Yang Li, Sameshima Hiroshi, Ikenoue Tsuyomu
Department of Obstetrics and Gynecology, Faculty of Medicine, University of Miyazaki, Japan.
J Obstet Gynaecol Res. 2010 Oct;36(5):1102-7. doi: 10.1111/j.1447-0756.2010.01273.x. Epub 2010 Aug 17.
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 (≤ 25% of the surface area), moderate (25-50%) or severe (≥ 50%).
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.
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.
