ABSTRACT
<p><b>OBJECTIVE</b>To explore the effect of auricular points sticking-pressing (APSP) in treating post-cesarean hypogalactia (PCH).</p><p><b>METHODS</b>A randomized, controlled, single-blinded clinical trial on 116 patients with PCH was carried out. They were equally assigned to the treatment group and the control group. The treatment group received APSP, with the pellets pressed for 4 times daily, while the control group was only asked to do lactation to meet infant demand. The therapeutic efficacy and the changes in scores of traditional Chinese medicine (TCM) syndrome, volume of milk secretion, supplementary feeding and serum level of prolactin (PRL) in the two groups were estimated and compared after the patients had been treated for 5 days.</p><p><b>RESULTS</b>The cured and markedly effective rate in the treatment group was 89.7%, which was significantly higher than that in the control group (27.6%, P<0.05), 95% CI (0.1543, 0.2527). The improvement of TCM syndrome, elevation of milking volume, decrease of the supplementary feeding and increase of PRL level revealed in the treatment group were all superior to those in the control group, showing statistical significance (P<0.01).</p><p><b>CONCLUSION</b>APSP shows an apparent efficacy in treating PCH and is worthy of application in clinical practice.</p>
Subject(s)
Adult , Female , Humans , Infant, Newborn , Pregnancy , Young Adult , Acupuncture Points , Acupuncture, Ear , Methods , Cesarean Section , Rehabilitation , Infant Nutritional Physiological Phenomena , Lactation , Physiology , Lactation Disorders , Blood , Therapeutics , Medicine, Chinese Traditional , Methods , Milk, Human , Bodily Secretions , Postoperative Complications , Therapeutics , Pressure , Prolactin , Blood , Treatment OutcomeABSTRACT
The aim of this study was to, from the point of neurogenic inflammation, explore the pathogenesis of colitis and to provide direct evidence for the neurogenic colitis hypothesis. Male Sprague-Dawley rats (180-220 g) anesthetized with chloral hydrate were intrathecally (ith) implanted with polyethylene-10 (PE-10) catheter to reach the spinal cord T₁₂-L₅ level. Substance P (SP) was ith injected once a day for 14 d. The disease active index (DAI) score was calculated by rat body weight and stool. The macroscopic and HE staining-microscopic pathologies of colon/spinal tissue were evaluated. By immunofluorescence staining, the protein expression of a pro-inflammatory cytokine, migration inhibitory factor (MIF), in colon tissue was detected and was semi-quantitatively analyzed. The results showed that in the colon tissue, inflammation was dose-dependently aggravated by ith SP 10 μ and 20 μ, whereas in the spinal tissue, only slight edema and congestion were seen in SP 20 μ group. The MIF protein of colon tissue was increased in ith SP 10 μ and 20 μ groups (P<0.05, P<0.01 as compared to normal saline group respectively), but in the spinal tissue, there was no obvious MIF protein expression either in SP groups or in normal saline group. Pretreatment with neurokinin-1 (NK₁) receptor antagonist ([D-Pro2, D-Trp7, 9] -SP, 22.4 μ, ith, 10 min before ith SP) prolonged the latency of DAI rising and reduced the DAI amplitude, as well as prevented the high MIF expression induced by ith SP. These results suggest that rat colitis can be induced by direct SP stimulation in lumbar spine via activating central NK₁ receptor; and that colonic MIF is possibly one of the inflammatory factors involved in this pathogenesis. These data provide a reasonable support to the hypothesis of colitis being a neurogenic inflammation. In addition, a potential clinical significance for the finding that higher concentration of spinal SP can induce colitis via NK₁ receptor is discussed.