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C J Gordon

Publications and source records attributed to C J Gordon.

At least 73 records · Page 4Linked to original sources
PubMed1990

Thermal biology of the laboratory rat.

The purpose of this paper is to thoroughly review the literature and present a data base of the basic thermoregulatory parameters of the laboratory rat. This review surveys the pertinent papers dealing with various aspects of the thermal biology of the laboratory rat, including: metabolism, thermoneutrality, core and brain temperature, thermal tolerance, thermal conductance and insulation, thermoregulatory effectors (i.e., thermogenesis, peripheral vasomotor tone, evaporation, and behavior), thermal acclimation, growth and reproduction, ontogeny, aging, motor activity and exercise, circadian rhythm and sleep, gender differences, and other parameters. It is shown that many facets of the thermoregulatory system of the laboratory rat are typical to that of most homeothermic species. However, is several instances the rat exhibits unique thermoregulatory responses which are not comparable to other species.

Acclimatization↗
PubMed1990

Effects of methanol on autonomic thermoregulation of rats at different ambient temperatures.

To measure the effect of methanol on autonomic thermoregulation, male Fischer rats were injected intraperitoneally with saline or 1 or 3 g/kg methanol (20% w/v in saline). The rats were then placed in a chamber, set at an ambient temperature (Ta) of 5, 15, 25, or 35 degrees C, for 60 min while total activity, metabolic rate (MR), evaporative water loss (EWL), and dry thermal conductance were measured. After 60 min, the rat was removed from the chamber and colonic temperature (Tc) was measured. The rats developed a significant hypothermia following the 3 g/kg dosage of methanol at Ta's from 5 to 25 degrees C, while the change in Tc at 35 degrees C was not significant. Total activity decreased following 3 g/kg methanol at Ta's from 15 to 35 degrees C. At a Ta of 25 degrees C, MR was at basal levels and methanol had no effect, but at the other Ta's, where MR was elevated, methanol caused a significant reduction in MR. EWL and thermal conductance were elevated at 35 degrees C in control rats, and methanol reduced EWL at this Ta while it had no effect on conductance at this or any other Ta. These data suggest that the methanol-induced hypothermia and its depressive effect on activity and MR were related. The effect of methanol on the heat loss effectors (EWL, conductance) was not significant or was in the direction of heat conservation. Thus, methanol exposure leads to a significant hypothermia in rats by an inhibitory action on heat production pathways.

Animals↗
PubMed1990

Hypothermia and hypometabolism: sensitive indices of whole-body toxicity following exposure to metallic salts in the mouse.

To investigate the practicality of hypothermia and hypometabolism as sensitive indices of toxicity in the mouse, oxygen consumption was monitored continuously and body temperature was measured at 30 min postinjection following the intraperitoneal administration of various metal salts. Eleven metal ions were tested: Al3+, Cd2+, Co2+, Cr2+, Cu2+, Hg2+, Mg2+, Mn2+, Ni2+, Pb2+, and Zn2+. All metals induced dose-dependent reductions in both oxygen consumption (hypometabolism) and deep body (colonic) temperature. Comparative toxicity of the metal ions was evaluated by calculating the dose of metal ion in dimensions of mmol/kg body mass needed to reduce colonic temperature to 35 degrees C. The order of toxicity from lowest to highest was as follows: Cr less than Al less than Pb less than Mn less than Mg less than Zn less than Cu less than Co less than Ni less than Hg less than Cd. The threshold doses for reducing body temperature were less than 5% of the LD50 in 6 of the metals studied. Metal salts with relatively low LD50 doses such as Hg, Cd, and Ni were most efficacious in inducing hypothermia and hypometabolism. Moreover, there was a direct linear relationship between dose for inducing hypothermia or hypometabolism and the reported LD50. Hence, the hypothermia and hypometabolism test may prove to be a sensitive and rapid test for the evaluation of toxicity of environmental contaminants.

Acclimatization↗
PubMed1990

Ethnic differences in the renal sodium dopamine relationship. A possible explanation for regional variations in the prevalence of hypertension?

