海水浸泡爆炸伤延期植皮最佳时机的研究

目的确定海水浸泡爆炸伤延期植皮的最佳时机。方法建立海水浸泡爆炸伤动物模型后，分别于0、3、7、14d切取创面组织作病理切片，镜下观察创面受床的病理改变；同期对创区实施植皮术，通过计算机全自动图像分析系统准确计算出各组的皮片成活率。结果分别于伤后0、3、7、14d，对皮肤缺损区施行植皮术，发现不同时机植皮成活率不同，伤后7d对海水浸泡爆炸伤皮肤缺损区植皮，皮片成活率最高。结论海水浸泡爆炸伤延期7d后植皮是对创面实施植皮术的最佳时机。     

海水浸泡兔脑挫伤后caspase-8及caspase-3表达的研究

目的建立海水浸泡颅脑挫裂伤模型,观察海水浸泡对实验性脑挫裂伤后创伤性脑水肿的影响及研究兔脑挫伤后不同时间caspase-8及caspase-3表达的变化。方法采用立体定向自由落体伤模型进行持续海水浸泡作为实验组,对照组采用同样的方法致伤后不进行海水浸泡。观察创伤组织的病理改变,并通过免疫组化染色和计算机图像分析技术用半定量化的方法检测不同干预不同时程caspase-8和caspase-3的活性表达强弱差异。结果实验组和对照组均发生了创伤性脑水肿,但水肿高峰期出现时间不一致,严重程度也不一致。实验组caspase-8和caspase-3活性表达强度均高于对照组。结论海水浸泡促进了挫裂伤周边缺血水肿区神经细胞凋亡的增加。     

Effects of seawater immersion combined with open abdominal injury on the expression of NF-κB,and IκBαof small intestine in rats

Objective To observe effects of seawater immersion combined with open abdominal injury on the expression of NF-κB,and IκBαas well as the change pattern in rats. Methods Ninety-one Wistar rats were randomly divided into 3 groups: the control group (n =7), the open abdominal injury group(n =42) and open abdominal injury combined with 1-hour seawater immersion group ( n =42). The expression of NF-κB,andIκBαin small intestine tissues was measured by Western blot and statistical analyses were also made in the study. Results The expression of NF-κB,in the seawater immersion combined with open abdominal injury group increased significantly 3 hours after injury, when compared with that of the open abdominal injury group(P<0. 05), whereas the expression of NF-κB, of the pure injury group was slightly lower than that of the control group, but no statistical differences could be seen between them(P>0.05). The change pattern in the expression of IκBαwas quite the opposite to that of NF-κB. Conclusions NF-κB seemed to be rapidly and persistently involved in the whole inflammatory response to trauma induced by opened abdominal injury and seawater immersion, when a comparison was made with the pure open abdominal injury group. Injuries for the rats in the open abdominal injury combined with seawater immersion group were serious, and the feedback mechanism for NF-κB was not established for quite a long time.     

海水浸泡弹烧复合伤血细菌学与内脏病理学的变化

目的 探讨海水浸泡弹烧复合伤伤后血液细菌学变化与内脏病理学变化之间的关系。方法 建立海水浸泡弹烧复合伤模型后，依模型将15只成年杂种犬随机分为单纯弹烧复合伤组(简称非浸泡组，7只)和海水浸泡弹烧复合伤组(简称浸泡组，8只)，于伤后即刻和4、7、10、20、28h共6个时相点抽取静脉血进行血细菌培养。另于伤后28h和濒死期将动物活杀，取心、肝、肺、肾行病理学观察。结果 浸泡组动物菌血症出现较早且严重。导致菌血症的细菌来源复杂，不仅有肠道菌群，还有海水特有菌群和皮肤常驻菌群。在内脏器官组织病理学上，不仅有不同程度的血液循环障碍及退行性变，还有严重的炎症反应。结论 在海水浸泡弹烧复合伤中，伤后出现的严重菌血症进一步加重了内脏器官损伤。     

海水浸泡对失血性休克并腹部开放伤实验大鼠肿瘤坏死因子α及肠道热休克蛋白HSP-70的影响

目的探讨海水浸泡失血性休克并腹部开放伤对实验大鼠血浆肿瘤坏死因子α(TNFα-)和肠道热休克蛋白HSP-70水平变化的影响。方法建立失血并腹腔海水浸泡伤动物模型。实验大鼠随机分为对照组(n=6)、失血创伤组(n=14)、失血创伤海水浸泡组(n=14),失血创伤组为单纯失血性休克并腹部开放伤,失血创伤海水浸泡组将动物致伤后置入人工配置的海水中,于伤前和浸泡后30m in及1,1.5,3 h取血测定TNFα的变化,取肠道组织测定HSP-70的表达。结果失血创伤海水浸泡组血中TNFα较失血创伤组伤后明显升高并且高峰出现时间明显提前,肠道损伤病理变化明显重于失血创伤组,肠道组织中HSP-70含量在创伤早期显著升高,后又明显降低。结论TNFα-的过度表达在失血性休克并腹部开放伤后海水浸泡的病理生理变化中起重要作用,肠道组织细胞中HSP-70的异常表达在肠道组织细胞的应激反应机制中,可能有重要的意义。     

