A randomized controlled study comparing oral misoprostol with intramuscular oxytocin in active management of third stage of labour.

OBJECTIVE: The study aimed to compare the effectiveness and side effects of 600 µg of oral Misoprostol with 10 international units (IU) intramuscular oxytocin in managing the third stage of labor. METHODS: This open-label, randomized controlled trial included 260 low-risk women in the second stage of labor with anticipated vaginal delivery. They were randomly assigned, to receive either 600 µg of misoprostol orally or 10 IU of oxytocin intramuscularly. The primary outcomes were blood loss during delivery and incidence of postpartum hemorrhage, evaluated using intention-to-treat analysis. Significance was set at P≤0.05. RESULTS: Baseline characteristics were similar in both groups (P>0.05). The misoprostol group had a significantly lower blood loss than that of the oxytocin group (306.57±176.44 mL vs. 349.37±135.50 mL; relative difference, -12.251 [95% confidence intervals [CI], -22.528 to -1.575]; P=0.012). Incidence of postpartum hemorrhage was similar in both the groups (relative risk [RR], 0.952 [95% CI, 0.543 to 0.671]; P=0.865). Additional oxytocic therapy requirement was also comparable (RR, 1.143 [95% CI, 0.671 to 1.947]; P=0.623). Nausea, shivering, and mean increase in temperature were significantly more common in the misoprostol group than in the oxytocin-parturient group. CONCLUSION: In this study, 600 µg oral misoprostol was superior to intramuscular 10 IU oxytocin in reducing blood loss at birth, and equally effective in preventing postpartum hemorrhage. However, misoprostol exhibited more side effects compared to that of oxytocin.

Impact of apoE deficiency during synaptic remodeling in the mouse olfactory bulb.

In this study we examined the role of apoE on the rate of synaptic recovery in the olfactory bulb (OB) following olfactory epithelium (OE) lesioning in mice. We used both immunoblotting and immunohistochemical techniques to compare the density of OB synaptophysin (Syn, a synaptic marker) in apoE-gene deficient/knockout (KO) mice and wild-type (WT) mice following OE lesion. We found that the whole bulb concentrations of Syn, measured by immunoblotting, declined sharply following injury in both WT and KO mice during the degenerative phase (3-7 days). After this initial decline, the Syn concentration gradually increased to normal levels by 56 days in WT mice. In contrast, Syn concentration in KO mice did not recover by day 56 when Syn density in WT was essentially normal. Glomerular Syn density, measured by immunohistochemistry, found a lower density in KO mice at all time points post-lesion. This lower concentration of whole bulb Syn parallels the slower recovery of glomerular area in KO mice. The data indicate that apoE deficiency in KO mice is associated with a delayed recovery of the glomerular area and a slower recovery in Syn concentration in the OB.

The distribution of apolipoprotein E in mouse olfactory epithelium.

Previous studies from our laboratory suggest that apolipoprotein (apoE), a lipid transporting protein, facilitates olfactory nerve regeneration. We have shown that apoE is enriched in the olfactory nerve and around the glomeruli of the olfactory bulb (OB). The studies reported herein were undertaken to identify possible sources of apoE in the olfactory epithelium (OE). Immunoblotting results revealed apoE expression in the OE of wild-type (WT) mice, but not in apoE deficient/knockout (KO) mice. Immunohistochemical studies revealed that the perikarya and processes of sustentacular (Sus) cells expressed apoE-like immunoreactivity. Minimal neuronal apoE immunostaining was seen, although apoE was observed in the interstial spaces between olfactory receptor neurons (ORN). Substantial apoE-like immunoreactivity was localized to the endfeet and terminal process of Sus cells surrounding the basal cells. Double labeling immunocytochemical studies confirmed that the cell bodies and endfeet of Sus cells expressed high levels of apoE. The endothelial cells of blood vessels were intensely stained for apoE in the lamina propria. Cells forming Bowman's gland also immunostained for apoE. The apoE staining in the nerve fascicles was less intense, but was uniformly distributed throughout the core of the nerve bundles. Heavily stained cells, probably ensheathing glia, surrounded the nerve fascicles. These results revealed that apoE is expressed in the adult OE and lamina propria at strategic locations where it could facilitate the differentiation, maturation and axonal growth of the ORN, perhaps by recycling lipids from degenerating ORN for use by growing axons.

Reconstitution of the olfactory epithelium following injury in apoE-deficient mice.

ApoE, a protein component of lipoproteins, is extensively expressed in the primary olfactory pathway. Because apoE has been shown to play a vital role in nerve repair and remodeling, we hypothesized that apoE expression will increase in the injured olfactory epithelium (OE), and that apoE deficiency in apoE knockout (KO) mice will lead to delayed/incomplete reconstitution of the OE following injury. To directly test this hypothesis, we compared OE regeneration in wild-type (WT) and KO mice following injury induced by intranasal irrigation of Triton X-100. OE was collected at 0, 3, 7, 21, 42, and 56 days post lesion. The amount and distribution of apoE in the regenerating OE was measured by immunoblotting and immunohistochemistry. Rate of OE reconstitution in WT and KO mice was assessed by using three independent measures: (1) OE thickness was measured in cresyl-violet stained sections, (2) basal cell proliferation was determined by using bromodeoxyuridine (BrdU) staining, and (3) differentiation and maturation of olfactory sensory neurons were measured by immunoblotting and immunohistochemical analysis of growth associated protein (GAP) 43 and olfactory marker protein (OMP). The results revealed that apoE expression in the OE is highly regulated during the entire course of OE reconstitution post injury, and that apoE deficiency in apoE KO mice leads to delayed recovery of mature OMP(+) cells in the reconstituting OE. The data suggest that apoE production increases in the injured OE to facilitate maturation of olfactory sensory neurons.