Asian Cardiovasc Thorac Ann 2004;12:58-60
© 2004 Asia Publishing EXchange Ltd
Lung Perfusion with Oxygenated Blood During Aortic Clamping Prevents Lung Injury
Jing-Hao Zheng, MD,
Zhi-Wei Xu, MD,
Wei Wang, MD,
Zhu-Ming Jiang,
Xiao-Qing Yu,
Zhao-Kang Su, MD,
Wen-Xiang Ding, MD
Department of Pediatric Thoracic and Cardiovascular Surgery, Xin Hua Hospital, Shanghai Children’s Medical Center and Shanghai Second Medical University Shanghai, People’s Republic of China
For reprint information contact: Jing-Hao Zheng, MD Tel: 86 21 5783 2020 Fax: 86 21 5839 1515 Email: zhjh{at}sh163a.sta.net.cn Department of Pediatric Thoracic and Cardiovascular Surgery, Shanghai Children’s Medical Center, 1678 Dongfang Road, Pudong, Shanghai 200127, People’s Republic of China.
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ABSTRACT
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To evaluate the protective effect of continuous pulmonary perfusion with oxygenated blood during aortic crossclamping, 12 mixed-breed piglets (7–12 kg) were placed on cardiopulmonary bypass for 130 minutes. An experiment group of 6 (group E) had continuous pulmonary perfusion with oxygenated blood during cardiopulmonary bypass, while the other 6 served as controls (group C). Pulmonary function was measured at the beginning and end of cardiopulmonary bypass and one hour later. Histology was compared before and after cardiopulmonary bypass. Pulmonary function after cardiopulmonary bypass was significantly better in group E than group C. There was preservation of the normal pulmonary parenchyma in group E, whereas group C had marked intra-alveolar edema and abundant intra-alveolar neutrophils. Anoxia of lung tissue during aortic crossclamping on cardiopulmonary bypass is probably the major factor in lung injury. Continuous pulmonary perfusion was effective in preventing lung injury during aortic crossclamping.
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INTRODUCTION
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As the technique of cardiopulmonary bypass (CPB) has continued to improve, better results of cardiac surgery have followed. However, lung injury, especially in small babies with severe pulmonary hypertension, is still a serious and potentially fatal complication. Lung injury follows an inflammatory reaction of the whole body, with accumulation of neutrophils in the pulmonary circulation.1 During CPB, pulmonary tissue is supplied only by the parenchymal blood flow.2 Thus, there is potential injury from anoxia and reperfusion in lung tissue. Maintaining circulation in the lung during CPB, especially while the aorta is clamped, is believed to protect lung function. The aim of this experiment was to evaluate the protective effect on pulmonary function of continuous pulmonary perfusion with oxygenated blood during aortic crossclamping.
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MATERIALS AND METHODS
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Twelve mixed-breed piglets weighing 7–12 kg were divided into two groups of 6: an experimental group E, and a control group C. They were anesthetized with ketamine 15–20 mg·kg-1 and thiopental sodium 26–50 mg·kg-1, and ventilated with a volume-controlled respirator (Siemens Servo 900C; Siemens Elema AB, Berlin, Germany). The respirator was regulated using blood gas analysis from a systemic arterial line that was also used for blood pressure monitoring. The fraction of inspired oxygen (FiO2) was kept at 0.8–1.0, the tidal volume was 15–20 mL·kg-1, and the respiratory rate was 20–25 breaths·min-1. Through a mid-sternal incision, the ascending aorta and both venae cavae were catheterized, and CPB was started after infusion of heparin 300 IU·kg-1. The arterial line from the pump was divided into two; one line going to the systemic arterial circulation and the other to the pulmonary artery through another roller pump. When the rectal temperature was lowered to 30°C, the aorta was clamped and cardioplegic solution at 4°C was infused into the aortic root. At the same time, the roller pump was started to perfuse the pulmonary artery with blood at 25 mL·kg-1·min-1 for continuous pulmonary perfusion in group E. The pulmonary circulation flowed back to a reservoir. The mean systemic blood pressure was kept at 40–50 mmHg and the rate of blood flow at 120–180 mL·kg-1·min-1. The aorta was clamped for 50 min, and the duration of parallel circulation was 50 min before stopping CPB. Total CPB time was 130 min. On parallel circulation, continuous pulmonary perfusion was stopped after the heart resumed beating. Separate small catheters were inserted into the left atrium and the pulmonary artery to monitor pressure. After CPB, white blood cell (WBC) counts in samples of left and right atrial blood were determined in both groups. Pulmonary function was assessed by measurements of respiratory peak pressure (Ppeak, cmH2O), pause pressure (Ppause, cmH2O), tidal volume (TV, mL), respiratory frequency (F), fraction of inspired oxygen (FiO2), and inspiratory proportion (insp%). The static lung compliance (Cstat) was calculated from these data:
The respiratory resistance of the lung (Raw) was calculated as:
Using the pressures of arterial oxygen and carbon dioxide, the pulmonary artery–alveolar oxygen gradient (AaDO2) was calculated:
where R (respiratory quotient) = 0.8.
