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Biomedical subjects

C J Gordon

Publications and source records attributed to C J Gordon.

At least 127 records · Page 7Linked to original sources
PubMed1982

Effects of ambient temperature and exposure to 2450-MHz microwave radiation on evaporative heat loss in the mouse.

Whole-body evaporative heat loss was measured as whole-body evaporative water loss in mice during a 90-min exposure to 2450-MHz microwave radiation at an ambient temperature of 20 degrees C and in non-exposed mice maintained at ambient temperatures of 20, 25, 30, 33, and 35 degrees C. The ambient-temperature threshold for increasing evaporative water loss was between 30 and 33 degrees C. A specific absorption rate of microwave radiation in excess of 29 W/kg was required to produce an increase in heat loss. For absorption rates ranging from 29 to 44 W/kg, the mouse dissipated 65% of the total absorbed heat by water evaporation; the remainder was dissipated passively. The data collected in the mouse may be extrapolated to larger species, such as man, but only by an exponential relationship. Using this relationship, it was shown that a threshold specific absorption rate of 29 W/kg in a 0.033-kg mouse was equivalent to approximately 0.25 W/kg in a 70-kg human.

Animals↗
PubMed1982

Open-loop gain of evaporative heat loss during radiant heat exposure in the mouse.

Whole-body evaporative water loss of the mouse during radiant heating was determined at ambient temperatures of 20-35 degrees C. The ratio of evaporated to absorbed heat per gram body weight, which is equal to open-loop gain (OLGEHL), increased over sixfold with each 1 degrees C increase in ambient temperature. At 35 degrees C, OLGEHL was equal to 0.8, which implies that the mouse evaporates 80% of the absorbed radiant heat. At 20 degrees C, less than 1% of the absorbed heat is evaporated and the remainder of the heat load is dissipated passively. A previous estimate of OLG for the mouse is similar to the data from this study at an ambient temperature of 35 degrees C. Determining OLG with natural ambient stimulation may make future studies in thermoregulation comparable.

Animals↗
PubMed1982

Action of preoptic injections of beta-endorphin on temperature regulation in rabbits.

Male New Zealand White rabbits, Oryctolagus cuniculus, were stereotaxically implanted with a guide tube above the preoptic/anterior hypothalamus area (PO/AH) for the injection of the opioid peptide, beta-endorphin (beta-E), naloxone, sodium salicylate, or physiological saline. PO/AH and ear temperature, oxygen consumption, and evaporative heat loss (EHL) were recorded in free-moving rabbits before and after injection of saline followed with beta-E, naloxone, or sodium salicylate at ambient temperatures (Ta) of 2-31 degrees C. A 5-micrograms injection of beta-E promoted a rapid reduction in ear temperature followed by a prolonged rise in PO/AH (body) temperature. Preinjection with an isovolumetric amount of the opiate antagonist, naloxone, inhibited the thermoregulatory effects of beta-E. The beta-E-induced rise in body temperature was directly correlated with Ta. beta-E had no effect on oxygen consumption at Ta's of 5 and 27 degrees C. When measured 30 min after injection, beta-E demonstrated a significant inhibition of EHL at Ta's of 27 and 31 but not 5 degrees C. The beta-E-induced rise in body temperature was not antagonized with preinjections of sodium salicylate in the PO/AH. These data indicate that beta-E promotes a regulated increase in body temperature. The mechanism of activation appears to be distinct from that of an infectious fever.

Animals↗
PubMed1982

Effect of heating rate on evaporative heat loss in the microwave-exposed mouse.

Male CBA/J mice were administered heat loads of 0-28 J X g-1 at specific absorption rates (SARs) of either 47 or 93 W X kg-1 by exposure to 2,450-MHz microwave radiation at an ambient temperature of 30 degrees C while evaporative heat loss (EHL) was continuously monitored with dew-point hygrometry. At an SAR of 47 W X kg-1 a threshold heat load of 10.5 J X g-1 had to be exceeded before EHL increased. An approximate doubling of SAR to 93 W X kg-1 reduced the threshold to 5.2 J X g-1. Above threshold the slopes of the regression lines were 1.15 and 0.929 for the low- and high-SAR groups, respectively. Thus the difference in threshold and not slope attributes to the significant increase in EHL when mice are exposed at a high SAR (P less than 0.02). In separate experiments a SAR of 47 W X kg-1 raised the deep body temperature of anesthetized mice at a rate of 0.026 degrees C X s-1, whereas 93 W X kg-1 raised temperature at 0.049 degrees C X s-1. Hence the sensitivity of the EHL mode of heat dissipation is directly proportional to the rate of heat absorption and to the rate of rise in body temperature. These data contradict the notion that mammals have control over whole-body heat exchange only (i.e., thermoregulation) but instead indicate that the EHL system is highly responsive to the rate of heat absorption (i.e., temperature regulation).

