Vernon D D, Banner W, Dean J M
Department of Pediatrics, University of Utah School of Medicine, Salt Lake City 84103.
Ann Emerg Med. 1989 Aug;18(8):863-6. doi: 10.1016/s0196-0644(89)80214-8.
The hemodynamic effects of severe iron poisoning were studied in five mongrel dogs. Anesthetized animals were instrumented with arterial, venous, and pulmonary artery thermodilution catheters. Iron intoxication was induced by orogastric administration of ferrous sulfate (600 mg/kg elemental iron). Pulmonary artery wedge pressure values were maintained near preintoxication values by saline infusion, and sodium bicarbonate (1.5 mEq/kg/dose) was given for pH less than 7.25. Hourly hemodynamic measurements were obtained for five hours. Cardiac output, mean arterial pressure, pH, and heart rate decreased significantly (P less than .05), whereas systemic vascular resistance, left ventricular stroke work, and oxygen consumption did not change. All animals developed metabolic acidosis despite saline (3.6 +/- 0.9 L, mean +/- SD) and bicarbonate administration (4.2 +/- 0.8 mEq/kg). These findings suggest that decreased cardiac output was partially due to decreased heart rate but not to decreased preload or abnormal left ventricular afterload. Alkali therapy and maintenance of oxygen consumption did not prevent development of metabolic acidosis.
在五只杂种狗身上研究了重度铁中毒的血流动力学效应。对麻醉后的动物插入动脉、静脉和肺动脉热稀释导管。通过经口胃管给予硫酸亚铁（600mg/kg元素铁）诱导铁中毒。通过输注生理盐水使肺动脉楔压值维持在中毒前水平附近，对于pH值低于7.25的情况给予碳酸氢钠（1.5mEq/kg/剂量）。连续五小时每小时进行血流动力学测量。心输出量、平均动脉压、pH值和心率显著下降（P<0.05），而全身血管阻力、左心室搏功和氧耗量未发生变化。尽管给予了生理盐水（3.6±0.9L，平均值±标准差）和碳酸氢钠（4.2±0.8mEq/kg），所有动物仍出现代谢性酸中毒。这些发现表明心输出量降低部分是由于心率下降，而非前负荷降低或左心室后负荷异常。碱疗法和氧耗量的维持并不能预防代谢性酸中毒的发生。
