Mechanisms governing protective pregnancy-induced adaptations of the pelvic floor muscles in the rat preclinical model.
Mechanisms governing protective pregnancy-induced adaptations of the pelvic floor muscles in the rat preclinical model.
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DOI：
10.1016/j.ajog.2021.11.1353
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发表时间：
2022-05
影响因子：
9.8
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中科院分区：
文献类型：
--
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有和没有分娩损伤的女性盆腔软组织的内在特性可能是不同的。然而，人们对此知之甚少。大鼠骨盆底肌肉经历保护性妊娠诱导的结构适应--肌角化和肌内胶原含量的增加--保护免受产伤。我们旨在检验以下假设：（1）妊娠子宫的机械负荷增加驱动产前适应;（2）负荷引起的变化足以保护骨盆肌肉免受分娩损伤。在3至4月龄Sprague-Dawley大鼠中检测了与妊娠激素环境解耦的负荷的独立效应，这些大鼠随机分为以下4组，每组N为5至14：（1）负荷-/妊娠激素-（对照），（2）负荷+/妊娠激素-，（3）减少负荷/妊娠激素+，和（4）负荷+/妊娠激素+。通过用与胎鼠大小和重量相似的珠子称重子宫角来模拟妊娠子宫的机械负荷。单侧子宫角结扎后单侧妊娠可减轻负荷。为了评估肉瘤发生所需的急性和慢性阶段，在珠加载后4小时或21天处死大鼠。收集尾骨肌、髂尾肌、耻骨尾肌和非骨盆胫骨前肌用于肌纤维和肌节长度测量。肌内胶原含量采用羟脯氨酸测定法进行评估。另外20只负荷+/妊娠激素-大鼠进行阴道扩张，以确定负荷诱导的变化是否足以保护其免受各种程度的分娩相关应变引起的机械性肌肉损伤。使用双因素重复测量方差分析比较数据，然后进行成对比较，以平均值±平均值标准误表示。负荷的急性增加导致显著的盆底肌肉拉伸，伴随着肌节长度的急性增加，与非负荷对照肌肉相比（尾骨：2.69±0.03 vs 2.30±0.06 μm，P<0.001;耻骨尾肌：2.71±0.04 vs 2.25±0.03 μm，P<0.0001;髂尾肌：分别为2.80±0.06和2.35±0.04 μm，P<0.0001）。持续负荷21天后，所有骨盆肌肉的肌节均恢复到正常长度（P> 0.05）。然而，在尾骨中，负荷+/妊娠激素-组的肌纤维比负荷-/妊娠激素-组的肌纤维明显更长（分别为13.33±0.94和9.97±0.26 mm，P<.0001）和耻骨尾肌（分别为21.20±0.52和19.52±0.34 mm，P<0.04），与负荷+/妊娠激素+无差异（分别为12.82±0.30和22.53±0.32 mm，P> 0.1），表明持续负荷诱导了这些肌肉的肌角化。负荷+/妊娠激素-组的尾肌肌内胶原蛋白含量显著高于对照组（分别为6.55±0.85和3.11 ±0.47 μg/mg，P<.001），（5.93±0.79 vs 3.46±0.52 μg/mg，P<0.05），与负荷+/孕激素+（分别为7.45±0.65和6.05±0.62 μg/mg，P> 0.5）无差异。髂尾肌的成肌需要机械和内分泌两方面的刺激。胫骨前肌不受机械或内分泌改变的影响。尽管适应程度相当，但负荷引起的变化只能部分防止肌节超伸长。负荷诱导骨盆底固有肌肉成分的可塑性，从而防止机械性产伤。这种保护作用因个体肌肉和应变程度而异，并因妊娠激素的存在而进一步增强。最大限度地提高机械负荷在怀孕期间对盆底肌肉的影响，如专门的盆底肌肉拉伸方案，是一个潜在的可操作的目标，用于增强妊娠诱导的适应，以减少分娩损伤的妇女谁否则可能有不完全的产前肌肉适应。
The intrinsic properties of pelvic soft tissues in women who do and do not sustain birth injuries are likely divergent. However, little is known about this. Rat pelvic floor muscles undergo protective pregnancy-induced structural adaptations-sarcomerogenesis and increase in intramuscular collagen content-that protect against birth injury. We aimed to test the following hypotheses: (1) the increased mechanical load of a gravid uterus drives antepartum adaptations; (2) load-induced changes are sufficient to protect pelvic muscles from birth injury. The independent effects of load uncoupled from the hormonal milieu of pregnancy were tested in 3- to 4-month-old Sprague-Dawley rats randomly divided into the following 4 groups, with N of 5 to 14 per group: (1) load−/pregnancy hormones− (controls), (2) load+/pregnancy hormones−, (3) reduced load/pregnancy hormones+, and (4) load+/pregnancy hormones+. Mechanical load of a gravid uterus was simulated by weighing uterine horns with beads similar to fetal rat size and weight. A reduced load was achieved by unilateral pregnancy after unilateral uterine horn ligation. To assess the acute and chronic