Over the last three years we have carried out studies on the urine output of both sodium and dopamine in five different ethnic groups: whites, Ghanaians, Zimbabweans, Iranians and Thais. Sodium was measured by ion specific electrode and dopamine by HPLC with electrochemical detection (using epinine as an internal standard). In several groups salt loading studies were also carried out. The five ethnic groups differed substantially with regard to the correlation between their urinary sodium and dopamine outputs. Three groups (whites, Thais and Zimbabweans) showed a strong positive correlation (P less than .001) and this may reflect their traditionally salt rich diet. In two groups (Ghanaians and Iranians) there was no correlation and this may reflect a salt scarce environment. Taken together with our previously reported studies showing that normotensive Ghanaians do not mobilize dopamine on salt loading, this would suggest that certain ethnic groups are predisposed to develop hypertension on salt loading--that is, they are 'salt sensitive.' This genetic trait may have passed from the West Coast of Africa, with the slaves, to America and the Caribbean. Other workers have reported deficiencies in vasodilator systems in the American black, such as dopamine, kallikrein and the renal prostaglandins. These defects may lead to the nosologic entity of 'low renin' hypertension, well described in American blacks, and could open up avenues of therapy based either on DA1 activators (such as fenoldopam) or on renal prodrugs (such as gludopa).

Africa, Western↗
PubMed1990

Thermal effects of MR imaging: worst-case studies on sheep.

The objective of this study was to provide a worst-case estimate of thermal effects of MR imaging by subjecting anesthetized unshorn sheep to power deposition at specific absorption rates (SARs) well above approved standards for periods of time in excess of normal clinical imaging protocols. A control period with no RF power was followed by 20-105 min of RF power application. Afterward, there was a 20-min or longer recovery period with no RF power. Eight sheep were given whole-body RF exposure (1.5- to 4-W/kg SAR) while rectal and skin temperatures were monitored. Four sheep were subjected to 4-W/kg head scans for an average of 75 min while temperatures of the cornea, vitreous humor, head skin, jugular vein, and rectum were measured. In head scanning experiments, skin and eye temperatures increased about 1.5 degrees C. Jugular vein temperature rose a maximum of 0.4 degrees C after an average exposure of 75 min. In whole-body exposures, elevation of rectal temperature was correlated with energy input. Deep-body temperature rises in excess of 2.0 degrees C were attained for 4-W/kg whole-body exposure periods greater than 82 min. Animals exposed for 40 min to 4 W/kg in either body coil (three sheep) or head coil (two sheep) were recovered and observed to be in good health for 10 weeks; no cataracts were found. MR power deposition at SAR levels well above typical clinical imaging protocols caused body temperature to increase. For exposure periods in excess of standard clinical imaging protocols the temperature increase was insufficient to cause adverse thermal effects. Studies in healthy humans are needed to determine whether enhanced heat-loss effector mechanisms are likely to cause deep-body temperatures to plateau at an acceptable level, and to elucidate mechanisms that determine subcutaneous temperature.

Animals↗
PubMed1989

Metoclopramide versus metoclopramide and lorazepam. Superiority of combined therapy in the control of cisplatin-induced emesis.

Sixty-four patients treated with cisplatin-containing regimens were entered into a randomized, double-blinded study examining the antiemetic efficacy of metoclopramide with and without lorazepam for control of cisplatin-induced emesis. Metoclopramide was administered to all patients at 2 mg/kg, intravenously, 30 minutes before chemotherapy and 1.5, 3.5, and 5.5 hours posttreatment. Patients randomized to receive combined antiemetic therapy were administered lorazepam at 2 mg/m2 (maximum, 4 mg dose) intravenously, 30 minutes before chemotherapy. Those patients not receiving lorazepam were given normal saline placebo. Degree of nausea and number of vomiting episodes were recorded on a data flow sheet with a visual analogue scale. Drug toxicities were evaluated before each administered dose. Patients receiving both metoclopramide and lorazepam experienced significantly less vomiting episodes (P less than 0.05) and nausea (P less than 0.01) when compared to patients given metoclopramide alone. Forty-four percent of those receiving the combined therapy reported no nausea or vomiting episodes compared to only 22% receiving metoclopramide alone. Sedation was significantly more common in patients receiving lorazepam (88%) as opposed to patients receiving only metoclopramide (43%), P less than 0.01. Amnesia was seen in 25% receiving lorazepam. No significant difference in diarrhea, dystonia, or disinhibition was observed between the two arms. The authors conclude that the combination of lorazepam and metoclopramide was superior to metoclopramide alone in the prevention of cisplatin-induced nausea and vomiting, with sedation and amnesia more commonly observed in the combined regimen.

Adult↗
PubMed1989

Ethnic differences in the renal sodium-dopamine relationship: a possible explanation for regional variation in the prevalence of hypertension?

Twenty-four-h urinary sodium and dopamine output by normotensive adults from 5 different ethnic groups have been measured. The groups differed substantially in the correlation between the urinary output to sodium and dopamine. Those with a traditionally salt rich diet (Thais, Caucasians, Zimbabweans) showed a strong positive correlation (p less than 0.001), whereas no such relationship was found in West Africans and Iranians, who come from traditionally salt scarce environments. It is hypothesised that in some races the lack of or uncoupling of the renal sodium-dopamine relationship, possibly as a mechanism to help conserve dietary sodium, predisposes to the development of hypertension when the individuals encounter a salt rich diet.

