This experiment tested the effects of an intracerebroventricular injection of prostaglandin E1 on the sympathetic activation and the thermogenic changes in rats with ibotenate lesions of the ventromedial hypothalamus. Under pentobarbital anesthesia, twelve Sprague-Dawley male rats were lesioned bilaterally in the ventromedial hypothalamus with an injection of ibotenic acid (30 nmol into each side). Sham lesions were carried out in other twelve control rats. After 48 h, all animals were anesthetized with ethyl-urethane. The firing rate of the sympathetic nerves innervating the interscapular brown adipose tissue and the colonic and interscapular brown adipose tissue temperatures were monitored before and after an intracerebroventricular injection of prostaglandin E1 (500 ng) or saline. Prostaglandin E1 induced an increase in the firing rate of sympathetic nerves and the colonic and interscapular brown adipose tissue temperatures. These effects were reduced by the ventromedial hypothalamic lesion. Since ibotenic acid destroys cell bodies, the findings indicate that neurons of the ventromedial hypothalamus play a considerable role in the control of sympathetic activation and the thermogenic changes during prostaglandin E1 hyperthermia., M. Monda, A. Sullo, V. De Luca, A. Viggiano., and Obsahuje bibliografii
Our study was aimed to characterize the phenotype and functional endpoints of local microwave hyperthermia (LHT, 42 °C) on tumor infiltrating and spleen leukocytes. The effectiveness of LHT applied into the tumor of B16F10 melanoma-bearing C57/BL6 mice was compared with anesthetized and non-treated animals. Subpopulations of leukocytes were analyzed using the flow cytometry, and the cytotoxic activity of splenocytes against syngeneic B16F10 melanoma and NK-sensitive YAC-1 tumor cell lines was evaluated in 51 Cr-release assay. Similarly, the in vitro modification of the heat treatment was performed using healthy and melanoma-bearing splenocytes. We found a 40 % increase of activated monocytes (CD11b+CD69+) infiltration into the tumor microenvironment. In the spleen of experimental animals, the numbers of cytotoxic T lymphocytes (CTLs-CD3+CD8+) and NK cell (CD49b+NK1.1+) raised by 22 % and 14 %, respectively, while the NK1.1+ monocytes decreases by 37 %. This was accompanied by an enhancement of cytotoxic effector function against B16F10 and YAC-1 targets in both in vivo and in vitro conditions. These results demonstrate that LHT induces better killing of syngeneic melanoma targets. Furthermore, LHT evokes the homing of activated monocytes into the tumor microenvironment and increases the counts of NK cells and CTL in the spleen., J. Kubeš, J. Svoboda, J. Rosina, M. Starec, A. Fišerová., and Obsahuje bibliografii a bibliografické údaje
We investigated the effects of repeated hyperthermic bouts on the heat shock response of heat s hock protein ( HSP ) 72 in skeletal muscle. Rats were assigned to control and hyperthermia groups which were exposed to heated water at 42 °C. The hyperthermia group was further divided into sub -groups: a single bout (H30) or four bouts of hyperthermia for 30 min (H30x4). There was an increase in HSP72 protein content of the H30 groups in both extensor digitorum longus (EDL) and soleus muscles. Moreover, HSP72 protein expression in H30x4 group was significantly higher than in H30 group in both EDL and soleus muscles. The HSP72 mRNA was markedly increased from control levels in the H30 and H30x4 group in both types of muscles . However, HSP72 mRNA of the H30x4 group was lower than that of the H30 group in soleus muscles. Heat shock response of HSP72 is activate d even after repeated bouts of hyperthermia, with a differential regulation between muscle types., J. Lee, K. Himori, D. Tatebayashi, M. Abe, T. Yamada., and Obsahuje bibliografii
The aim of our study was to test the in fluence of short exposure (6 h) of preimplantation rabbit embryos to elevated temperatures (41.5 ºC or 42.5 ºC) in vitro on their developmental capacity. Fertilized eggs recovered from female oviducts at the pronuclear stage (19 hpc) were cultured at standard temperature (37.5 ºC) until the morula stage (72 hpc). Afterwards, the embryos were divided into two groups, cultured for 6 h either at hyperthermic (41.5 ºC or 42.5 ºC) or standard temperature (control 37.5 ºC), post-incubated overnight (16-20 h) at 37.5 ºC and then evaluated for developmental stages, apoptosis (TUNEL), proliferation (cell number), actin cytoskeleton and presence of heat-shock proteins Hsp70. It was observed that hyperthermia at 41.5 ºC did not alter progression of embryos to higher preimplantation stages (expanded and hatching/hatched blastocysts), rate of apoptosis, total cell number of blastocysts and structure of actin filament compared to 37.5 ºC. We stern-blotting revealed the presence of heat stress-induced 72 kDa fraction of Hsp70 proteins in granulosa cells (exposed to 41 ºC) and embryos (exposed to 41.5 ºC). Following the elevation of temperature to 42.5 ºC embryo development was dramati cally compromised. The embryos were arrested at the morula or early blastocyst stage, showed an increased rate of apoptosis and decreased total cell number compared to control. The structure of actin filaments in most of blastomeres was damaged and such blastomeres often contained apoptotic nuclei. In this group a presence of heat-stress-induced fraction of Hsp70 proteins had not been confirmed. This is the first report demonstrating a threshold of thermotolerance of rabbit preimplantation embryos to hyperthermic exposure in vitro. A detrimental effect of higher temperature on the embryo is probably associated with the loss of their ability to produce Hsp70 de novo, which leads to cytoskeleton alterations and enhanced apoptosis., A. V. Makarevich, L. Olexiková, P. Chrenek, E. Kubovičová, K. Fréharová, J. Pivko., and Obsahuje bibliografii a bibliografické odkazy
The present study investigated the effects of head cooling during endurance cycling on performance and the serotonergic neuroendocrine response to exercise in the heat. Subjects exercised at 75 % VO2max to volitional fatigue on a cycle ergometer at an ambient temperature of 29±1.0 °C, with a relative humidity of approximately 50 %. Head cooling resulted in a 51 % (p<0.01) improvement in exercise time to fatigue and Borg Scale ratings of perceived exertion were significantly lower throughout the exercise period with cooling (p<0.01). There were no indications of peripheral mechanisms of fatigue either with, or without, head cooling, indicating the importance of central mechanisms. Exercise in the heat caused the release of prolactin in response to the rise in rectal temperature. Head cooling largely abolished the prolactin response while having no effect on rectal temperature. Tympanic temperature and sinus skin temperature were reduced by head cooling and remained low throughout the exercise. It is suggested that there is a co-ordinated response to exercise involving thermoregulation, neuroendocrine secretion and behavioural adaptations that may originate in the hypothalamus or associated areas of the brain. Our results are consistent with the effects of head cooling being mediated by both direct cooling of the brain and modified cerebral artery blood flow, but an action of peripheral thermoreceptors cannot be excluded., L. Ansley, G. Marvin, A. Sharma, M. J. Kendall, D. A. Jones, M. W. Bridge., and Obsahuje bibliografii a bibliografické odkazy