Patients who underwent renal transplantation in childhood have abnormal LV diastolic function and impaired exercise capacity, despite preserved LV longitudinal systolic deformation.
Objective: 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. Design: 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 ( 220 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. Results: 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). Conclusion: 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. M yocardial dysfunction, hypotension, and increased pulmonary vascular resistance are well known consequences of hypoxic-ischaemic insults in neonates, 1 with a relation between low alveolar oxygen tension and increased pulmonary vascular resistance.2 In contrast with chronic hypoxia, the effects are reversible with reoxygenation after insults of short duration.
Myocardial dysfunction, hypotension, and increased pulmonary artery pressure are induced by asphyxia in neonates. We sought to define left ventricular (LV) systolic function by measuring longitudinal and radial contraction by strain Doppler echocardiography (SDE) in hypoxemic newborn pigs. Hypoxemia was induced in 11 anesthetized and instrumented newborn pigs by ventilation with 8% O 2 in nitrogen. When mean arterial blood pressure (BP) decreased to 15 mm Hg or arterial base excess reached Ϫ20 mmol/L or less, the pigs were reoxygenated and ventilated for 150 min. Echocardiography was performed at baseline and during hypoxemia and reoxygenation. Baseline measurements of myocardial peak systolic strain demonstrated normal longitudinal shortening and radial thickening. During hypoxemia, systolic longitudinal shortening in the mid-posterior and septal segments changed to systolic stretching. Peak strain in the mid-lateral and anterior segments decreased but without signs of paradox wall motion. Short-axis peak strain remained positive during hypoxemia, although the amplitude was reduced and delayed with respect to timing. In the newborn pig heart, we found a complex and heterogeneous systolic pattern with distinct regional differences during global hypoxemia. Rapid changes in LV function during hypoxemia and reoxygenation are assessable by SDE, and the results indicate that longitudinal systolic contraction is more vulnerable to hypoxemic changes than radial contraction. To explore the full picture of a global hypoxemic injury, both long-and short-axis functions have to be considered.
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