Adaptation, Physiological↗
PubMed1989

Temperature regulation following nickel intoxication in the mouse: effect of ambient temperature.

1. The purpose of this study was to examine the interaction between ambient temperature (Ta) and the effects of nickel chloride on the thermoregulatory system of the mouse. 2. Male mice of the BALB/c strain were injected with nickel chloride at dosages of 0, 0.1, 1.0, 2.5, 5.0 and 10.0 mg/kg intraperitoneally and placed in an environmental chamber set at a Ta of either 10, 20, 30 or 35 degrees C for 60 min. Colonic temperature was then measured after one hour of exposure at a given Ta. 3. The thermoregulatory effects of nickel chloride were highly dependent on Ta. Nickel chloride had no effect on body temperature at Ta's of 30 and 35 degrees C. 4. 10 mg/kg dosage of nickel chloride caused a significant reduction in colonic temperature at a Ta of 20 degrees C. At a Ta of 10 degrees C the 5 and 10 mg/kg dosages of nickel chloride caused a significant lowering of body temperature. 5. Using segmented linear regression techniques it was shown that the threshold dose of nickel chloride for causing hypothermia was 9.6 and 3.3 mg/kg at Ta's of 20 and 10 degrees C, respectively. 6. This study has shown that two stressors, low Ta and nickel chloride intoxication, when applied independently have no effect on body temperature; however, when applied simultaneously, they have a significant toxic effect on thermoregulation.

Animals↗
PubMed1989

Modulating effect of body temperature on the toxic response produced by the pesticide chlordimeform in rats.

Previous studies from this laboratory have demonstrated significant deficits in cardiovascular function in rats exposed to the pesticide chlordimeform (CDM) when body core temperature (TCO) was maintained at 37 degrees C. To investigate the role of TCO on CDM toxicity, similar experiments were conducted over a range of TCO values. Adult rats (n = 30) were anesthetized with sodium pentobarbital (35 mg/kg) and randomly assigned to one of six equal groups. Groups were paired and TCO was maintained in the rats in each of the respective group pairs at one of three levels (37, 35, or 33 degrees C). Rats in one group at each temperature level (groups T37, T35, and T33) were injected intraperitoneally with 60 mg/kg of CDM. Animals in the corresponding temperature-matched groups (groups C37, C35, and C33, respectively) received volume-matched injections of normal saline vehicle and served as time-paired controls. The electrocardiogram and heart rate (HR) were monitored throughout the experimental procedure. There was a significant decrease in HR in all CDM-treated groups when compared to the control group animals. The magnitude of the observed cardiac effect was attenuated in the T35 group when compared to that of the other treated groups. Similarly, lethality rates (number of deaths/total) for the T37, T35, and T33 groups were 2/5, 0/5, and 3/5, respectively; there were no deaths among the control-group animals. From these and previous data from this laboratory, we conclude there may be a beneficial effect of moderate hypothermia in rats exposed to toxic agents while more severe hypothermia appears to offer no advantage and may actually exacerbate the toxic effect.

Amidines↗
PubMed1989

Thermoregulatory responses of the rabbit to central neural injections of sulfolane.

Systemic exposure of the rabbit to sulfolane results in hypothermia; however, the mechanism of this thermoregulatory effect is unknown. This study was designed to determine the thermoregulatory effects of sulfolane on the central nervous system (CNS) of the rabbit. Male rabbits were stereotaxically implanted with an injection cannula over the preoptic/anterior hypothalamic area (POAH) or into the lateral cerebral ventricle. POAH temperature (TPOAH), ear temperature (Te), and metabolic rate (MR) were recorded at an ambient temperature (Ta) of 15 degrees C. No changes were observed in any of the thermoregulatory indices following injections of saline or sulfolane in dosages of 100, 300, and 1000 micrograms directly into the POAH. Intracere-broventricular (ICV) injection of saline also had no effect on thermoregulation. However, ICV sulfolane in dosages of 300, 1000, and 3000 micrograms caused TPOAH to rise 0.23, 0.47, and 0.56 degrees C, respectively. This hyperthermia was significant at a dosage of 3000 micrograms. There was no change in Te or MR at these three dose levels. Microinjection of 10,000 micrograms sulfolane ICV caused a slight decrease in TPOACH for 30 min which was accompanied by an increase in Te. Following the slight decrease, TPOAH increased to + 0.54 degrees C at 120 min after injection as Te returned to baseline values. The data suggest that the previously observed thermoregulatory effects of sulfolane following systemic exposure cannot be attributed to a direct action of the parent compound on the CNS.