海水浸泡对腹部开放伤实验犬肝脏功能及形态学的影响

目的 探讨腹部开放伤后海水浸泡对实验犬肝功能及肝脏病理形态学的影响.方法 20只实验犬致伤后随机分为对照组(n=10)和浸泡组(n=10).对照组为单纯腹部外伤,浸泡组于致伤后置入人工配制的海水中.分别于致伤前(0h)及出水后4、8、12、16、20h取血测定总胆红素(TB)、ALT、AST、LDH、血氨(NH3)、凝血酶原时间(PT)、肿瘤坏死因子-α(TNF-α)、白介素6(IL-6)、内毒素(ETX)水平,于24h处死动物对肝组织进行病理检查.结果 与对照组比较,浸泡组TB、ALT、AST和PT增高,16h后升高明显.浸泡组伤后4h和12h LDH明显高于对照组,伤后4h血NH3明显高于对照组(P＜0.05).TNF-α、IL-6和ETX的变化与肝功能的损害程度呈正比.与对照组比较,浸泡组肝脏的病理形态学改变明显.结论 海水浸泡可导致实验犬的肝功能损伤和肝细胞病理形态学变化.     

海水浸泡伤大鼠胃黏膜和血浆中神经激肽A和降钙素基因相关肽的动态变化

目的： 观察腹腔海水浸泡伤后大鼠胃黏膜和血浆中神经激肽A（NKA）和降钙素基因相关肽（CGRP）水平的动态变化，以探讨感觉神经肽在急性胃黏膜病变中的作用。方法：32只SD大鼠随机分成正常对照组和腹腔浸泡伤组，后者又分为1 h、2 h、3 h 3组，取大鼠胃黏膜和血浆，采用酶标法和放免法测定胃黏膜和血浆中NKA和CGRP水平。结果：随着浸泡时间的延长，腹腔浸泡伤组大鼠胃黏膜NKA和CGRP水平进行性低于正常大鼠（P<0.05），而血浆NKA和CGRP水平进行性高于正常大鼠。结论：海水浸泡伤是一损伤性因素，可引起胃黏膜中NKA和CGRP水平降低、血浆中NKA和CGRP水平升高，提示NKA和CGRP等感觉神经肽在急性胃黏膜病变发生发展过程中可能有重要作用。     

Thermal regulatory responses to submaximal cycling following lower-body cooling in humans

This study compared the effects of pre-exercise cooling with control water immersions on exercise-induced thermal loads derived from steady-state submaximal exercise. Eight healthy male participants [mean (SEM) age 29 (1) years, maximal oxygen uptake 3.81 (0.74) l·min^–1, and body surface area 1.85 (0.11) m²] took part in experiments that included 30 min of baseline data collection [ambient temperature 21.3 (0.2°C)], 30 min of immersion in water to the level of the supra-iliac crest [water temperatures of 35.1 (0.3)°C for thermoneutral and 17.7 (0.5)°C for precooled treatments], and 60 min of cycling exercise at 60% of maximal oxygen uptake. No significant differences were noted during exercise in net mechanical efficiency, metabolic rate, O₂ pulse, or ratings of perceived exertion between the two treatments. Precooling resulted in a significant negative body heat storage during immersion and allowed greater heat storage during exercise. However, net body heat storage for the entire protocol was no different between treatments. Cooling significantly lowered rectal, mean skin, and mean body temperatures as well as more than doubling the exercise time until a 0.5°C rectal temperature increase was observed. The cooling trial significantly delayed onset of sweating by 19.62 min and decreased sweat rate by 255 ml·h^–1 compared to control. Thermal and sweat sensation scores were lower after the cooling treatment compared to control. These data suggest that lower-body precooling is effective at decreasing body heat storage prior to exercise and decreases reliance on heat dissipation mechanisms during exercise. Therefore, this unique, well-tolerated cooling treatment should have a broader application than other precooling treatments. Electronic Publication     

Effects of sympathetic inhibition on blood pressure and renal responses to central hypervolaemia in normal humans

The purpose of this study was to evaluate the effects of short-term sympathetic inhibition with clonidine on blood pressure and renal responses to central hypervolaemia induced by thermoneutral head-out water immersion. Eleven healthy subjects were randomly studied on two occasions, during a 1 h pre-immersion period, 2 h of water immersion and a 1 h post-immersion period, after either placebo or clonidine treatment. Clonidine caused a significant suppression of plasma adrenaline, plasma noradrenaline, urinary noradrenaline excretion and mean arterial blood pressure. Blood pressure remained constant during water immersion after both placebo and clonidine, compared with the respective pre-immersion control values. The suppression pattern of plasma catecholamines and urinary noradrenaline in response to water immersion during placebo was similar after clonidine treatment. Renal volume excretion was not affected by clonidine. In contrast, clonidine caused a significant attenuation of the immersion-induced stimulation of natriuresis (maximum -33±12%, P<0.01, compared with placebo). These data indicate that the renal capacity to excrete sodium is impaired during moderate blood pressure reduction by short-term sympathetic inhibition with clonidine, whereas the regulation of arterial blood pressure in response to central hypervolaemia is maintained.