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首页> 外文期刊>The journal of obstetrics and gynaecology research >Changes in heart rate patterns by lipopolysaccharide and intermittent hypoxia-ischemia in 7-day-old rats.
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Changes in heart rate patterns by lipopolysaccharide and intermittent hypoxia-ischemia in 7-day-old rats.

机译:7天大的大鼠中脂多糖和间歇性缺氧缺血引起的心率变化。

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摘要

AIM: We previously reported that lipopolysaccharide (LPS) and hypoxia-ischemia (HI) act additively to induce brain damage in the developing rat model. The present study was undertaken to determine whether LPS-HI-induced brain damage is associated with changes in heart rate (HR) patterns. MATERIAL & METHODS: Seven-day-old Wistar rats were administered LPS (1 mg/kg, n = 17) or saline (n = 15) intraperitoneally. After 4 h, the left common carotid artery was ligated and electrocardiogram electrodes were placed on the chest under ether anesthesia, followed by intermittent HI (8% oxygen for 6 min) at 10-min intervals for a total of 10 times. Seven days later, rats were sacrificed and brains removed for histological examination. Neuronal damage for a single section was categorized as mild (/= 50%). RESULTS: Brain damage was induced only in the LPS/HI group, which was statistically significant when compared to the saline/HI group. Baseline HR increased significantly due to LPS administration (P < 0.05). In the LPS/HI group, the amplitude of hypoxia-driven tachycardia decreased significantly in the last 5 hypoxic episodes in brain-damaged rats compared to rats with no visible damage (28 +/- 1 vs 16 +/- 2 bpm). Baseline HR variability was also suppressed significantly during the last five hypoxic episodes in brain-damaged rats compared to rats with no visible damage. CONCLUSIONS: LPS administration caused a gradual decrease in baseline HR variability and blunted tachycardia in response to repetitive HI, suggesting these signs are indicative of future neonatal brain damage.
机译:目的:我们先前曾报道脂多糖(LPS)和缺氧缺血(HI)会在发育中的大鼠模型中相加地诱导脑损伤。本研究旨在确定LPS-HI引起的脑损伤是否与心率(HR)模式的变化有关。材料与方法:对7日龄的Wistar大鼠腹膜内给予LPS(1 mg / kg,n = 17)或生理盐水(n = 15)。 4小时后,结扎左颈总动脉,将心电图电极置于乙醚麻醉下的胸部,然后以10分钟的间隔间歇性HI(8%氧气,持续6分钟),共10次。七天后,处死大鼠并取出大脑进行组织学检查。单个区域的神经元损伤分为轻度( / = 50%)。结果:仅LPS / HI组可诱发脑损伤,与生理盐水/ HI组相比有统计学意义。由于给予LPS,基线HR显着增加(P <0.05)。在LPS / HI组中,与无可见损伤的大鼠相比,在缺氧的最后5次缺氧发作中,缺氧引起的心动过速的幅度显着降低(28 +/- 1 vs 16 +/- 2 bpm)。与没有可见损伤的大鼠相比,在脑损伤的大鼠的最后五个低氧发作期间,基线HR变异性也得到了显着抑制。结论:LPS给药引起重复性HI导致基线心率变异性逐渐降低,心动过速减弱,表明这些迹象表明未来新生儿脑损伤。

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