment level than was observed in WA rats. However, no differences were observed between groups when changes in heart rate from pretreatment level were compared. A similar statement may be made for a higher dose of phenylephrine (150 micrograms/kg ip), although MBP were elevated to higher levels in both groups with the higher dose. Abrupt exposure of WA rats to cold (6 degrees C) resulted in a sharp increase in heart rate and a more gradual increase in MBP over a period of 1 h. Removal of CA rats from 6 to 25 degrees C resulted in a gradual decrease in heart rate with no significant change in MBP during the ensuing hour.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

PubMed1988

Prostaglandin E1 hyperthermia in water or food deprived rats.

The effect of 48 hours of water deprivation on the colonic temperature response to intrahypothalamic injection of prostaglandin E1 (PGE1) was investigated in adult male rats. Water deprivation did not alter colonic temperature of rats at a neutral ambient temperature. Administration of PGE1 at doses of 50, 200 and 400 ng gave rise to a short latency dose dependent hyperthermia in both control and water deprived rats. Water deprived rats had significantly greater increases in colonic temperature following the two higher doses of PGE1. Control rats and water deprived rats exposed to the cold (5 degrees C) had decreases in colonic temperature which were not significantly different. Water deprivation, which should increase the plasma levels of the putative endogenous antipyretic vasopressin, does not attenuate PGE1 hyperthermia but has a slight enhancing effect. Following food deprivation for 48 hours rats had a slight but significantly greater increase in colonic temperature following intrahypothalamic injection of 200 ng PGE1. Thus the water deprivation induced change in responsiveness to PGE1 may be due to the decrease in food intake which accompanies water deprivation. The mechanism by which rats exhibit an enhanced febrile response to PGE1 administration following food or water deprivation is not yet known.

Alprostadil↗

PubMed1987

Alpha-adrenergic mediation of the tail skin temperature response to naloxone in morphine-dependent rats.

Studies were undertaken to evaluate the role of central noradrenergic neurons in the tail skin temperature (TST) surge that accompanies morphine withdrawal in the rat. A 5 degrees C increase in TST and a 1-2 degrees C decrease in rectal temperature (Tr) was observed following administration of a dose of naloxone HCl (NAL, 1 mg/kg, s.c.) which precipitated withdrawal in morphine-dependent rats. Intracerebroventricular (i.c.v.) injection of clonidine HCl, a partial alpha 2-adrenergic agonist did not alter TST in morphine-dependent animals. However, clonidine (10 or 50 micrograms/rat, i.c.v.) given 10 min prior to the administration of NAL completely blocked the TST response to the opiate antagonist in the morphine-dependent animals. Although NAL and clonidine reduced Tr to a similar extent in morphine-dependent rats, their effects were not additive when the drugs were administered sequentially. Treatment with the alpha-adrenergic antagonist phentolamine (11.9 or 60 micrograms/rat, i.c.v.) failed to alter TST when administered alone, but the highest dose significantly reduced the TST response to naloxone in the morphine-dependent rat. In addition, phentolamine, at high doses only, moderately reduced Tr, but the alpha-adrenergic antagonist failed to modify the decline in Tr associated with NAL-precipitated morphine withdrawal. Collectively, these data indicate that brain noradrenergic neurons play a role in the TST surge which accompanies NAL-precipitated morphine withdrawal, and that the TST and Tr responses can be dissociated in the morphine-dependent rat.

Animals↗

PubMed1986

Effects of thyroid hormone replacement on beta-adrenergic responsiveness of food-deprived rats.

Thyroid hormone levels and beta-adrenergic responsiveness after stimulation with the beta-adrenergic agonist isoproterenol were studied in four groups of male rats. The groups used were control rats, rats deprived of food for 72 h, rats administered 50 micrograms thyroxine (T4)/kg daily for 4 days, and rats deprived of food for 72 h and administered 50 micrograms T4/kg daily for 4 days. Food deprivation significantly decreased serum T4 and triiodothyronine (T3) levels, and administration of T4 significantly increased serum T4 and T3 levels in both fed and food-deprived rats. Administration of T4 led to lower body weights in both fed and food-deprived rats. Administration of isoproterenol led to increases in colonic and tail skin temperatures and heart rate. Food deprivation significantly attenuated the increased body temperatures and heart rate induced by isoproterenol, and administration of T4 to food-deprived rats returned these adrenergic responses to control levels. Administration of T4 to fed rats significantly increased the thermal and cardiac responses to isoproterenol above those of the control rats. Administration of isoproterenol also increased plasma glucose levels. Food deprivation significantly decreased both postsaline- and isoproterenol-stimulated glucose levels. However, administration of T4 was without effect on either the postsaline- or isoproterenol-stimulated glucose levels of either the fed or food-deprived rats. The decreases in T4 and T3 that accompany food deprivation may thus be responsible for some, but not all, of the reductions in beta-adrenergic responsiveness observed in food-deprived rats.

