Anand I S, Chandrashekhar Y, Ferrari R, Poole-Wilson P A, Harris P C
Department of Cardiology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Br Heart J. 1993 Oct;70(4):357-62. doi: 10.1136/hrt.70.4.357.
Patients with chronic severe anaemia often retain salt and water. Fluid retention in these patients is not caused by heart failure and the exact mechanisms remain unclear. This study was designed to examine some of the possible mechanisms.
Haemodynamic variables, body fluid compartments, renal function, and plasma hormones were measured in four patients with oedema caused by chronic severe anaemia (mean (SE) haematocrit 13 (1.7)) who had never received any treatment. Cardiac output was increased (6.1 (0.6) l/min/m2) and right atrial (7.8 (1) mm Hg), mean pulmonary arterial (20.5 (2.0) mm Hg), and mean pulmonary arterial wedge (13 (2.7) mm Hg) pressures were slightly increased. The mean systemic arterial pressure (81 (1.3) mm Hg) and systemic vascular resistance (12.3 (1.1) mm Hg x min x m2/l were low. There were significant increases in total body water (+14%), extracellular volume (+32%), plasma volume (+70%), and total body exchangeable sodium (+30%). Renal blood flow was moderately decreased (-46%) and the glomerular filtration rate was slightly reduced (-24%). There were significant increases in plasma noradrenaline (2.1-fold), renin activity (15-fold), aldosterone (3.2-fold), growth hormone (6.3-fold), and atrial natriuretic peptide (12-fold).
In patients with oedema caused by chronic severe anaemia there is retention of salt and water, reduction of renal blood flow and glomerular filtration rate, and neurohormonal activation similar to that seen in patients with oedema caused by myocardial disease. However, unlike patients with myocardial disease, patients with anaemia have a high cardiac output and a low systemic vascular resistance and blood pressure. It is suggested that the low concentration of haemoglobin in patients with anaemia causes a reduced inhibition of basal endothelium-derived relaxing factor activity and leads to generalised vasodilatation. The consequent low blood pressure may be the stimulus for neurohormonal activation and salt and water retention.
慢性重度贫血患者常伴有盐和水潴留。这些患者的液体潴留并非由心力衰竭引起，确切机制尚不清楚。本研究旨在探讨一些可能的机制。
对4例因慢性重度贫血（平均（标准误）血细胞比容13（1.7））导致水肿且从未接受过任何治疗的患者，测量其血流动力学变量、体液分布、肾功能及血浆激素水平。心输出量增加（6.1（0.6）升/分钟/平方米），右心房压（7.8（1）毫米汞柱）、平均肺动脉压（20.5（2.0）毫米汞柱）及平均肺动脉楔压（13（2.7）毫米汞柱）略有升高。平均体动脉压（81（1.3）毫米汞柱）及全身血管阻力（12.3（1.1）毫米汞柱×分钟×平方米/升）较低。总体水（+14%）、细胞外液量（+32%）、血浆量（+70%）及总体可交换钠（+30%）均显著增加。肾血流量中度减少（-46%），肾小球滤过率略有降低（-24%）。血浆去甲肾上腺素（2.1倍）、肾素活性（15倍）、醛固酮（3.2倍）、生长激素（6.3倍）及心房利钠肽（12倍）均显著增加。
慢性重度贫血所致水肿患者存在盐和水潴留、肾血流量及肾小球滤过率降低，以及与心肌病所致水肿患者相似的神经激素激活。然而，与心肌病患者不同，贫血患者心输出量高，全身血管阻力及血压低。提示贫血患者血红蛋白浓度降低导致对基础内皮源性舒张因子活性的抑制减弱，进而引起全身血管扩张。由此导致的低血压可能是神经激素激活及盐和水潴留的刺激因素。
