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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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At least 37 records · Page 2

Central effects of some peptide and non-peptide opioids and naloxone on thermoregulation in the rabbit

The effects of several peptide and non-peptide opiods and naloxone on induced hyperthermia is studied in rabbits. The effect of tyical mu, kappa, and sigma receptor antagonists (morphine, ketocyclazcine and SKF 10,0 10, 047) and some opioid peptides (Beta-endorphin /BE/, methionine-enkaphalin /ME/, and D-Ala2-methionine-enkaphalin-amide /DAME/ are determined. The role of prostaglandins (PG), cAMP, and norepinephrine (NE) in morphine, BE, and DAME induced hyperthermia is investigated. In addition, the effect of naloxone on pyrogen, arachidonic acid, PGE2, prostacyclin, dibutyryl cAMP, and NE induced hyperthermia is determined. Among other results, it is found that the three receptor antagonists induced hyperthermia in rabbits. BE, ME, and DAME were also found to cause hyperthermia, and it is suggested that they act on the same type of receptor. It is also determined that neither NE nor cAMP is involved in the hyperthermia due to morphine, BE, and DAME. It is suggested that an action of endogenous peptides on naloxone sensitive receptors plays little role in normal thermoregulation or in hyperthermia.

Kandasamy, S. B.↗

Hyperthermic responses to central injections of some peptide and non-peptide opioids in the guinea-pig

The intracerebroventricular administration of prototype nonpeptide opioid receptor (mu, kappa, and sigma) agonists, morphine, ketocyclazocine, and N-allyl normetazocine and an agonist at both kappa and sigma receptors, pentazocine, was found to induce hyperthermia in guinea pigs. The similar administration of peptide opioids like beta endorphin, methionine endkephalin, leucine endkephaline, and several of their synthetic analogues was also found to cause hyperthermia. Only the liver-like transport system of the three anion transport systems (iodide, hippurate, and liver-like) present in the choroid plexus was determined to be important to the central inactivation of beta-endorphin and two synthetic analogues. Prostaglandins and norepinephrine (NE) as well as cAMP were not involved in peptide and nonpeptide opioid-induced hyperthermia. Naloxone-sensitive receptors were found to be involved in the induction of hyperthermia by morphine and beta-endorphin, while hyperthermic responses to ketocyclazocine, N-allyl normetazocine, pentazocine, Met-enkephalin, Leu-enkephalin, and two of the synthetic analogues were not antagonized by nalozone. The lack of antagonism of naloxone on pyrogen, arachidonic acid, PGE2, dibutyryl cAMP, and NE-induced hyperthermia shows that endogenous opioid peptides are not likely to be central mediators of the hyperthermia induced by these agents.

Kandasamy, S. B.↗

Muscle metaboreceptor modulation of cutaneous active vasodilation

PURPOSE: Isometric handgrip exercise in hyperthermia has been shown to reduce cutaneous vascular conductance (CVC) by inhibiting the cutaneous active vasodilator system. METHODS: To identify whether this response was initiated by muscle metaboreceptors, in seven subjects two 3-min bouts of isometric handgrip exercise in hyperthermia were performed, followed by 2 min of postexercise ischemia (PEI). An index of forearm skin blood flow (laser-Doppler flowmetry) was measured on the contralateral arm at an unblocked site and at a site at which adrenergic vasoconstrictor function was blocked via bretylium iontophoresis to reveal active cutaneous vasodilator function unambiguously. Sweat rate was measured via capacitance hygrometry, CVC was indexed from the ratio of skin blood flow to mean arterial pressure and was expressed as a percentage of maximal CVC at that site. In normothermia, neither isometric exercise nor PEI affected CVC (P > 0.05). RESULTS: The first bout of isometric handgrip exercise in hyperthermia reduced CVC at control sites and this reduction persisted through PEI (pre-exercise: 59.8 +/- 5.4, exercise: 49.8 +/- 4.9, PEI: 49.7 +/- 5.3% of maximum; both P < 0.05), whereas there were no significant changes in CVC at the bretylium treated sites. The succeeding bout of isometric exercise in hyperthermia significantly reduced CVC at both untreated (pre-exercise: 59.0 +/- 4.8, exercise: 47.3 +/- 4.0, PEI: 50.1 +/- 4.1% of maximum; both P < 0.05) and bretylium treated sites (pre-exercise: 61.4 +/- 7.3, exercise: 50.6 +/- 5.1, PEI: 53.9 +/- 6.0% of maximum, both P < 0.05). At both sites, CVC during PEI was lower than during the pre-exercise period (P < 0.05). Sweat rate rose significantly during both bouts of isometric exercise and remained elevated during PEI. CONCLUSIONS: These data suggest that the reduction in CVC during isometric exercise in hyperthermia, including the inhibition of the active vasodilator system, is primarily mediated by muscle metaboreceptors, whereas central command or muscle mechanoreceptors have less influence.

