Sustained Hyperthermia Research Articles

Hypothalamic, rectal, and muscle temperatures in exercising dogs: effect of cooling.

To investigate mechanisms that may be involved in the prolongation of exercise performance with body cooling hypothalamic (Thy), rectal (Tre), and exercising muscle (Tm) temperatures, as well as the heart rate, respiratory rate, blood lactic acid concentration ( [LA] ), and plasma osmolality (Osm) were measured in five dogs during exhaustive treadmill exercise at an ambient temperature (Ta) of 22 +/- 1 degree C without cooling (control) and with external cooling by use of ice packs. In both series of experiments, dehydration of animals was prevented. Compared with exercise with noncooling, exercise with cooling resulted in 1) increased exercise duration from 90 +/- 14 to 145 +/- 15 min (62%, P less than 0.05); 2) attenuated increases in Thy, Tre, and Tm; 3) decreased respiratory and heart rates; and 4) lowered LA. Significant negative correlations were found between both Tm and delta Tm attained at 60 min of the run and time of exercise until exhaustion (r = -0.72 and -0.74, respectively; P less than 0.02). This work failed to differentiate clearly changes or equilibrium levels of brain, core, or muscle temperature as separate factors affecting work tolerance. However, the inverse relationship between Tm reached at 60 min of the run (in both experiments) and the total duration of exercise indicates that sustained muscle hyperthermia may largely contribute to limitation of working ability.

Action of anorexigenic peptide injected into the brain: Dissociation of effect on body weight and feeding in the rat

Previous reports on the effect of anorexigenic peptide (AXP) administered systemically in the rodent are inconsistent in terms of the effect of the tri-peptide on food intake and body weight. The purpose of this study was to examine the effect of AXP infused into the brain on these measures. In post-pubescent female rats of the Sprague-Dawley strain, guide cannulae were permanently implanted in the lateral cerebral ventricle for repeated intracerebroventricular (ICV) infusion. Postoperatively, measures of food and water intake and body weight were obtained every day at the same time. After a 7-day base-line period, AXP was infused bilaterally in a total volume of 15 μl and in a dose of either 0.25 μg (n=7) or 1.25 μg (n=5), with artificial CSF vehicle serving as the control solution (n=6). ICV infusions were given once daily for 20 consecutive days, after which the same intake and body weight measures were recorded for another 7-day period. The rats given 0.25 μg AXP showed a significant suppression in weight gain with the overall slope of the growth curve being 0.358. In contrast, the growth slope of the rats given the 1.25 μg dose of AXP was 0.621, whereas those given the CSF was 0.823. Although the trends of intake of food tended to follow the curves of the rats' body weight, the difference between g/kg food intake of rats during ICV infusions of either dose of AXP was not significantly different from that of the CSF controls. Water intake also was unaffected by either dose of AXP. These results demonstrate that this tri-peptide derived from urine of patients afflicted with anorexia nervosa exerts a direct effect on the brain. Since the 0.25 μg dose of AXP infused acutely ICV caused a sustained hyperthermia, its mechanism of action is apparently a metabolic one; that is, the interruption in the gain in body weight of the rat is independent of the amount of food it ingests.

Somatosensory evoked potentials during whole body hyperthermia in humans

Somatosensory evoked potentials (SEPs) and body temperature were recorded in patients subjected to induced total hyperthermia for treatment of advanced neoplasms. Elevation of body temperature up to 42°C for 2 h was achieved using a computer-controlled external heating system. SEPs were recorded continuously on-line during the treatment using finger shock stimulation. Evoked potential components later than 160 msec disappeared in the early part of the treatment, but reappeared quickly during cooling. P50 and P50-N70 amplitudes decreased regularly and significantly over the whole duration of the heating period. During the plateau period, no evoked potential peaks could be detected but short latency peaks reappeared as soon as cooling started. The disappearance of SEPs to finger stimulation during sustained hyperthermia at 42°C confirms the findings obtained by EEG recording that a major neuronal dysfunction occurs under these circumstances which subsides quickly as temperature is dropped.

Hyperthermia produced by simulated intraventricular hemorrhage in the cat

The thermoregulatory effect of simulated intraventricular hemorrhage was examined in cats implanted with a guide cannula terminating in either the dorsal or ventral aspect of the third cerebral ventricle. Each cat received a slow intraventricular infusion of 500 μl control solution (artificial cerebrospinal fluid) followed 7 days later by a similar infusion of fresh autogenous venous blood. Animals were killed 4 to 48 h after blood infusion and the brains dissected immediately. Control infusions caused hyperthermia in only one cat. Blood infusion produced sustained hyperthermia in nine animals (mean latency, 28.4 min; mean maximum magnitude, 1.4°C). The characteristic of the blood distributions which best correlated with hyperthermia was the presence of clotted blood within the ventral portion of the third ventricle. Cats in which blood did not reach this locus ( N = 7), even though massive clots could be found in the lateral, dorsal third, and fourth ventricles and/or in the cisternal spaces, did not become febrile. With one exception, cats in which blood clotted in the ventral third ventricle exhibited hyperthermia. In the exceptional cat, the clot within the ventral third ventricle was limited entirely to the posterior aspect of this space. These findings suggest that hyperthermia consequent to ventricular bleeding is mediated by an action of blood on structures bordering on the ventral portion of the third ventricle, possibly the anterior hypothalamic and/or preoptic nuclei. These results have implications regarding the putative mechanisms through which blood could affect these structures.

TRH: a possible mediator of thermoregulation.

FELDBERG and Myers1 have reported that intraventricular injections of amines produce changes in the rectal temperature of unanaesthetised cats. They noted that more than 50 µg noradrenaline produced temporary hypothermia whilst 200 µg 5-hydroxytryptamine (5HT) induced a sustained hyperthermia. These results, coupled with earlier findings that these amines were concentrated in the hypothalamus2,3, led them to speculate that the regulation of body temperature in the cat may be mediated by the release of noradrenaline and 5HT within the hypothalamus.

Effects of chronic central cooling on alimentation and thermoregulation.

AbstractChronic local cooling in the forebrain of 4 un‐anesthetized goats was achieved by perfusion of cold water for 1–7 days through implanted silver thermodes. In 2 goats with thermodes located in the pre‐optic region, chronic central cooling resulted in a marked inhibition of water consumption while causing little alteration of food intake. In a third goat with a thermode in the posterior pre‐optic area and the rostral hypothalamus, central cooling inhibited water intake but also increased food intake slightly. In contrast, in a fourth goat bearing a thermode rostrally in the ventromedial hypothalamus, prolonged chilling resulted in a considerable increase in hay consumption while failing to inhibit drinking. These data provide additional evidence in support of the thermostatic theory of the regulation of food intake (Brobeck 1948) and of water intake (Andersson and Larsson 1961); further, they reveal a differential response in alimentation to cooling of separate areas of the forebrain. On central cooling, all thermode goats rapidly developed sustained hyperthermia without shivering declining over 1–3 days upon cessation of central cooling. The sustained hyperthermia may be the result of peripheral vasoconstriction combined with increased metabolism of non‐shivering origin. To explain the present results, there is no need to postulate the existence of central “cold receptors” or “hypothermia detectors” within the cooled part of the brain.