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. 2004 Mar;89(2):F156–F160. doi: 10.1136/adc.2002.020594

Resuscitation with 100% O2 does not protect the myocardium in hypoxic newborn piglets

W Borke, B Munkeby, L Morkrid, E Thaulow, O Saugstad
PMCID: PMC1756019  PMID: 14977902

Abstract

Background: Perinatal asphyxia is associated with cardiac dysfunction secondary to myocardial ischaemia. Cardiac troponin I (cTnI) is a marker of myocardial necrosis. Raised concentrations in the blood are related to perinatal asphyxia and increased morbidity.

Objective: To assess porcine myocardial damage from enzyme release during hypoxaemia induced global ischaemia, and subsequent resuscitation with ambient air or 100% O2. To investigate whether CO2 level during resuscitation influences myocardial damage.

Design: Newborn piglets (12–36 hours) were exposed to hypoxaemia by ventilation with 8% O2 in nitrogen. When mean arterial blood pressure had fallen to 15 mm Hg, or base excess to < -20 mmol/l, the animals were randomly resuscitated by ventilation with either 21% O2 (group A, n = 29) or 100% O2 (group B, n = 29) for 30 minutes. Afterwards they were observed in ambient air for another 150 minutes. During resuscitation, the two groups were further divided into three subgroups with different CO2 levels.

Analysis: Blood samples were analysed for cTnI, myoglobin, and creatine kinase-myocardial band (CK-MB) at baseline and at the end of the study.

Results: cTnI increased more than 10-fold (p < 0.001) in all the groups. Myoglobin and CK-MB doubled in concentration.

Conclusion: The considerable increase in cTnI indicates seriously affected myocardium. Reoxygenation with 100% oxygen offered no biochemical benefit over ambient air. CK-MB and myoglobin were not reliable markers of myocardial damage. Normoventilation tended to produce better myocardial outcome than hyperventilation or hypoventilation.

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Figure 1 .

Figure 1

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Mean arterial pressure (MAP). During hypoxaemia blood pressure decreased significantly, and during resuscitation it rose ending in a plateau about 20 mm Hg lower than at the start of the experiment.

Figure 2 .

Figure 2

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Cardiac troponin I (cTnI) related to CO2. cTnI release was significantly (p < 0.001) increased in all three groups resuscitated by the different ventilatory modes. cTnI release was lower in the normoventilated piglets than the piglets with high or low CO2 (NS).

Figure 3 .

Figure 3

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Cardiac troponin I (cTnI) related to O2. There was an increase in cTnI from baseline to end point (p < 0.001) confirming serious cardiac involvement. There were no significant differences between the groups resuscitated with ambient air and 100% O2.

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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