Non-NASA Center↗

Thermoregulation During Spaceflight

The purpose of this flight proposal is to investigate human thermoregulatory parameters during exercise in microgravity. The hypothesis to be tested is that microgravity-adopted astronauts will exhibit accentuated increases in their core temperature (excess hyperthermia) during exercise because of altered heat loss responses due to reduced sweating and/or accentuated vasodilation. The specific aims are (1) to compare core and skin temperature responses during moderate exercise before flight and inflight; (2) to determine whether the hypothesized inflight excessive hyperthermia is due to increased heat production, reduced, sweating, impaired peripheral vasodilation, or to some combination of these factors; and (3) to determine whether heat production at an exercise load of 60 percent of the maximal working capacity is similar preflight and inflight. It is expected that the astronauts will exhibit excessive hyperthermia during exposure to microgravity which will be caused by decreased sweating and decreased skin blood flow.

Greenleaf, John E.↗

Opposing actions of dibutyryl cyclic AMP and GMP on temperature in conscious guinea-pigs

It is shown that the intracerebroventricular administration of dibutyryl cyclic AMP (Db-cAMP) induced hyperthermia in guinea pigs which was not mediated through prostaglandins or norepinephrine since a prostaglandin synthesis inhibitor and an alpha-adrenergic receptor blocking agent did not antagonize the hyperthermia. However, the hyperthermic response to Db-cAMP was attenuated by the central administration of a beta-adrenergic receptor antagonist, which indicates that cAMP may be involved, through beta-adrenergic receptors, in the central regulation of heat production and conservation. The central administration of Db-cGMP produced hypothermia which was not mediated via histamine H1 or H2 receptors and serotonin. The antagonism of hypothermia induced by Db-cGMP and acetylcholine + physostigmine by central administration of a cholinergic muscarine receptor antagonist and not by a cholinergic nicotinic receptor antagonist suggests that cholinoceptive neurons and endogenous cGMP may regulate heat loss through cholinergic muscarine receptors. It is concluded that these results indicate a regulatory role in thermoregulation provided by a balance between opposing actions of cAMP and cGMP in guinea pigs.

Kandasamy, S. B.↗

Hypothermic and antipyretic effects of ACTH (1-24) and alpha-melanotropin in guinea-pigs

Intracerebroventricular administration of adrenocorticotropin (ACTH 1-24) and alpha-melanotropin (alpha-MSH), peptides which occur naturally in brain induced dose-related hypothermia in guinea-pigs at room temperature (21 C) and also produced greater hypothermia at low (10 C) ambient temperature. However, when the experiments were repeated in a warm (30 C) environment, no effect on body temperature was observed. These results indicate that the peptides did not reduce the central set-point of temperature control. The hypothermia induced by ACTH and alpha-MSH was not mediated via histamine H1- or H2-receptors and serotonin since the H1-receptor antagonist, mepyramine, the H2-receptor antagonist, cimetidine, and the serotonin antagonist, methysergide, had no antagonistic effects. The peptides were antipyretic since they reduced pyrogen-induced-fever and hyperthermia due to prostaglandin E2, norepinephrine and dibutyryl cAMP, at a dose which did not affect normal body temperature. The powerful central effects of these peptides on normal body temperature, fever and hyperthermia, together with their presence of the brain regions important to temperature control, suggest that they participate in thermoregulation.