Analysis of Variance↗

PubMed1986

Beta-adrenergic responsiveness in the rat following acute administration of ethanol.

Ethanol has been shown to induce a hypothermia in rats maintained in air at 26 degrees C. The objective of the present study was to assess the metabolic responsiveness of ethanol-treated rats to administration of isoproterenol, a beta-adrenoceptor agonist, and to assess whether ethanol per se, or the hypothermia accompanying its administration, contribute to changes in beta-adrenergic responsiveness. In the present study, administration of ethanol (3 g/kg, i.p.) reduced both colonic temperature (Tco) and rate of oxygen consumption (metabolic rate) of rats maintained at 26 degrees C to levels below those of saline-treated controls within 20 min after treatment. Maximal decreases in both parameters occurred within approximately 40 min. Administration of isoproterenol (50 micrograms/kg, s.c.) 10 min after treatment with either ethanol or saline was accompanied by an increase in the metabolic rates of both groups, although the magnitude of the increase in the ethanol-treated group was less than that of controls. Maximal increases in tail skin temperatures (Tsk) following treatment with isoproterenol were similar in both groups but an increase in Tsk occurred earlier in the ethanol-treated group. Tco increased after treatment with isoproterenol in the saline-treated group but decreased in the ethanol-treated group. When isoproterenol was administered 90 min after treatment with ethanol, increases in metabolic rate, Tsk, and Tco were similar in both groups, although the increase in Tsk of ethanol-treated animals was delayed until Tco reached pretreatment level. Exposure to 30 degrees C minimized ethanol-induced hypothermia. At this temperature the metabolic responses to administration of isoproterenol at 90 min after treatment with ethanol did not differ significantly between the two groups. These results suggest that the metabolic responsiveness to administration of a beta-adrenoceptor agonist is not altered by prior treatment with ethanol but is affected by the hypothermia accompanying its administration.

Animals↗

PubMed1985

Effect of beta-adrenergic antagonists on experimentally induced drinking in female rats.

The nonspecific beta-adrenergic antagonist d,l propranolol, the specific beta 1-adrenergic antagonist atenolol, and the specific beta 2-adrenergic antagonist butoxamine were administered intraperitoneally (IP) to ovariectomized female rats in order to determine the role of beta-adrenergic receptors in drinking. D,l propranolol and atenolol administered at doses of 6, 12, and 18 mg/kg significantly attenuated the one-hour water intakes of rats administered angiotensin II (200 micrograms/kg, SC) and the water intakes of rats deprived of water for 24 hours. D propranolol, which has little beta-adrenergic blocking ability, administered at doses of 6 and 12 mg/kg, and butoxamine, administered at doses of 25 and 35 mg/kg, had no significant effects on the water intakes of angiotensin II treated or water deprived rats. Regardless of the dose, d,l propranolol, atenolol, and butoxamine failed to significantly alter the water intakes of rats administered 1.0 M NaCl (10 ml/kg, IP) The results provide evidence that beta 1-adrenergic receptors, but not beta 2-adrenergic receptors, are involved in mediating the increased water intakes induced by angiotensin II and water deprivation. On the other hand the increased water intake due to administration of hypertonic saline does not appear to mediated by beta-adrenergic receptors.

Adrenergic beta-Antagonists↗

PubMed1983

Alteration of peripheral beta-adrenergic responsiveness in fasted rats.

Total food deprivation for 72 hrs (3 day fast) in female rats resulted in a reduction in serum thyroid hormones as well as a reduced peripheral beta-adrenergic responsiveness to isoproterenol. Food deprivation for 48 or 72 hrs significantly decreased both serum T3 and T4 values as compared to non-fasted controls. There were no significant differences in either T3 or T4 levels as a result of a 24 hr fast. Rats deprived of food for 72 hr had significantly smaller increases in oxygen consumption, colonic and tail skin temperatures following administration of isoproterenol (100 micrograms/kg b.w., s.c.) when compared to non-fasted control rats. Arterial blood pressure and heart rates were measured in unrestrained, unanesthetized, chronically cannulated rats. Food deprivation for 72 hrs significantly attenuated the decrease in blood pressure and the increase in heart rate associated with administration of isoproterenol (10 micrograms/kg b.w., s.c.). Possible mechanisms for the reduced beta-adrenergic responsiveness associated fasting are discussed.

Animals↗