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題名 | Effects of Erythropoietin on Catecholamines, Hemodynamics and Autonomic Functions in Patients Undergoing Regular Hemodialysis=紅血球生成素對血液透析病患之血流動力及自主神經功能之影響 |
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作者 | 遲守華; 林裕峰; 王家儀; 沈友直; 盧國城; 戴良恭; 林石化; 周雲英; 謝善德; | 書刊名 | 醫學研究 |
卷期 | 15:3 1994.11[民83.11] |
頁次 | 頁181-190 |
分類號 | 415.816 |
關鍵詞 | 紅血球生成素; 兒茶酚胺; 血流動力學; 自主神經功能; Erythropoietin; Catecholamines; Hemodynamics; Autonomic function; |
語文 | 英文(English) |
中文摘要 | 以人工合成紅血球生成素(rh-EPO)治療末期腎病患者之貧血症狀乃醫療上一大進步。然而,約有三分之一接受rh-EPO治療的病患會加重其原有的高血壓症狀或新生高血壓,其病因仍不明。因此我們對12位血液透析病患接受rh-EPO治療前後之血壓、血球容積、血流動力、血漿兒茶酚胺、和自主神經功能做研究。結果顯示,三個月的rh-EPO治療後,血壓呈有意義的上升(96.8±6.9 vs 89.5±5.7 mmHg, p<0.01),白血球容積增加(30.2±2.1 vs 25.6±1.4%, p<0.01);而血漿新腎上腺素(638.3±58.8 vs 433.3±26.5 pg/ml, p<0.01)、腎上腺素(210.6±19.3 vs 155.6±13.3 pg/ml,p<0.01)、及度巴明(216.6±13.3 vs 152.8±13.7 pg/ml, p<0.01)均上升;另外自主神經功能獲得改善。在血流動力學方面,總周邊血管阻力增加(p<0.05),心搏出量減少(p<0.05)。由以上結果可知,病患在接受rh-EPO治療後之血壓上升,與紅血球容積增加、總周邊血管阻力增加、和直立收縮壓獲得改善相關。結論:rh-EPO治療後引起之高血壓應是多因子的。而其中紅血球容積的增加、總周邊血管阻力增加、血漿兒茶酚胺上升、和自主神經功能的改善,均是促成其血壓上升的原因。 |
英文摘要 | Therapy with recombinant human erythropoietin (rh-EPO) is a major therapeutic advance in the treatment of anemia of end stage renal disease. However, blood pressure elevation during treatment with rh-EPO is of major concern and approximately one third of hemodialytic patients treated with rh-EPO will experience either an aggravation of pre-existing hypertension or develop de novo hypertension. The pathogenesis of rh-EPO induced hypertension is still conflicting. We then studied the influences of rh-EPO therapy on blood pressure, hematocrit, hemodynamic data, plasma catecholamines and autonomic functions in 12 regular dialytic patients. Our results showed elevated blood pressure (96.8±6.9 vs 89.5±5.7 mmHg, p<0.01), and increased hematocrit (30.2±2.1 vs 25.6±1.4%, p<0.01) after 3 months of rh-EPO therapy. Plasma catecholamines as measured by norepinephrine (NE 638.3±58.8 vs 433.3±26.5 pg/ml, p<0.01), epinephrine (EP 210.6±19.3 vs 155.6±13.3 pg/ml, p<0.01) and dopamine (DA 216.6±13.3 vs 152.8±13.7 pg/ml, p<0.01) also elevated after rh-EPO therapy as compared to those of baseline levels. Autonomic function also improved after rh-EPO therapy. Concerning the hemodynamic data, we observed increased total peripheral vascular resistance (p<0.05) and decreased cardiac output (p<0.05) after rh-EPO therapy. The increment in blood pressure after rh-EPO therapy correlated with increment in hematocrit, total peripheral vascular resistance and improvement in orthostatic systolic pressure. We conclude that the mechanisms of rh-EPO induced hypertension must be multifactorial. Among these, increased red cell mass, increased total peripheral vascular resistance, augmented plasma cate cholamines and improved autonomic functions all contribute to the elevated blood pressure after rh-EPO therapy. |
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