Kandasamy, S. B.↗

Role of heat shock protein Hsp25 in the response of the orofacial nuclei motor system to physiological stress

Although expression of the small heat shock protein family member Hsp25 has been previously observed in the central nervous system (CNS), both constitutively and upon induction, its function in the CNS remains far from clear. In the present study we have characterized the spatial pattern of expression of Hsp25 in the normal adult mouse brain as well as the changes in expression patterns induced by subjecting mice to experimental hyperthermia or hypoxia. Immunohistochemical analysis revealed a surprisingly restricted pattern of constitutive expression of Hsp25 in the brain, limited to the facial, trigeminal, ambiguus, hypoglossal and vagal motor nuclei of the brainstem. After hyperthermia or hypoxia treatment, significant increases in the levels of Hsp25 were observed in these same areas and also in fibers of the facial and trigeminal nerve tracts. Immunoblot analysis of protein lysates from brainstem also showed the same pattern of induction of Hsp25. Surprisingly, no other area in the brain showed expression of Hsp25, in either control or stressed animals. The highly restricted expression of Hsp25 implies that this protein may have a specific physiological role in the orofacial motor nuclei, which govern precise coordination between muscles of mastication and the pharynx, larynx, and face. Its rapid induction after stress further suggests that Hsp25 may serve as a specific molecular chaperone in the lower cholinergic motor neurons and along their fibers under conditions of stress or injury. Copyright 1998 Elsevier Science B.V.

Non-NASA Center↗

Magnetic microspheres and tissue model studies for therapeutic applications

The use of magnetic fluids and magnetic particles in combinatorial hyperthermia therapy for cancer treatment is reviewed. The investigation approach adopted for producing thermoregulating particles and tissue model studies for studying particle retention and heating characteristics is discussed.

Review↗

Physiological responses to heat of resting man with impaired sweating capacity

The effects of total-body heat exposure were studied in three groups of subjects with varied degrees of impaired sweating capacity. The responses of two ectodermal dysplasic men, six quadriplegic men, and a man with widespread burned scar tissue were compared with the responses of three able-bodied men resting in the heat. It was found that the able-bodied and burned subjects competed successfully with a controlled environment of 38 C and 20% relative humidity for up to 150 min, whereas the quadriplegic and ectodermal dysplasic men developed hyperthermia, hyperventilation, and distress after only 120 and 75 min of heat exposure, respectively. The intolerance to heat is thus ascribed directly to the inability to produce and evaporate sweat.

Totel, G. L.↗

The effect of direct heating and cooling of heat regulation centers on body temperature

Experiments were done on 28 rabbits in which puncture instruments were left in the brain for 1-2 days until the calori-puncture hyperthermia had passed and the body temperature was again normal. The instrument remaining in the brain was then used as a galvanic electrode and a second fever was produced, this time due to the electrical stimulus. It was concluded that heat is a centrally acting antipyretic and that cold is a centrally acting stimulus which produces hyperpyrexia cold-induced fever.

Barbour, H. G.↗

Temperature uniformity in hyperthermal tumor therapy

Mouse mammary tumors heated by water bath or by microwave-induced hyperthermia exhibit a response that varies sharply with treatment temperature; therefore, uniform heating of the tumor is essential to quantitate the biological response as a function of temperature. C3H tumors implanted on the mouse flank were easily heated to uniformities within 0.1 C by using water baths. Cold spots up to 1 C below the desired treatment temperature were observed in the same tumors implanted on the hind leg. These cold spots were attributed to cooling by major blood vessels near the tumor. In this case temperature uniformity was achieved by the deposition of 2450 MHz microwave energy into the tumor volume by using parallel-opposed applicators.

