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Relationships between gastric slow wave frequency, velocity, and extracellular amplitude studied by a joint experimental‐theoretical approach

机译:通过联合实验理论方法研究胃慢波频率,速度和细胞外振幅之间的关系

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Abstract Background Gastric slow wave dysrhythmias are accompanied by deviations in frequency, velocity, and extracellular amplitude, but the inherent association between these parameters in normal activity still requires clarification. This study quantified these associations using a joint experimental‐theoretical approach. Methods Gastric pacing was conducted in pigs with simultaneous high‐resolution slow wave mapping (32‐256 electrodes; 4‐7.6?mm spacing). Relationships between period, velocity, and amplitude were quantified and correlated for each wavefront. Human data from two existing mapping control cohorts were analyzed to extract and correlate these same parameters. A validated biophysically based ICC model was also applied in silico to quantify velocity‐period relationships during entrainment simulations and velocity‐amplitude relationships from membrane potential equations. Key Results Porcine pacing studies identified positive correlations for velocity‐period (0.13?mm?s ?1 per 1?s, r 2 =.63, P .001) and amplitude‐velocity (74?μV per 1?mm?s ?1 , r 2 =.21, P =.002). In humans, positive correlations were also quantified for velocity‐period (corpus: 0.11?mm?s ?1 per 1?s, r 2 =.16, P .001; antrum: 0.23?mm?s ?1 per 1?s, r 2 =.55; P .001), and amplitude‐velocity (94?μV per 1?mm?s ?1 , r 2 =.56; P .001). Entrainment simulations matched the experimental velocity‐period relationships and demonstrated dependence on the slow wave recovery phase. Simulated membrane potential relationships were close to these experimental results (100?μV per 1?mm?s ?1 ). Conclusions and Inferences These data quantify the relationships between slow wave frequency, velocity, and extracellular amplitude. The results from both human and porcine studies were in keeping with biophysical models, demonstrating concordance with ICC biophysics. These relationships are important in the regulation of gastric motility and will help to guide interpretations of dysrhythmias.
机译:摘要背景胃慢波缺陷伴随着频率,速度和细胞外幅度的偏差,但正常活动中这些参数之间的固有关联仍需要澄清。本研究使用联合实验理论方法量化了这些关联。方法胃起搏在具有同时高分辨率慢波测定的猪中进行(32-256个电极;4-7.6Ωmm间距)。定量时段,速度和振幅之间的关系,对每个波前的量化和相关。分析来自两个现有映射控制群组的人类数据以提取和关联这些相同的参数。验证的生物物理学的ICC模型也应用于硅中,以量化夹夹模拟期间的速度周期关系和来自膜电位方程的速度幅度关系。关键结果猪起搏研究确定了速度周期的正相关(0.13?mmΔs≤1,R 2 = .63,p&速度)和幅度 - 速度(每1Ω·μV74Ω·μV? s?1,r 2 = .21,p = .002)。在人类中,对于速度 - 时段(Corpus:0.11Ω·mΩ·s≤10,r 2 = .16,p& antrum:0.23?mm?s≤0.23?mm?s≤10 ?S,R 2 = .55; p& .001)和幅度速度(每1Ω·μV为94ΩμVΩ·s≤1,r 2 = .56; p <.001)。夹带模拟符合实验速度 - 周期关系,并依赖于慢波恢复阶段的依赖。模拟膜潜在关系接近这些实验结果(100≤μV/1Ω·s≤1)。结论和推断这些数据量化了慢波频率,速度和细胞外幅度之间的关系。人类和猪研究的结果都与生物物理模型保持一致,与ICC生物物理学展示了一致性。这些关系在调节胃动力中是重要的,并有助于引导对缺血性的解释。

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