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Journal Article
Research Support, Non-U.S. Gov't
Autoregulative function in the brain in an endotoxic rat shock model.
Inflammation Research : Official Journal of the European Histamine Research Society ... [et Al.] 2008 November
OBJECTIVE AND DESIGN: Autoregulative function in the brain gets relevant in hypodynamic conditions of a sepsis syndrome. We investigated the temporal pattern and dose dependent effects of LPS-induced shock on autoregulative function in rats.
MATERIAL AND SUBJECTS: Chloralose-anesthetized and mechanically ventilated male CD-rats (n = 30).
TREATMENT: Animals were subjected to vehicle, 1 or 5 mg/kg b.w. lipopolysaccharide (LPS) from E. coli given intravenously.
METHODS: Autoregulative function was tested repeatedly with a carotid compression technique assessing the transient hyperemic response ratio (THRR) in the cortex with laser Doppler flowmetry up to 270 min. THRR data from exsanguination experiments served as controls.
RESULTS: Despite lower blood pressure levels in the high dose group (control: 114 +/- 7 mmHg; 1 mg/kg LPS group: 82 +/- 16 mmHg; 5 mg/kg LPS group: 62 +/- 16 mmHg; p < 0.05) progressive cerebral hyperemia occurred similarly in both groups. Compared to exsanguinations experiments autoregulative compensation for lower blood pressure levels was lacking in the high LPS dose group at the end of experiments.
CONCLUSIONS: Cerebral autoregulation was affected by LPS-induced shock supporting the notion of vasoregulative failure in endotoxic shock.
MATERIAL AND SUBJECTS: Chloralose-anesthetized and mechanically ventilated male CD-rats (n = 30).
TREATMENT: Animals were subjected to vehicle, 1 or 5 mg/kg b.w. lipopolysaccharide (LPS) from E. coli given intravenously.
METHODS: Autoregulative function was tested repeatedly with a carotid compression technique assessing the transient hyperemic response ratio (THRR) in the cortex with laser Doppler flowmetry up to 270 min. THRR data from exsanguination experiments served as controls.
RESULTS: Despite lower blood pressure levels in the high dose group (control: 114 +/- 7 mmHg; 1 mg/kg LPS group: 82 +/- 16 mmHg; 5 mg/kg LPS group: 62 +/- 16 mmHg; p < 0.05) progressive cerebral hyperemia occurred similarly in both groups. Compared to exsanguinations experiments autoregulative compensation for lower blood pressure levels was lacking in the high LPS dose group at the end of experiments.
CONCLUSIONS: Cerebral autoregulation was affected by LPS-induced shock supporting the notion of vasoregulative failure in endotoxic shock.
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