Harrison, G. H.↗

Research and technology, 1983

Highlights of major accomplishments and applications made during the past year illustrate the broad range of research and technology activities at the Langley Research Center. Advances are reported in the following areas: systems engineering and operation; aeronautics; electronics; space applications; aircraft and spacecraft structures; composite structures; laminar flow control; subsonic transport aircraft; and supersonic fighter concepts. Technology utilization efforts described cover a hyperthermia monitor, a lightweight composite wheelchair; and a vehicle ride quality meter.

Source record↗

Hypothalamic, rectal, and muscle temperatures in exercising dogs - Effect of cooling

An experimental investigation of the mechanisms of performance prolongation during exercise is presented. Measurements were obtained of the rectal, muscle, and hypothalamic temperature of dogs during treadmill exercise at an ambient temperature of 22 + or - 1 C, with and without cooling by use of ice packs. In comparison with exercise without cooling, exercise with cooling was found to: (1) increase exercise duration from 90 + or - 14 to 145 + or - 15 min; (2) attenuate increases in hypothalamic, rectal and muscle temperature; (3) decrease respiratory and heart rates; and (4) lower blood lactic acid content. It is shown that although significant differences were found between the brain, core, and muscle temperatures during exercise with and without cooling, an inverse relation was observed between muscle temperature and the total duration of exercise. It is suggested that sustained muscle hyperthermia may have contributed to the limitation of working ability in exercise with and without cooling.

Kruk, B.↗

Primate body temperature and sleep responses to lower body positive pressure

Cephalic fluid shifts, induced by lower body positive pressure (LBPP) are known to influence various physiological systems (i.e., cardiovascular and renal). In earlier experiments, an apparent change in the arousal state of primates in such LBPP conditions was observed. This study was designed to examine the effects of LBPP on arousal state and body temperature level which is normally correlated with sleep. Chair-restrained male squirrel monkeys were exposed to 40 mmHg LBPP for 90-100 minutes between the daytime hours of 13:00-15:00. Each monkey was placed in a specially modified restraint chair to which they were highly trained. Deep body temperature (DBT) was collected from 10 animals. Sleep parameters were obtained from six animals chronically implanted for sleep recording. A video camera was used to observe each animal's apparent state of arousal. LBPP resulted in an approximate 0.9 C decrease in DBT. During video observation, some animals appeared drowsy during LBPP; however, sleep recording revealed no significant changes in the state of arousal. Thus, LBPP is capable of inducing a mild hyperthermia. Further, the mechanisms underlying the observed lowering of body temperature appear to be independent of arousal state.

Edgar, D. M.↗

Tissue simulating gel for medical research

A tissue simulating gel and a method for preparing the tissue simulating gel are disclosed. The tissue simulating gel is prepared by a process using water, gelatin, ethylene gylcol, and a cross-linking agent. In order to closely approximate the characteristics of the type of tissue being simulated, other material has been added to change the electrical, sound conducting, and wave scattering properties of the tissue simulating gel. The result of the entire process is a formulation that will not melt at the elevated temperatures involved in hyperthermia medical research. Furthermore, the tissue simulating gel will not support mold or bacterial growth, is of a sufficient mechanical strength to maintain a desired shape without a supporting shell, and is non-hardening and non-drying. Substances were injected into the tissue simulating gel prior to the setting-up thereof just as they could be injected into actual tissue, and the tissue simulating gel is translucent so as to permit visual inspection of its interior. A polyurethane spray often used for coating circuit boards can be applied to the surface of the tissue simulating gel to give a texture similar to human skin, making the tissue simulating gel easier to handle and contributing to its longevity.

Companion, John A.↗