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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
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 preexisting 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 twelve 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 three 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- choIamines and improved autonomic functions all contribute to the elevated blood pressure after rh-EPO therapy.
並列摘要
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 preexisting 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 twelve 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 three 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- choIamines and improved autonomic functions all contribute to the elevated blood pressure after rh-EPO therapy.