Original Articles
Effects of ischemia on pulmonary dysfunction after cardiopulmonary bypass

Presented at the Poster Session of the Thirty-fourth Annual Meeting of The Society of Thoracic Surgeons, New Orleans, LA, Jan 26–28, 1998.
https://doi.org/10.1016/S0003-4975(99)00096-XGet rights and content

Abstract

Background. Pulmonary hypertension and lung injury secondary to cardiopulmonary bypass (CPB) are probably caused by a combination of ischemia and inflammation. This study was undertaken to investigate the potential ischemic effects of cessation of pulmonary arterial flow during CPB on pulmonary injury.

Methods. Twenty neonatal piglets (2.5 to 3.1 kg) were randomly assigned to two groups. Group A (n = 10) underwent 90 minutes of CPB at full flow (100 mL · kg−1 · min−1) and clamping of the main pulmonary artery (PA). Group B (n = 10) underwent 90 minutes of partial CPB (66 mL · kg−1 · min−1) with continued mechanical ventilation and without clamping of the PA. All hearts were instrumented with micromanometers and a PA ultrasonic flow probe. Endothelial function was assessed by measuring endothelial-dependent relaxation (measured by change in pulmonary vascular resistance after PA infusion of acetylcholine) and endothelial-independent relaxation (measured by change in pulmonary vascular resistance after ventilator infusion of nitric oxide and PA infusion of sodium nitroprusside).

Results. All groups exhibited signs of pulmonary injury after CPB as evidenced by significantly increased pulmonary vascular resistance, increased alveolar–arterial O2 gradients, and decreased pulmonary compliance (p < 0.05); however, pulmonary injury was significantly worse in group A (p < 0.05).

Conclusions. This study suggests that although exposure to CPB alone is enough to cause pulmonary injury, cessation of PA flow during CPB contributes significantly to this pulmonary dysfunction.

Section snippets

Material and methods

Twenty neonatal piglets (1 week old, 2.5 to 3.1 kg) were randomly assigned to two separate groups. All animals received humane care in accordance with the “Guide for the Care and Use of Laboratory Animals” published by the National Institutes of Health (NIH publication 85-23, revised 1985) and as approved by the Duke University Animal Care and Use Committee.

Anesthesia was induced in all piglets with intramuscular ketamine (20 mg/kg) and acepromazine (1 mg/kg). The piglets were intubated and

Arterial blood gases and hemodynamic data

There were no significant differences in the arterial blood gases between the two groups. Left atrial pressures were maintained at 3 to 7 mm Hg with volume infusions and were not significantly different between the two groups. Fluid requirements for each group were not significantly different. Results are summarized in Table 1.

Pulmonary vascular resistance

Pulmonary vascular resistance increased significantly after 90 minutes of CPB in all groups compared with baseline values (p < 0.005). There was no significant

Comment

In this study, CPB resulted in lung injury in both the full and partial CPB groups as evidenced by increased PVR, increased A–a O2 gradients, and decreased pulmonary compliance. This supports previous studies indicating that exposure to CPB can cause pulmonary injury 6, 7, 8. When the full and partial CPB groups were compared with each other, there was a greater degree of injury present in the full CPB group, suggesting that cessation of pulmonary arterial flow is an important factor in the

References (21)

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