The influence of labor epidural analgesia on maternal, uteroplacental and fetoplacental hemodynamics in normotensive parturients: a prospective observational study.

BACKGROUND: Epidural analgesia provides sufficient analgesia during labor but can cause hypotension despite various prophylactic measures. We studied its effects on pre-placental, fetoplacental, and fetal hemodynamics using Doppler ultrasound. The primary endpoint was the pulsatility index of the umbilical artery at 30 min after establishing epidural analgesia. Secondary endpoints included maternal blood pressures and neonatal outcome data. METHODS: We included healthy parturients at a cervical dilation ≥2 cm, with or without a request for epidural analgesia (n=32 per group). Ultrasound studies of the uterine arteries, umbilical artery and fetal middle cerebral artery were performed before insertion of the epidural catheter, and 30, 60 and 90 min after; the same time-points were assessed in the non-epidural control group. Maternal blood pressure was measured by a continuous non-invasive arterial pressure monitor. RESULTS: Ultrasound studies detected no significant differences in pulsatility indices over time in any blood vessel. In contrast to the control group, maternal blood pressures were significantly lower for all measures after the onset of analgesia compared with baseline values (mean systolic pressure decreased from 132.7 ±â€¯15.9 mmHg to 123.1 ±â€¯14.4 mmHg at 30 min, P=0.003). The mean pH value of the umbilical arterial blood was 7.29 (±0.06) in the epidural group versus 7.31 (±0.08) in the control group (P=0.33). The median Apgar score at 5 min was 10 in both groups. CONCLUSIONS: Pre-placental, fetoplacental and fetal hemodynamics remained stable despite a statistically significant decrease in maternal blood pressure in laboring parturients receiving epidural analgesia.

CCR6 identifies lymphoid tissue inducer cells within cryptopatches.

The chemokine receptor CCR6 is expressed by dendritic cells, B and T cells predominantly within the organized structures of the gut-associated lymphatic tissue. Its ligand CCL20 is synthesized by the follicle-associated epithelium and is crucial for the development of M cells within Peyer's patches. In addition, lineage-negative c-kit positive lymphocytes within cryptopatches (CP) express CCR6. CCR6-deficient mice exhibit an altered intestinal immune system containing increased amounts of intraepithelial lymphocytes and show smaller Peyer's patches, while progression of cryptopatches to mature isolated lymphoid follicles (ILF) is inhibited. In this report, we show that lin(-) c-kit(+) lymphocytes express a variety of different chemokine receptors and that CCR6 identifies those cells located within CP. In contrast, cells found outside CP are positive for CXCR3 and exhibit a different surface marker profile, suggesting that at least two different populations of lin(-) c-kit(+) cells are present. The presence of CCR6 does not influence the expression of Notch molecules on lin(-) c-kit(+) cells, nor does it influence Notch ligand expression on bone marrow-derived dendritic cells. In the human gut, CCR6 identifies clusters of lymphocytes resembling murine CP. CCR6 seems to have an important role for lin(-) c-kit(+) cells inside CP, is expressed in a regulated manner and identifies potential human CP.