Animals↗
PubMed1988

Temperature regulation in laboratory mammals following acute toxic insult.

The purpose of this paper is to provide a concise review of the effects of acute chemical toxicity on thermoregulation in mammals, with particular emphasis on the effects of xenobiotic compounds in laboratory rodents. It has been shown that acute administration of compounds such as nickel, cadmium, lead, and some pesticides causes a reduction in the body temperature of mice when tested at normal room temperatures. When provided with the option of selecting their preferred ambient temperature, the toxic-treated animals generally select cool temperatures which augment the hypothermic effect of the toxic compounds. It would appear that many of the xenobiotic compounds have central as well as peripheral effects on the control of body temperature. That is, the hypothermic animals select cool temperatures, a condition indicative of a centrally mediated decrease in the set-point. This decrease in set-point, or regulated hypothermia, may be beneficial to survival since the lethality of most xenobiotic compounds increases with rising body temperature. The observation that acute doses of various compounds leads to behaviorally and autonomically mediated changes in body temperature may have significant implications for the measurement of other biological effects of these chemical agents (e.g., CNS dysfunction, bradycardia, immunosuppression).

Animals↗
PubMed1988

Thermoregulatory responses of the rabbit to subcutaneous injection of sulfolane.

Earlier studies have shown that intraperitoneal injection of the industrial solvent sulfolane (tetrahydrothiophene-1,1-dioxide) caused a decrease in metabolic rate and a rapid, regulated hypothermia in mice and rats. In the present study, subcutaneous injections of 0, 100, 200, 400, 600, and 750 mg/kg sulfolane at an ambient temperature (Ta) of 10 degrees C caused a dose-dependent decrease in colonic temperature (Tc) of rabbits. Metabolic rate (MR) remained unchanged during the initial phase of the hypothermia for all dose groups; but peripheral vasodilation, as indicated by an increase in ear skin temperature, was seen at the higher dose levels. The observed thermoregulatory response to sulfolane was a function of Ta. Thus, at Tas of 10 and 20 degrees C, injection of 600 mg/kg sulfolane had no effect on MR but caused an increase in ear skin temperature. The magnitude of the hypothermia was similar at these two Tas, indicating the sulfolane-treated rabbits had some control over Tc. At a Ta of 28 degrees C, however, the animals became hyperthermic upon injection of 600 mg/kg sulfolane.

Animals↗
PubMed1988

Effect of ethyl alcohol on thermoregulation in mice following the induction of hypothermia or hyperthermia.

This study was designed to assess the effects of ethyl alcohol (ethanol) administration on behavioral and autonomic thermoregulation in mice subjected to severe hypothermia or hyperthermia. Male mice of the BALB/c strain were injected intraperitoneally with ethanol at dosages of 0, 0.3, 1.0, or 3.0 g/kg and then placed within a hot environmental chamber to raise their body temperature to 41 degrees C or, alternatively, within a cold chamber to lower it to 28 degrees C. Once the desired hypothermic or hyperthermic state was achieved, the mice were removed from the chamber and placed in either a temperature gradient to monitor behavioral thermoregulatory responses or in an environmental chamber thermostabilized at an ambient temperature (Ta) of 28 degrees C to monitor metabolic rate. The 3.0 g/kg dosage significantly affected behavioral thermoregulatory responses of the hyperthermic mice when initially placed in the temperature gradient. The ability to increase metabolic rate following hypothermia was significantly suppressed at 3.0 g/kg. Dosages of 1.0 and 3.0 g/kg inhibited metabolic rate of hyperthermic mice. Both hypothermic and hyperthermic mice given 3.0 g/kg of ethanol had colonic temperatures significantly below normal after placement in the temperature gradient and metabolic chamber. In conclusion, relatively large dosages of ethanol impair behavioral and autonomic thermoregulation and may lower the set-point for the control of body temperature in mice.

Animals↗
PubMed1988

Thermoregulatory responses in mice following acute administration of principal nitrogenous excretory substances.

