Caspi J, Coles J G, Benson L N, Herman S L, Act J A, Wilson G J
Division of Cardiovascular Surgery, Hospital For Sick Children, Toronto, Ontario, Canada.
Pediatr Res. 1994 Jul;36(1 Pt 1):49-54. doi: 10.1203/00006450-199407001-00008.
Neonates undergoing heart surgery are exposed to high levels of circulating catecholamines. Our objective was to determine to what extent epinephrine (E)-related cardiotoxicity can be attributed to induced tachycardia. We assessed left ventricle function by pressure-volume data obtained by conductance catheter/micromanometer technique and correlated it with ultrastructure in newborn piglets (3 to 7 d old). Group A (n = 6) received E (1 microgram/kg/min) for 2 h, whereas group B piglets (n = 6) were atrially paced at a rate (220/min) matched to group A. Left ventricle peak systolic pressure and stroke work were significantly higher (p < 0.05) in group A. End-systolic elastance increased during E infusion (70%) versus no significant change in group B. After 2 h of E infusion, end-systolic elastance was significantly reduced in group A from 9.8 +/- 3.5 to 5 +/- 2.4 mm Hg/mL (p < 0.05). Chamber stiffness index increased during E infusion from 0.36 +/- 0.2 to 0.6 +/- 0.3 mL-1 (p < 0.05) and remained elevated (0.58 +/- 0.2 mL-1) after E infusion was discontinued versus no change in group B. E-induced left ventricle dysfunction was associated with scattered but irreversible ultrastructural changes consisting of sarcolemmal rupture and loss of mitochondrial architecture, whereas only minor reversible changes such as microvesicular lipid accumulation and mitochondrial swelling were seen in group B. We conclude that E cardiotoxicity in the neonate is independent of induced tachycardia.
接受心脏手术的新生儿会暴露于高水平的循环儿茶酚胺中。我们的目的是确定肾上腺素（E）相关的心脏毒性在多大程度上可归因于诱导的心动过速。我们通过电导导管/微压力计技术获得的压力-容积数据评估左心室功能，并将其与新生仔猪（3至7日龄）的超微结构相关联。A组（n = 6）接受E（1微克/千克/分钟）持续2小时，而B组仔猪（n = 6）以与A组匹配的速率（220次/分钟）进行心房起搏。A组的左心室收缩压峰值和每搏功显著更高（p < 0.05）。E输注期间，收缩末期弹性增加（70%），而B组无显著变化。E输注2小时后，A组的收缩末期弹性从9.8±3.5显著降低至5±2.4毫米汞柱/毫升（p < 0.05）。E输注期间，心室僵硬度指数从0.36±0.2增加至0.6±0.3毫升-1（p < 0.05），E输注停止后仍保持升高（0.58±0.2毫升-1），而B组无变化。E诱导的左心室功能障碍与散在但不可逆的超微结构变化相关，包括肌膜破裂和线粒体结构丧失，而B组仅出现轻微的可逆变化，如微泡状脂质积聚和线粒体肿胀。我们得出结论，新生儿中E的心脏毒性与诱导的心动过速无关。
