Splanchnic tissues undergo hypoxic stress during whole body hyperthermia
Splanchnic tissues undergo hypoxic stress during whole body hyperthermia
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DOI：
10.1152/ajpgi.1999.276.5.g1195
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发表时间：
1999-05-01
影响因子：
4.5
通讯作者：
Gisolfi, CV
中科院分区：
文献类型：
--
作者：
Hall, DM;Baumgardner, KR;Gisolfi, CV
有意识的动物暴露于环境热应激增加门静脉自由基含量。观察到的热应激诱导的自由基分子的性质表明，高温在肝脏和肠道中产生细胞缺氧应激。为了研究这一假设，清醒的大鼠轴承留置门静脉和股动脉导管暴露于常温或高温条件。在热应激期间和热暴露后24 h监测血气水平。热疗显着增加动脉O-2饱和度，内脏动静脉O-2差，静脉PCO 2，而降低静脉O-2饱和度和静脉pH值。热暴露后一小时，肝糖原水平下降了20%。热暴露两小时后，尽管T-c正常，但热应激动物的内脏动脉-静脉O-2差异仍然升高。第二组大鼠暴露于类似的条件下，同时接受动脉内注射缺氧细胞标记物[H-3]misonidazole。对肝脏和肠进行活组织检查，并对[H-3]米索硝唑含量进行定量。热应激增加组织[H-3]米索硝唑保留80%在肝脏和29%在小肠。在肠上皮细胞和肝2区和3区肝细胞以及枯否细胞中，细胞[H-3]米索硝唑水平显著升高。这种效应在近端小肠和小肝叶中最为突出。这些数据提供的证据表明，高温产生细胞缺氧和内脏组织的代谢应激，并表明，细胞代谢应激可能有助于自由基的产生在热应激。
Exposure of conscious animals to environmental heat stress increases portal venous radical content. The nature of the observed heat stress-inducible radical molecules suggests that hyperthermia produces cellular hypoxic stress in liver and intestine. To investigate this hypothesis, conscious rats bearing in-dwelling portal venous and femoral artery catheters were exposed to normothermic or hyperthermic conditions. Blood gas levels were monitored during heat stress and for 24 h following heat exposure. Hyperthermia significantly increased arterial O-2 saturation, splanchnic arterial-venous O-2 difference, and venous PCO2, while decreasing venous O-2 saturation and venous pH. One hour after heat exposure, liver glycogen levels were decreased similar to 20%. Two hours after heat exposure, the splanchnic arterial-venous O-2 difference remained elevated in heat-stressed animals despite normal T-c. A second group of rats was exposed to similar conditions while receiving intra-arterial injections of the hypoxic cell marker [H-3]misonidazole. Liver and intestine were biopsied, and [H-3]misonidazole content was quantified. Heat stress increased tissue [H-3]misonidazole retention 80% in the liver and 29% in the small intestine. Cellular [H-3]misonidazole levels were significantly elevated in intestinal epithelial cells and liver zone 2 and 3 hepatocytes and Kupffer cells. This effect was most prominent in the proximal small intestine and small liver lobi. These data provide evidence that hyperthermia produces cellular hypoxia and metabolic stress in splanchnic tissues and suggest that cellular metabolic stress may contribute to radical generation during heat stress.