Krous H F, Catron A C, Farber J P
Pediatr Pathol. 1984;2(1):115-22. doi: 10.3109/15513818409041193.
Autonomic nervous system abnormalities have been implicated in infants dying of or considered at high risk of sudden infant death syndrome (SIDS). In a rat model, norepinephrine (0.02 mg/kg) caused systemic hypertension and numerous pulmonary petechiae, the latter a common finding in SIDS. Petechiae were not seen below the diaphragm. The animals were killed by tracheal occlusion 5 min after the intravenous administration of norepinephrine. The number of pulmonary petechiae was greatly reduced by alpha-adrenergic blockade (phentolamine) and dopaminergic blockade (haloperidol) but not by beta-adrenergic blockade (timolol). A significantly greater reduction of peak mean systemic arterial pressure occurred after alpha-adrenergic blockade than with other blocking agents. It is conceivable that hypoxia-induced endogenous catecholamine release contributes to the pathogenesis of pulmonary petechiae found at necropsy of SIDS victims.
自主神经系统异常与死于婴儿猝死综合征(SIDS)或被认为有SIDS高风险的婴儿有关。在一个大鼠模型中,去甲肾上腺素(0.02mg/kg)引起全身性高血压和大量肺瘀点,后者是SIDS中的常见发现。在横膈膜以下未见到瘀点。在静脉注射去甲肾上腺素5分钟后,通过气管闭塞处死动物。α-肾上腺素能阻断(酚妥拉明)和多巴胺能阻断(氟哌啶醇)可大大减少肺瘀点的数量,但β-肾上腺素能阻断(噻吗洛尔)则不能。与其他阻断剂相比,α-肾上腺素能阻断后平均体动脉压峰值的降低更为显著。可以想象,缺氧诱导的内源性儿茶酚胺释放有助于SIDS受害者尸检时发现的肺瘀点的发病机制。