This study was designed to assess the effects of some key excretory nitrogenous substances on body temperature and selected ambient temperature (Ta) in the mouse. In the first experiment, a dosage-response curve was developed to assess the effects of urea, creatinine, and ammonium chloride on colonic temperature at a Ta of 20 degrees C. All three substances elicited a drop in body temperature at a critical dosage. The threshold dosages were 3280 mg/kg for urea, 1279 mg/kg for creatinine, and 365 mg/kg for ammonium chloride. In a second experiment the selected Ta was monitored using a temperature gradient system. Mice were injected with dosages of the nitrogenous substances that had previously been shown to cause hypothermia at a Ta of 20 degrees C. Urea and ammonium chloride had no significant effect on the selected Ta nor on the colonic temperature after 90 min in the temperature gradient. Creatinine elicited a slight lowering of the selected Ta but had no effect on colonic temperature. The thermoregulatory responses to extremely toxic dosages of the nitrogenous substances appear to be quite dissimilar to that when animals are treated with xenobiotic compounds.

Ammonium Chloride↗
PubMed1988

Behavioral thermoregulation in the rat following the oral administration of ethanol.

To assess if ethyl alcohol (ethanol) causes a reduction in the set-point for control of body temperature, behavioral thermoregulatory responses in the Fischer rat were measured following a single oral administration of ethanol. In a preliminary study, five rats were given 3.0 g/kg ethanol dissolved in saline (20%; v/v) by gavage and placed in a longitudinal temperature gradient for 2 hr. The temperature gradient permitted the rats to behaviorally thermoregulate (i.e. select a thermal preferendum). The selected ambient temperature (Ta) in the temperature gradient was notably lower during the initial and final stages of the test period when compared to the response of rats administered similar volumes of saline. Colonic temperature upon removal from the gradient was approximately 1.0 degree C below that of the saline-treated animals. In a follow-up study, rats were placed in the temperature gradient for 1 hr for accommodation purposes. The rats were then gavaged with 0, 1.0 or 3.0 g/kg ethanol and placed back in the gradient for another 2 hr. Selected Ta was significantly reduced in the 3.0 g/kg group during the second hour post-ethanol exposure. The 1.0 g/kg dosage had little effect on selected Ta. As in the preliminary study, the colonic temperature of the rats in the follow up study given 3.0 g/kg was 1.0 degree C below that of the control at 2 hr post-injection. Because the 3.0 g/kg treated animals were significantly hypothermic and selected cooler Tas in the temperature gradient, it was concluded that ethanol exerted a lowering of the set-point for control of body temperature.

Adaptation, Physiological↗
PubMed1988

Simultaneous measurement of preferred ambient temperature and metabolism in rats.

A recent study from this laboratory found that rats placed in a temperature gradient preferred ambient temperatures (Ta) that were significantly below the lower critical Ta of the thermoneutral zone for elevating metabolic rate (MR). To further evaluate the interaction between preferred Ta and MR in the rat, a system was developed where preferred Ta, MR (i.e., O2 consumption), and activity could be automatically monitored in the unrestrained rat. Two groups of male Sprague-Dawley rats, a light-weight group and a heavy-weight group, were placed in a longitudinal temperature gradient for 90 min. These animals were further divided into two groups. One group was permitted free run in the gradient with a temperature range of 7-40 degrees C, whereas another group was restricted to the warm end of the gradient where the coolest available temperature was approximately equal to the lower critical Ta (29 degrees C). The preferred Ta and MR data were statistically analyzed over the last 20 min of the experimental run. Rats allowed to run freely in the gradient selected Ta of 17-20 degrees C and had MR significantly higher than animals restricted to a range of Ta no cooler than the lower critical Ta. Animals that selected the cooler Ta were much more active than those forced to remain at the warmer Ta. In conclusion, the interaction between behavioral and autonomic thermoregulation in the rat is unique compared with other rodent species such as the mouse, hamster, and guinea pig, which prefer Ta associated with thermoneutrality.

Animals↗
PubMed1987

Normalizing the thermal effects of radiofrequency radiation: body mass versus total body surface area.

The current guideline for exposure to radiofrequency radiation (RFR) was developed through assessment of the biological effects data collected primarily from the rat. The consensus that a lack of hazardous biological effects occurred below a whole-body-averaged specific absorption rate (SAR) of 4.0 W/kg led to the proposition of a 0.4 W/kg guideline with a built-in safety factor of 10. This paper demonstrates that if the RFR absorption rate in the rat had been normalized with respect to total body surface area rather than body mass, the exposure guideline would be 2.3 W/m2, which translates to an SAR of approximately 0.06 W/kg for an adult human. It is further shown that a given RFR absorption rate, normalized as a fraction of a species' heat loss per unit of surface area, is independent of body mass over a range of 0.03-100 kg; however, a normalization of the RFR absorption rate to heat loss per unit of body mass is highly dependent on the species' mass. Normalizing the rate of RFR absorption to the surface area of the rat indicates that the current RFR exposure guideline of 0.4 W/kg may be too high.

Animals↗