Animals↗
PubMed1981

Acoustically driven thermal-identified neurons in the preoptic area of unanesthetized rabbits.

The convergence of acoustically stimulated neural activity onto central and peripheral thermal-stimulated neurons in the preoptic/anterior hypothalamus (POAH) was studied in the unanesthetized rabbit. POAH single units were either directly thermally stimulated with a water-perfused thermode, or indirectly stimulated by warming the ears with an infrared lamp. There was no statistical distinction in the way central thermal-stimulated neurons responded to an 89 dB, 510 Hz sound pulse. There was a significant interaction in the response of neurons inhibited by skin heating (cold-responsive) to acoustic stimulation with 52% facilitated, 33% inhibited and 15% unaffected. It is possible that some neurons in the POAH are part of a common pathway leading to an activation of thermal- and acoustically-induced changes in motor activity.

Acoustic Stimulation↗
PubMed1981

Effect of beta-endorphin on the thermal excitability of preoptic neurons in the unanesthetized rabbit.

The opioid peptide, beta-endorphin (beta-E), will promote changes in body temperature when injected into the brain. It is possible that beta-E alters body temperature by affecting the activity of thermoregulatory neurons in the preoptic anterior hypothalamus (POAH). Single unit activity in the POAH was recorded in unanesthetized rabbits while radiant heat was applied to the dorsal skin. Beta-E was then microinjected into the POAH, and the peripheral heating was repeated. Seventy-seven percent of the POAH neurons were responsive to skin heating. Beta-E and equal excitatory and inhibitory effects on warm-excited and warm-inhibited neurons. Four of six warm-excited neurons were converted to warm-inhibited or unresponsive following beta-E injection. Six out of ten warm-inhibited neurons were converted to warm-excited or unresponsive by beta-E. Beta-E-induced shifts in thermal excitability of POAH neurons may be responsible for the ability of POAH injections of beta-E to elevate body temperature in the rabbit.

Animals↗
PubMed1981

Effect of slow and rapid skin heating on the activity of single neurons in the preoptic area of unanesthetized rabbits.

Skin temperature was increased at slow and rapid rates while single unit activity was recorded in the medial preoptic/anterior hypothalamus (POAH) of the unanesthetized rabbit. Of 69 units tested with slow skin heating, activity increased in 14, decreased in 38, and was unchanged in 17. The responsive units exhibited either an immediate or delayed change in firing rate during skin heating. During rapid skin heating, 6 of 19 units which could be tested underwent a qualitative change from their thermal responsiveness during slow skin heating. Rapidly responding neurons could provide an instantaneous indication of changes in skin temperature, whereas the activation of slowly responding units requires a relatively long period of skin heating. Qualitative shifts in thermal responsiveness during rapid skin heating could provide an additional mechanism for detecting abrupt changes in ambient temperature. Thus, POAH thermal responsive neurons provide input regarding both steady state and rapid changes in skin temperature.

Animals↗
PubMed1981

Rapid brain cooling in the free-running hamster Mesocricetus auratus.

A thermocouple reentrant tube was stereotaxically implanted in the rostral brain stem of the golden hamster, Mesocricetus auratus. Brain temperature was continuously recorded while the hamster was permitted volitional running on an activity wheel. There was an immediate decrease in brain temperature at the start of running activity, reaching a mean of 0.49 degrees C below the prerunning level. Spontaneous or forced cessation of running activity was associated with a rapid recovery of brain temperature. The time course of brain cooling during exercise greatly differed from the exponential decay of brain temperature in hyperthermic and dead animals. Air flow through the nose may contribute to the maintenance of a low brain temperature because nasal blockade promotes an increase in brain temperature. Below an ambient temperature of 33 degrees C, the resting hamster maintains its brain temperature below deep-body (abdominal) temperature. Vinyl acetate casts of the arterial and venous systems revealed several potential sites for heat exchange that might account for brain cooling under resting and exercising conditions.

Animals↗
PubMed1980

Effects of prostaglandin E2 on the activity of thermosensitive and insensitive single units in the preoptic/anterior hypothalamus of unanesthetized rabbits.

Toe eliminate depressant effects of anesthetics on neuron activity, we recorded the single unit activity of thermoregulatory neurons in the POAH of unanesthetized rabbits. Intraventricularly applied PGE2 induced consistent excitatory effects (190% increase in firing rate) on cold-excitable cells and inhibited the firing rate (50%) of warm-sensitive neurons. Single units that were insensitive or had uncreelatable changes in firing rate with POAH temperature were either facilitated or inhibited by PGE2. The consistent effects of PGE2 on the thermoregulatory neurons found in this study support the proposal of PGE modulation of thermoregulatory neurons during the development of a fever.