The respiratory index (RI) was derived from AaDO2:
A 3 x 3 cm sample of pulmonary tissue was obtained by wedge resection of the right middle lobe both before and after CPB. The samples were fixed in formaldehyde and embedded in wax for electron microscopy. The right and left pulmonary tissue wet weight (PWW) was measured, and the dry weight (PDW) was determined after keeping the tissue at a constant temperature of 60°C for 72 hours. Pulmonary water content (PWC) was calculated as:
For statistical analysis, the mean and standard deviation of each variable was determined. Means were compared by the Student t test, and the two groups were compared by analysis of variance. Differences were considered significant when p < 0.05.
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RESULTS
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There were no significant differences between the two groups of piglets in terms of age, weight, duration of CPB, or aortic crossclamp time. A comparison of pulmonary function parameters is shown in Table 1
. The WBC counts are listed in Table 2. After CPB, the pulmonary water content of the experimental group was 73.5% ± 12.1% which was not significantly different from the control group value of 75.9% ± 10.3%. Electron microscopy of the pulmonary tissue from group C showed edema in the mesenchyme surrounding the pulmonary alveoli, abundant neutrophils in the pulmonary alveoli, with hemorrhage or hyperemia in some alveoli. Pulmonary structure was normal in group E.
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DISCUSSION
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Although the effects of CPB on the body have been studied intensively, impairment of pulmonary function after CPB is still a severe problem, especially in infants with congenital heart disease and severe pulmonary hypertension.1 It is known that contact between blood and artificial material can stimulate the complement system to cause a systemic reaction and also trigger adhesion molecule production by endotheliocytes, which in turn promotes complement activation of WBCs to adhere to the surface of the endothelium. The injurious effects of WBCs might be the primary cause of lung damage after CPB.
In addition to the systemic reaction to CPB, anoxia and reperfusion impair lung function. Anoxia and reperfusion can adversely affect the structure and function of the endotheliocyte and damage many organs of the body.1 During this process, WBCs play an important role.2 During total CPB, the lung is supplied only by blood from the bronchial arteries, and there is a possibility of anoxic injury. It has been reported that blood flow through the lung during total CPB is reduced to 11% of that before bypass.3 In partial CPB, the lung is perfused via the pulmonary artery, and blood flow during CPB is only reduced to 41% of that before bypass, so that postoperatively, the adenosine triphosphate level in the lung is unchanged. Based on these findings, it has been suggested that increasing the blood flow in the pulmonary artery during total CPB might reduce the degree of lung injury.3 Because aortic crossclamping during CPB is considered to be the time when most serious injury of the lung occurs, continuous pulmonary perfusion with oxygenated blood is advocated only during the period of crossclamping. As excessive blood flow, such as in cases of patent ductus arteriosus, may cause perfusion injury of the lung during CPB, the pulmonary perfusion was maintained at 25 mL·kg-1·min-1.
In this study, lung function and pulmonary gas exchange were significantly better in the experimental group than the control group, with the most marked difference being for Cstat. Because the pulmonary water content of the two groups was the same after CPB, it can be concluded that perfusion of the lungs with oxygenated blood during crossclamping did not increase the lung water content or injure the lung. This is supported by the electron microscopy observations of normal lung structure after CPB in the experiment group. Not only did continuous pulmonary perfusion attenuate the degree of reperfusion injury, but it also inhibited WBC accumulation in the lung tissue. This may result from prevention of the reaction between WBCs and endotheliocytes, which could explain the difference in atrial WBC counts after CPB in the two groups.
Blood flow in the bronchial arteries is usually 6% to 8% of the systemic blood flow. Some experiments have shown that if blood flow in the bronchial arteries is more than 25% of the systemic blood flow, or if a pulmonary flow rate of 30 mL·kg-1·min-1 is maintained during CPB, impairment of pulmonary function is reduced.4 The bronchial arterial flow required for optimal protection of pulmonary function is unknown, but it is certain that a higher flow than that usually obtained during CPB is required for protection of pulmonary function.5
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ABSTRACT
INTRODUCTION
