Contraction of the crural diaphragm increases the lower esophageal sphincter (LES)
pressure, which is important for preventing gastroesophageal reflux.
膈肌的收縮增加了食管下括約肌(LES)壓力,這對於預防胃食管反流很重要。
The pressure generated from the contraction of LES smooth muscle
is called the LES pressure, and pressure due to contraction
of the crural diaphragm is termed the crural diaphragm pressure.
由LES平滑肌的收縮產生的壓力稱為LES壓力,將因膈肌的收縮而產生的壓力稱為膈肌的壓力。
lower esophageal sphincter (LES)
食管下括約肌(LES)
Esophageal contraction amplitude showed a positive correlation with LES pressure
(r = 0.49, P < 0.01).
食管收縮幅度與LES壓力呈正相關(r = 0.49,P <0.01)。
Signal Transduction in Normal Lower Esophageal Sphincter (LES) Circular Muscle.
The body of the esophagus is normally relaxed and contracts only briefly
when required to produce peristalsis. In contrast, the lower esophageal sphincter (LES)
maintains a sustained pressure, and relaxes to allow the passage of a bolus.
正常下食管括約肌(LES)環形肌肉的信號轉導。食道的身體通常是放鬆的,
並且在需要產生蠕動時僅短暫收縮。相反,下食管括約肌(LES)保持持續的壓力,
並放鬆以允許推注通過。
The Ca2+ levels, released by agonist-induced activity of phospholipase C,
determine which contractile pathway is activated.
由激動劑誘導的磷脂酶C活性釋放的Ca2+(鈣離子)水平決定了哪種收縮途徑被激活。
acetylcholine (ACh)
乙醯膽鹼(ACh)
(1)In esophageal muscle ACh-induced contraction requires influx of extracellular Ca2+
(1)在食管肌肉中,ACh誘導的收縮需要細胞外Ca2+(鈣離子)的流入
(2)In LES muscle ACh-induced contraction utilizes intracellular Ca2+
release arising from metabolism of phosphatidylinositol (PI),
and a calmodulin-myosin light chain kinase-dependent pathway.
(2)在LES肌肉中,ACh誘導的收縮利用由磷脂酰肌醇(PI)代謝產生的細胞內Ca2+(鈣離子)釋放,以及鈣調蛋白 - 肌球蛋白輕鏈激酶依賴性途徑。
Lab 8: Gastrointestinal Motility: Measuring the effects of
various conditions on smooth muscle contraction
實驗8:胃腸動力:測量平滑肌收縮各種條件的影響
It has already been established that calcium concentration plays a large
role in smooth muscle contraction.
已經確定鈣濃度在平滑肌收縮中起重要作用。
This is seen through the variation of contractility, which is dependent
on the concentration of Ca2+ inside the cell
which helps determine the frequency of slow waves, thus controlling the rate of segmentation
and peristalsis (Al-Shboul, 2013, p.4).
這可以通過收縮性的變化來看出,這取決於細胞內Ca2+的濃度,這有助於確定慢波的頻率
,從而控制分割和蠕動的速率(Al-Shboul,2013,第4頁)。
小結1:
由以上可知,LES是平滑肌,因為收縮產生壓力,而LES的收縮需要神經傳遞質乙醯膽鹼(ACh)的誘導+鈣的內流。
乙醯膽鹼的合成依照這裡
脹氣怎麼治總整理Part-II(腸胃蠕動的真相,缺鎂鋅硒維它命ABC,建議一天一粒善存+豆漿)
告訴我們:
膽鹼乙醯轉移酶(縮寫為ChAT)活性可以通過視黃酸(維生素A的活性代謝物)在培養物中調節
補鋅導致神經生長因子增加,對膽鹼乙醯轉移酶(ChAT)的活性具有顯著影響
硒參與輔酶A的合成
乙醯輔酶A合成酶,該酶依賴於Mg2+(鎂)
需要鎂鋅硒
voltage-insensitive Ca2+ channels (VICC)
電壓不敏感的Ca2 +通道(VICC)
Vitamin D rapidly increases Ca2+ influx through VICC
維生素D通過VICC快速增加Ca2+的內流
在維生素D缺乏症組中,平均Zn(鋅)水平顯著低於對照組。
分析表明,較高水平的Zn(鋅)增加了更高水平的VitD的機率。
胃食道逆流(英文:Gastroesophageal reflux disease、heartburn reflux,縮寫:GERD)
the plasma parathyroid hormone concentration before treatment was 0.21, after treatment 0.73.
治療前血漿甲狀旁腺激素濃度為0.21,治療後為0.73。
The concentration of calcium is statistically significantly reduced
in patients with GERD by 22.5% and increased by 10% after treatment.
GERD患者的鈣濃度在統計學上顯著降低22.5%,治療後增加10%。
節錄自https://www.ncbi.nlm.nih.gov/pubmed/29783225
意思是GERD患者的甲狀旁腺表達(需要鎂)低,血鈣低。
However, the magnesium to calcium ratio was statistically significantly lower
in both GERD and asthma children as compared with control group.
然而,與對照組相比,GERD和哮喘兒童的鎂鈣比率在統計學上顯著降低。
(所謂的鎂鈣比率低可能鎂低、鈣也低)
小結2:
由以上可知,鎂鋅硒合成乙醯膽鹼,維它命D+鈣促進LES平滑肌收縮。
總結以上:
胃食道逆流缺少鎂鋅硒合成乙醯膽鹼,維它命D+鈣促進LES平滑肌收縮。