Animals↗
PubMedDate not supplied

Protocols for clinical care.

This paper describes the work of the DILEMMA project to provide protocol-based decision support in a variety of clinical domains. We give an outline of the generic protocol model that DILEMMA has produced, and the protocol task manager (PTM) software developed to assist protocol use in routine clinical practice. We summarise the validation of the model carried out to date, and take a quick look at the place of protocols in the wider context of clinical decision support.

Clinical Protocols↗
PubMedDate not supplied

Technique for applying neurotropic substances onto single units in awake animals.

Methods are shown for the stereotaxic placement of twin cannulae, one for recording single unit activity and the other for microinjecting test substances directly on the recording site. The device is inexpensive, occupies a small space on the calvarium, and remains operational in the same animal for several months. This technique is being used to study the effects of various neurotranmitters and neuromodulators on the activity of single units in the hypothalamus of unanesthetized rabbits.

Animals↗
PubMedDate not supplied

Slow bursting thermal sensitive neurons in the preoptic area of the rabbit.

Recent data have shown the presence of some hypothalamic neurons with a slow bursting activity. This study reports the interactions of slow bursting neurons with thermoregulatory control in the preoptic/anterior hypothalamus (POAH). Ninety-seven single units studied with direct thermal stimulation and with central injections of norepinephrine (NE) or serotonin (5-HT) were assessed for slow bursting activity. Twenty-one percent of the neurons had slow bursting activity patterns with frequencies ranging from 0.02-0.10 Hz. Intraventricular or direct POAH injected monoamines frequently inhibited bursting activity during normothermia and/or POAH thermal stimulation. Slow bursting neurons may elicit rhythmic thermoregulatory motor outputs, neurosecretion, and infraslow DC potentials in the central nervous system.

Animals↗
PubMedDate not supplied

Effect of alcohol on behavioral and autonomic thermoregulation in mice.

Male, BALB/c mice were injected intraperitoneally with ethyl alcohol (ethanol) in dosages of 0, 0.03, 0.1, 0.3, 1.0, or 3.0 g/kg and then placed in a temperature gradient which permitted the measurement of preferred ambient temperature (Ta). The 3 g/kg dosage of ethanol resulted in a slight, but statistically equivocal, lowering of the preferred Ta during the first 30 min of placement in the gradient. A replication of this experiment using a higher sample size indicated that a 3 g/kg dosage of alcohol caused a statistically significant decrease in preferred Ta. In another experiment, BALB/c mice were treated with the aforementioned ethanol dosages while metabolic rate (MR), evaporative water loss (EWL), and colonic temperature were measured 60 min postinjection at Ta's of 20, 30, and 35 degrees C. At a Ta of 20 degrees C a dosage of 3 g/kg caused a significant decrease in MR, EWL, and colonic temperature. At a Ta of 30 degrees C this same dosage caused significant reduction in colonic temperature, however; at a Ta of 35 degrees C ethanol had no effect on these parameters. In conclusion, mice treated with a relatively large dose of ethanol will select a significantly cooler Ta, which is associated with hypothermia. These combined behavioral and autonomic thermoregulatory effects suggest that ethanol led to a decrease in the set-point body temperature.

Animals↗
PubMedDate not supplied

Thermoregulation at a high ambient temperature following the oral administration of ethanol in the rat.

This study was designed to assess the thermoregulatory mechanisms responsible for the elevation in body temperature following ethanol administration when exposed to a high ambient temperature (Ta). Male rats of the Fischer 344 strain were gavaged with 20% ethanol at doses of 0, 2.0, 4.0, 6.0, or 8.0 g/kg and were then placed in an environmental chamber set at a Ta of 37 degrees C. Metabolic rate normalized to body mass0.75 (MR), evaporative water loss (EWL), and motor activity were recorded for 60 min. Ethanol elicited a significant increase in colonic temperature and decrease in MR, EWL, and motor activity. Ethanol also significantly reduced the quantity of evaporated water per milliliter of oxygen consumed (E/M). Multiple linear regression analysis indicated that the two major factors which were associated with the ethanol-induced elevation in body temperature were an increase in MR and a decrease in E/M. Visual observation of behavior indicated that the normal grooming of saliva onto the fur during heat stress was impaired in ethanol-treated animals. Thus, during exposure to a high Ta, the acute ethanol-induced elevation in body temperature appears to be attributed to a suppression in both autonomic and behavioral mechanisms of heat dissipation.

Administration, Oral↗