phases required for sarcomerogenesis, the rats were sacrificed at 4 hours or 21 days after bead loading. The coccygeus, iliocaudalis, pubocaudalis, and nonpelvic tibialis anterior musles were harvested for myofiber and sarcomere length measurements. The intramuscular collagen content was assessed using a hydroxyproline assay. An additional 20 load+/pregnancy hormones− rats underwent vaginal distention to determine whether the load-induced changes are sufficient to protect from mechanical muscle injury in response to parturition-associated strains of various magnitude. The data, compared using 2-way repeated measures analysis of variance followed by pairwise comparisons, are presented as mean±standard error of mean. An acute increase in load resulted in significant pelvic floor muscle stretch, accompanied by an acute increase in sarcomere length compared with nonloaded control muscles (coccygeus: 2.69±0.03 vs 2.30±0.06 μm, respectively, P<.001; pubocaudalis: 2.71±0.04 vs 2.25±0.03 μm, respectively, P<.0001; and iliocaudalis: 2.80±0.06 vs 2.35±0.04 μm, respectively, P<.0001). After 21 days of sustained load, the sarcomeres returned to operational length in all pelvic muscles (P>.05). However, the myofibers remained significantly longer in the load+/pregnancy hormones− than the load−/pregnancy hormones− in coccygeus (13.33±0.94 vs 9.97±0.26 mm, respectively, P<.0001) and pubocaudalis (21.20±0.52 vs 19.52±0.34 mm, respectively, P<.04) and not different from load+/pregnancy hormones+ (12.82±0.30 and 22.53±0.32 mm, respectively, P>.1), indicating that sustained load-induced sarcomerogenesis in these muscles. The intramuscular collagen content in the load+/pregnancy hormones− group was significantly greater relative to the controls in coccygeus (6.55±0.85 vs 3.11 ±0.47 μg/mg, respectively, P<.001) and pubocaudalis (5.93±0.79 vs 3.46±0.52 μg/mg, respectively, P<.05) and not different from load+/pregnancy hormones+ (7.45±0.65 and 6.05±0.62 μg/mg, respectively, P>.5). The iliocaudalis required both mechanical and endocrine cues for sarcomerogenesis. The tibialis anterior was not affected by mechanical or endocrine alterations. Despite an equivalent extent of adaptations, load-induced changes were only partially protective against sarcomere hyperelongation. Load induces plasticity of the intrinsic pelvic floor muscle components, which renders protection against mechanical birth injury. The protective effect, which varies between the individual muscles and strain magnitudes, is further augmented by the presence of pregnancy hormones. Maximizing the impact of mechanical load on the pelvic floor muscles during pregnancy, such as with specialized pelvic floor muscle stretching regimens, is a potentially actionable target for augmenting pregnancy-induced adaptations to decrease birth injury in women who may otherwise have incomplete antepartum muscle adaptations.
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