查詢結果分析
來源資料
相關文獻
- Long-Term Administration of Aminoguanidine Ameliorates Hyperdynamic Circulation and Sodium Retention in Portal Hypertensive Rats
- Involvement of Constitutive Nitric Oxide Synthase in the Portal-Systemic Collaterals of Portal Hypertensive Rats
- Nitro変-L-Arginine Methyl Ester Decreases Minimum Alveolar Concentration of Isoflurane and Reduces Brain Nitric Oxide Synthase Activity in Rats
- 長期阻斷內生性一氧化氮對血壓的影響:正常鼠與高血壓鼠間的比較
- 使用吸入性一氧化氮(NO)治療成人呼吸窘迫症(ARDS):利?或弊?
- Altering Sphingomyelin Signaling in Vessels from Stroke-prone Spontaneously Hypertensive Rats
- 運動對一氧化氮合成酶基因表現的影響
- 一氧化氮與上呼吸道
- 敗血性休克的致病機轉和治療之探討:生理、生化、藥物和藥理的角度
- 聚醣類誘導魚隻產生一氧化氮
頁籤選單縮合
題名 | Long-Term Administration of Aminoguanidine Ameliorates Hyperdynamic Circulation and Sodium Retention in Portal Hypertensive Rats=長期aminoguanidine治療可改善門脈高壓老鼠之高血流動力循環及鈉滯留 |
---|---|
作者 | 詹哲彰; 李發耀; 王聖賢; 陳建廷; 黃惠君; 李壽東; | 書刊名 | 中華民國消化系醫學雜誌 |
卷期 | 18:1 2001.03[民90.03] |
頁次 | 頁1-8 |
分類號 | 415.534 |
關鍵詞 | 氧化氮; 門脈高壓; 鈉滯留; Aminoguanidine; Nitric oxide; Portal hypertension; Sodium retention; |
語文 | 英文(English) |
中文摘要 | 鈉滯留是肝硬化常見的合併症而週邊血管擴張可能是鈉滯留的誘因。氧化氮(nitric oxide)是內生性的血管擴張物質,可導致肝硬化患者之廣泛性血管擴張。本研究探討長期皮下注射aminoguanidine(AG,∼100mg╱Kg╱Day,一種選擇性誘發型氧化氮合成�t的抑制劑),是否能改善門脈高壓老鼠的鈉滯留。老鼠以隨機方式分成三組:門脈部份結紮(PVL)的門脈高壓老鼠接受安慰劑組(蒸餾水),假手術接受安慰劑組(Sham)及門脈高壓接受AG組。蒸餾水或AG以皮下注射方式給予,時間從術前2天直到術後14天。實驗分為兩部分分別測量(a)系統及門脈血流動力學(b)血清鈉濃度及尿鈉排出量。所有老鼠均給予定量的鈉(2.56mmol╱日),之後再以熱稀釋法測量系統及門脈血流動力學,以代謝籠測量尿鈉排出量及計算鈉平衡。 接受安慰劑治療的老鼠中,PVL組較 Sham 組,有較低的平均動脈壓、系統性血管阻力、尿鈉排出量,並有明顯較高的心輸出量指數、門脈壓力及正鈉平衡。 在PVL的老鼠中,接受AG治療可使心輸出量指數降低,並增加平均動脈壓及系統性血管阻力(P<0.05),但未改變門脈壓力(P>0.05);並且AG治療可使PVL老鼠的尿鈉排出量明顯的增加並減少正鈉平衡(P<0.05)。長期使用AG皮下注射治療門脈高壓的老鼠可矯正高血流動力循環,提高尿鈉排出量並改善鈉滯留。AG的作用可能是抑制氧化氮改善週邊血管擴張的結果。 |
英文摘要 | Sodium retention is a common complication of portal hypertension and peripheral vasodilatation could be the initial event. Nitric oxide, an endogenous vasodilator, was found to be involved in the peripheral vasodilatation. This study investigated whether long-term treatment of aminoguanidine (AG), a preferential inducible nitric oxide synthase inhibitor, could prevent sodium retention in portal hypertension. Rats were randomly allocated to three groups: partial portal vein ligated (PVL) plus placebo distilled water), sham operation (Sham) plus placebo, and PVL plus AG groups. Distilled water or AG (∼100mg/kg/day) was administered subcutaneously from 2 days prior to and 14 days after the operation. Two series of experiments were performed to measure (a)systemic and portal hemodynamics and (b)serum sodium concentration and urine sodium excretion. All rats were given a constant daily sodium intake (2.56 mmol sodium). The hemodynamic studies were performed with a thermodilution technique and urine sodium excretion was determined using metabolic cages. In rats given placebo, PVL rats had a significantly lower mean arterial pressure, systemic vascular resistance, and urine sodium output associated with a significantly higher cardiac index, portal pressure and sodium balance than Sham rats. In PVL rats, AG treatment lowered cardiac index and increased mean arterial pressure and systemic vascular resistance (P<0.05) without changing portal pressure (P>0.05). In addition, AG administration increased sodium output and produced a less positive sodium balance (P<0.05). Long-term AG treatment ameliorated the hyperdynamic circulation and sodium retention in portal hypertensive rats. The effect of AG on sodium retention may due to alleviation of peripheral vasodilatation via inhibition of nitric oxide. |
本系統之摘要資訊系依該期刊論文摘要之資訊為主。