Fugelseth D, Børke W B, Lenes K, Matthews I, Saugstad O D, Thaulow E
Department of Paediatric Research, Rikshospitalet University Hospital, Oslo, Norway.
Arch Dis Child Fetal Neonatal Ed. 2005 May;90(3):F229-34. doi: 10.1136/adc.2004.056986.
To assess the consequences of hypoxaemia and resuscitation with room air versus 100% O(2) on cardiac troponin I (cTnI), cardiac output (CO), and pulmonary artery pressure (PAP) in newborn pigs.
Twenty anaesthetised pigs (12-36 hours; 1.7-2.7 kg) were subjected to hypoxaemia by ventilation with 8% O(2). When mean arterial blood pressure fell to 15 mm Hg, or arterial base excess was < or = -20 mmol/l, resuscitation was performed with 21% (n = 10) or 100% (n = 10) O(2) for 30 minutes, then ventilation with 21% O(2) for 120 minutes. Blood was analysed for cTnI. Ultrasound examinations of CO and PAP (estimated from tricuspid regurgitation velocity (TR-Vmax)) were performed at baseline, during hypoxia, and at the start of and during reoxygenation.
cTnI increased from baseline to the end point (p<0.001), confirming a serious myocardial injury, with no differences between the 21% and 100% O(2) group (p = 0.12). TR-Vmax increased during the insult and returned towards baseline values during reoxygenation, with no differences between the groups (p = 0.11) or between cTnI concentrations (p = 0.31). An inverse relation was found between increasing age and TR-Vmax during hypoxaemia (p = 0.034). CO per kg body weight increased during the early phase of hypoxaemia (p<0.001), then decreased. Changes in CO per kg were mainly due to changes in heart rate, with no differences between the groups during reoxygenation (p = 0.298).
Hypoxaemia affects the myocardium and PAP. During this limited period of observation, reoxygenation with 100% O(2) showed no benefits compared with 21% O(2) in normalising myocardial function and PAP. The important issue may be resuscitation and reoxygenation without hyperoxygenation.
评估新生猪低氧血症以及使用室内空气与100%氧气复苏对心肌肌钙蛋白I(cTnI)、心输出量(CO)和肺动脉压(PAP)的影响。
20只麻醉猪(12 - 36小时龄;体重1.7 - 2.7千克)通过8%氧气通气造成低氧血症。当平均动脉血压降至15毫米汞柱,或动脉碱剩余≤ -20毫摩尔/升时,分别用21%(n = 10)或100%(n = 10)氧气进行30分钟的复苏,然后用21%氧气通气120分钟。分析血液中的cTnI。在基线、低氧血症期间、复氧开始时及复氧期间,通过超声检查CO和PAP(根据三尖瓣反流速度(TR - Vmax)估算)。
cTnI从基线升至终点(p<0.001),证实存在严重心肌损伤,21%氧气组和100%氧气组之间无差异(p = 0.12)。TR - Vmax在损伤期间升高,复氧期间恢复至基线值,两组之间无差异(p = 0.11),cTnI浓度之间也无差异(p = 0.31)。在低氧血症期间,发现年龄增长与TR - Vmax呈负相关(p = 0.034)。每千克体重的CO在低氧血症早期升高(p<0.001),随后下降。每千克体重CO的变化主要归因于心率变化,复氧期间两组之间无差异(p = 0.298)。
低氧血症影响心肌和PAP。在这一有限观察期内,与21%氧气相比,100%氧气复氧在使心肌功能和PAP恢复正常方面未显示出优势。重要的问题可能是避免高氧的复苏和复氧。