Demeclocycline attenuates hyponatremia by reducing aquaporin-2 expression in the renal inner medulla.
通過減少腎內髓質中水通道蛋白-2的表達來減輕低鈉血症。
FIGURE22.1.
Activation of basolateral CaSR by peritubular calcium and magnesium inhibits
ADH-induced incorporation of AQP-2 water channels into the apical IMCD membrane
管週鈣和鎂激活基底外側CaSR抑制ADH誘導的AQP-2水通道向頂端IMCD膜的摻入
Hepatic Encephalopathy(HE) in Cirrhotic Patients
肝性腦病在肝硬化患者中
Results: Cirrhotic patients suffering from HE had lower serum zinc level when compared to those without HE.
結果:與沒有HE的患者相比,患有HE的肝硬化患者的血清鋅水平較低。
Cirrhotic patients without HE had their serum level of sodium >130 mmol/L
while patients with HE their serum level of sodium <130 mmol/L.
沒有HE的肝硬化患者血清鈉水平> 130 mmol / L,HE患者血清鈉水平<130 mmol / L。
There was significant negative correlation between serum sodium and grades of HE.
血清鈉與HE等級之間存在顯著的負相關。(血清鈉越低,HE越嚴重,又上方寫患有HE的肝硬化患者的血清鋅水平較低。)
表一 造成低血鈉的原因
B、水分過多
(一)原發性劇渴症
原發性劇渴症一般發生在慢性精神疾病患者身上,臨床觀察約有百分之五至二十的慢性精神分裂症患者合併有原發性劇渴症
The patient reported here was a 64 year old woman with a known history of mitral valve disease
but no other relevant past history. On the evening before her death, she began compulsively
drinking water in vast quantities, estimated at between 30 and 40 glasses, and this was
interspersed with episodes of vomiting. She became hysterical and also distressed, shouting
that she had not drunk enough water.
這里報告的患者是一名64歲的女性,患有二尖瓣病史,但沒有其他相關的既往病史。
在她去世的前一天晚上,她開始大量飲用水,估計在30到40杯之間,這裡散佈著嘔吐事件。
她變得歇斯底里,也很苦惱,大聲說她沒有喝足夠的水。
She declined medical attention but continued to drink water after
she had gone to bed. She later fell asleep and died some time later.
她拒絕了醫療,但在她上床睡覺後繼續喝水。她後來睡著了,一段時間後死了。
心臟二尖瓣脫垂缺鋅的機率非常高
二尖瓣關閉不全及主動脈瓣關閉不全應該都缺鋅
總結以上:
水中毒或劇渴症主要應該缺鎂鋅
建議一天一粒男性/女性善存綜合維它命礦物質或一天兩罐草莓亞培安素或桂格特級完膳
含鎂高的食物(由多至少依序排列):海苔、松子、榛果、亞麻籽、南瓜子、甘草、小茴香、桑葚、芥末、核桃、黑芝麻、葵花籽、杏仁、蕎麥、菊花、黑豆
含鋅高的食物(由多至少依序排列):小麥胚芽
延伸閱讀:
尿失禁,怎麼治?
副交感神經→內括約肌鬆弛(排尿)鬆弛張開才能排尿
交感神經→內括約肌收縮(使尿液停止)縮緊才能止尿
鎂、錳抑制交感神經過亢,興奮副交感神經
銅、鋅抑制副交感神經過亢,興奮交感神經。
Chronic primary polydipsia (POLY) in humans is associated with impaired urinary concentrating ability.
人體慢性原發性煩渴(POLY)與尿液濃縮能力受損有關。
Control rats (CTL)
對照大鼠
inner medulla AQP-2 protein abundance was decreased in POLY rats compared with CTL rats
與CTL大鼠相比,POLY大鼠的內髓質AQP-2蛋白豐度降低
We conclude that the impaired urinary concentrating ability associated
with primary POLY in rats is due to impaired osmotic equilibration
in the collecting duct that is mediated primarily by decreased AQP-2 protein abundance.
我們得出結論,與大鼠原發性POLY相關的尿液濃縮能力受損是由於收集管中的滲透平衡受損,
這主要是由AQP-2蛋白豐度降低所介導的。
Manganese promotes intracellular accumulation of AQP2 via
modulating F-actin polymerization and reduces urinary concentration in mice.
錳通過調節F-肌動蛋白聚合促進AQP2的細胞內累積( Finally, MnCl2 treatment in mice resulted in significant polyuria
and reduced urinary concentration
最後,小鼠中的MnCl2(氯化錳)處理導致顯著的多尿(錳促進排尿。)