Abstract. The aim of the present study was to investigate the effect of acute heat stress on the neuroendocrine and immunological function in rats. Male Sprague-Dawley rats were randomly divided into two groups and respectively exposed to heat (32˚C) or to room temperature (24˚C). After 7 days of heat exposure, the heat-stress rat model was established. The organ coefficients of the pituitary and adrenal glands were determined. The body temperature was measured by telemetry. The average contents of adrenocorticotropic hormone (ACTH), cortisol (Cor), interleukin-2 (IL-2) and IL-12 in serum were detected. The expression of apoptotic genes in the spleen was measured. The results showed that acute heat stress did not evidently affect the body temperature and body weight (P>0.05), but the exposure increased the organ coefficients of the pituitary and adrenal glands (P<0.05). Heat exposure significantly elevated the level of ACTH, Cor, IL-2 and IL-12 (P<0.05). The expression of caspase-3 and Bax were not changed significantly (P>0.05), while Bcl2 was reduced (P<0.05).

The repair of peripheral nerve injury is still a great challenge in clinic. Autologous nerve transplantation is the gold standard for the treatment of long-distance peripheral nerve defects, but this method remains associated with high morbidity of the donor site and lack of matching donor. In this study, a novel chitosan scaffold (CS) loaded with control-released basic fibroblast growth factor (bFGF) was used to repair 20 mm sciatic nerve defects in adult rat. The ultrastructure of bFGF-CS was observed by scanning electron microscope. The tensile tester and nano-indentation were used to evaluate its mechanical properties. Cholera toxin B-subunit (CTB) tracing, sciatic nerve function index, electromyography, immunofluorescence staining of regenerated nerve and motor endplate were used to evaluate the regeneration of sciatic nerve in rats. The results showed that the structure and mechanical properties of bFGF-CS was beneficial to the regeneration of sciatic nerve. At 12 weeks after operation, bFGF-CS facilitated sciatic nerve regeneration in rat. CTB successfully crossed the sciatic nerve defect area to reach the cell body of sciatic nerve. The motor endplate was reconstructed, thus promoting the behavioral recovery. These findings suggest that the bFGF-CS provides an effective means of repairing 20 mm sciatic nerve defects and shows great potential for clinical application.

Abstract. The aim of the present study was to investigate the effect of one week dehydration heat exposure on thoracic aorta reactivity in rats. Eighteen Male Sprague-Dawley rats were randomly divided into 3 groups (n=6 each group): Control group (CN), heat exposure group (HE), dehydration heat exposure group (DHE). The CN group was exposed to a room temperature of 24˚C, while the HE and DHE groups were exposed to a heat temperature of 32˚C. After 7 days of heat exposure, the heart rate and blood pressure of the rats were measured, and the noradrenaline (NA)-induced contraction on the aorta rings was measured by tension recording. The average contents of malondialdehyde (MDA) and superoxide dismutase (SOD) in serum were detected using ELISA. The expression of apoptotic genes in the thoracic aorta was measured using RT-PCR. Compared with CN, the heart rate in the HE and DHE groups had a tendency to become retarded, but there was no significant difference (P>0.05). In the HE group, the systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial pressure (MAP) of the rats were significantly higher than that of the CN (P<0.05). In the DHE group, the SBP of rats was significantly higher than that of the CN (P<0.05), while the SBP, DBP, and MAP of the rats were decreased compared to the rats in the HE group, although there was no statistical significance (P>0.05). In the HE and DHE groups, the NA-induced contraction on the rats thoracic aorta ring was larger than that of the CN (P<0.05), albeit there was no significant difference between the HE and DHE groups (P>0.05). The serum SOD content decreased in the HE and DHE groups, however, the reduction was significant only in the DHE group (P<0.05). The content of MDA in serum was significantly increased in the DHE group (P<0.05). The expression of BAX was significantly upregulated whereas Bcl2 expression was decreased in the DHE group (P<0.05). The results showed that a high temperature was harmful to the body, especially in the case of lack of food and water. Additionally, the heat exposure elevated blood pressure, and increased arterial reactivity, which were related to the elevated production of MDA, led to the impaired production of SOD, and an increase of cell apoptosis. These findings are useful to understand the influence of dehydrated heat exposure on the vascular function, and they provide certain theoretical and experimental guidance for protection under high temperature. IntroductionHigh temperature has a severe influence on an individual's work, life and body, and it is easy for the individual to become exhausted, irritable and exasperation. A high temperature constitutes a risk factor for the occurrence of cerebrovascular, heart and respiratory diseases; consequently, the death rate increases correspondingly, particularly among the elderly (1-3). At present, the effect of a high temperature especially the dehydration of thermal on the physiological function of human, is lacking in terms of comprehensive knowledge and understanding.On the ...

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Abstract. The purpose of this study was to investigate the effect of a hot and humid environment on thoracic aorta damage in spontaneously hypertensive rats (SHRs). Wistar-Kyoto (WKY) rats were randomly divided into three groups (n=8 in each group): Control group (WKY-CN), heat exposure for 8 h group (WKY-8) and heat exposure for 24 h group (WKY-24). The CN group was exposed to room temperature (24˚C); WKY-8 and WKY-24 group were exposed to heat (32˚C) and 65% relative humidity for 8 and 24 h, respectively. Accordingly, SHRs were randomly divided into three groups (n=8 each group): SHR-CN, SHR-8 and SHR-24. After 7 days of heat exposure, the weight, food consumption and blood pressure of rats was measured. Noradrenaline (NA)-induced contraction of aorta rings was measured using an organ bath system, and vascular morphology was observed. Expression levels of apoptotic genes and proteins in the thoracic aorta were also measured. The experimental results indicated that, in the heat exposure environment, rat food intake was reduced. Rat weight was significantly increased in all groups except SHR-24 (all P<0.01 except SHR-8, P<0.05). Heat exposure significantly increased the blood pressure of rats in the WKY-24 (P<0.01 for systolic; P<0.05 for diastolic), SHR-8 and SHR-24 (all P<0.01) groups. This effect was more notable in SHR compared with WKY. NA-induced contraction of aorta rings significantly increased in the SHR-CN group, compared with the WKY-CN group (P<0.01). Heat exposure significantly elevated the NA-induced contraction in both 8 h groups compared with the CN groups (P<0.01). This effect was accompanied by structural damage to the thoracic aorta and increased expression of apoptotic genes and proteins. In conclusion, thoracic aorta damages in SHRs were more sensitive to heat exposure. The enhanced NA-induced contraction may have partly been due to increased apoptosis in the thoracic aorta.