ABSTRACT
Background: Researchers have shown that diet is associated with hypertensive disorders of pregnancy, and there are some reports of performed meta-analyses on observational studies. However, very few randomized-controlled trials have systematically summarized. Thus, we reviewed and meta-analyzed the effects of nutritional interventions on risks of gestational hypertension (GH) or/and preeclampsia (PE). Materials and Methods: A systematic search was performed using Medline, Cochrane library, Google Scholar, ISI Web of Science, Scopus, and ProQuest to find randomized clinical trials assessing the effect of nutritional interventions on incidences of GH or/and PE compared to control or placebo interventions. Results: After considering duplicates, 1066 articles were screened from the database searches. Full-text articles were retrieved for 116 records, while 87 did not have the inclusion criteria and were later omitted. Twenty-nine studies were eligible, but 8 studies were not included in the meta-analysis due to insufficient data. Finally, seven studies were included in qualitative analysis. Furthermore, 7 studies (693 in intervention vs. 721 in control) were pooled for managed nutritional interventions, three (1255 vs. 1257) for a Mediterranean-style diet, and 4 (409 vs. 312) for sodium restricted. Our results revealed that managed nutritional programs were effective in reducing the incidence of GH (odds ratio [OR] = 0.37; 95% confidence interval [CI] = 0.15, 0.92); I2 = 66.9%; P = 0.010), but not for PE (OR = 0.50; 95% CI = 0.23, 1.07); I2 = 58.9%; P = 0.032. The Mediterranean-style diets in three trials (1255 vs. 1257) did not reduce the risk of PE (OR = 1.10; 95% CI = 0.71, 1.70); I2 = 2.3%; P = 0.359). Likewise, sodium-restricted interventions in four trials (409 vs. 312) did not decrease total risk of GH (OR = 0.99; 95% CI = 0.68, 1.45); I2 = 0%; P = 0.520). Meta-regression did not indicate any significant association between maternal age, body mass index, gestational weight gain, and start time of all interventions with the incidence of GH or/and PE (P > 0.05). Conclusion: The present meta-analysis showed that Mediterranean-style diets and sodium-restriction interventions did not decrease the incidence of GH or/and PE in healthy pregnancies; however, managed nutritional programs reduced the risk of GH, the total incidence of GH and PE, but not PE.
ABSTRACT
Background: CA1, as a major structure involved in learning and memory, has been shown to be affected by tramadol addiction. Both orexin and endocannabinoid receptors express in CA1 and play an important role in drug dependency. The aim of this study was to evaluate the modulatory effects of orexin-2 (OX2R) and endocannabinoid-1 (CB1R) receptors on neuronal activity in CA1, in response to tramadol in rats. Materials and Methods: Male Wistar rats were divided into 8 groups (n = 6-7); saline-dimethyl sulfoxide (DMSO), tramadol-DMSO, saline-TCS-OX2-29, saline-AM251, tramadol-TCS-OX2-29, tramadol-AM251, saline-TCS-OX2-29-AM251, tramadol-TCS-OX2-29-AM251. Tramadol was injected intraperitoneally, and then, AM251 (1 nmol/0.3 µL), CB1R antagonist and TCS-OX2-29 (1 nmol/0.3 µL), OX2R antagonist, were microinjected individually or concurrently into the CA1. Using in vivo extracellular single-unit recording, the firing of CA1 pyramidal neurons was investigated. Results: Tramadol decreased neuronal activity in CA1 (P < 0.01) but increased it after micro-injection of DMSO. TCS-OX2-29 increased neuronal activity in saline group (P < 0.05) but decreased it in tramadol group. AM251 had no effect on saline group but decreased neuronal activity in tramadol group (P < 0.05). Concurrent micro-injection of TCS-OX2-29 and AM251 had no effect on saline group but decreased neuronal activity in tramadol group (P < 0.05). Conclusions: Our findings suggest that neural activity in CA1 is rapidly affected by acute use of tramadol, and some of these effects may be induced through the endocannabinoid and orexin systems. Thus, the function of endocannabinoid and orexin systems in CA1 may play a role in tramadol addiction.
