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Ann Thorac Surg 2000;69:1402-1407
© 2000 The Society of Thoracic Surgeons

Original articles: Cardiovascular

Pulmonary artery perfusion with protective solution reduces lung injury after cardiopulmonary bypass

Yinglong Liu, MDa, Qiang Wang, MDa, Xiaodong Zhu, MDa, Dongqing Liu, BSa, Shiwei Pan, MDa, Yingmao Ruan, MDa, Yongli Li, BSa

a Department of Surgery, FuWai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China

Address reprint requests to Dr Liu, Department of Surgery, FuWai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China
e-mail: wq.lzhm{at}263.net


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 References
 
Background. The inflammatory response and higher temperature of lung tissue during cardiopulmonary bypass can result in lung injury. This study was to evaluate the protective effect of pulmonary perfusion with hypothermic antiinflammatory solution on lung function after cardiopulmonary bypass.

Methods. Twelve adult mongrel dogs were randomly divided into two groups. The procedure was carried out through a midline sternotomy, cardiopulmonary bypass was established using cannulas placed in the ascending aorta, superior vena cava, and right atrium near the entrance of the inferior vena cava. After the ascending aorta was clamped and cardioplegic solution infused, the right lung was perfused through a cannula placed in the right pulmonary artery with 4°C lactated Ringer’s solution in the control group (n = 6) and with 4°C protective solution in the antiinflammation group (n = 6). Antiinflammatory solution consisted of anisodamine, L-arginine, aprotinin, glucose-insulin-potassium, and phosphate buffer. Plasma malondialdehyde, white blood cell counts, and lung function were measured at different time point before and after cardiopulmonary bypass; lung biopsies were also taken.

Results. Peak airway pressure increased dramatically in the control group after cardiopulmonary bypass when compared with the antiinflammation group at four different time points (24 ± 1, 25 ± 2, 26 ± 2, 27 ± 2 cm H2O versus 17 ± 2, 18 ± 1, 17 ± 1, 18 ± 1 cm H2O; all p < 0.01). Pulmonary vascular resistance increased significantly in the control group than in the antiinflammation group at 5 and 60 minutes after cardiopulmonary bypass (1,282 ± 62 dynes · s · cm-5 versus 845 ± 86 dynes · s · cm-5 and 1,269 ± 124 dynes · s · cm-5 versus 852 ± 149 dynes · s · cm-5, p < 0.05). Right pulmonary venous oxygen tension (PvO2) in the antiinflammation group was higher than in the control group at 60 minutes after cardiopulmonary bypass (628 ± 33.3 mm Hg versus 393 ± 85.9 mm Hg, p < 0.05). The ratio of white blood cells in the right atrial and the right pulmonary venous blood was lower in the antiinflammation group than in the control group at 5 minutes after the clamp was removed (p < 0.05). Malondialdehyde were lower in the antiinflammation group at 5 and 90 minutes after the clamp was removed (p < 0.01 and p < 0.05, respectively). Histologic examination revealed that the left lung from both groups had marked intraalveolar edema and abundant intraalveolar neutrophils, whereas the right lung in the control group showed moderate injury and the antiinflammation group had normal pulmonary parenchyma.

Conclusions. Pulmonary artery perfusion using hypothermic protective solution can reduce lung injury after cardiopulmonary bypass.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 References
 
Although in recent years great progress has been achieved in techniques of surgery and extracoporeal circulation, lung dysfunction after cardiopulmonary bypass (CPB) remains an important clinical problem. The pathogenesis of postoperative pulmonary injury presumably consists of two aspects. The first is "whole body inflammatory response" triggered by the blood exposure to the surface of the cardiopulmonary bypass circuit [1], which induces a release of numerous inflammatory mediators and vasoactive substances that lead to pulmonary hypertension, increased pulmonary capillary permeability, and pulmonary edema [2, 3]. The second is "warm ischemic injury" caused by the absence of hypothermic blood perfusion after systemic venous blood transferred into the extracoporeal circuits. After lung reperfusion, many toxic agents, such as oxygen radicals, leukotriene, and elastase, are released by activated neutrophils sequestrated in the lung and induce more severe damage [4–7].

Aiming at both aspects, we designed a method of perfusing hypothermic antiinflammatory solution into pulmonary artery during CPB to lower the pulmonary temperature and minimize the inflammatory response in the lung.

Previous studies on pulmonary preservative solution have shown that storing the lung with UCLA, glucose-insulin-potassium, and Collins-Sachs solutions can improve pulmonary function after transplantation [8–10]. Other studies also demonstrated that L-arginine and aprotinin were effective in suppressing the inflammatory response [11–13]. On the basis of these studies, we composed a protective solution including anisodamine, L-arginine, aprotinin, glucose-insulin-potassium, and phosphate buffer. We hypothesized that canine pulmonary artery perfusion with this hypothermic solution during CPB would reduce pulmonary injury.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 References
 
All animals received humane care in compliance with the "Guide for the care and use of laboratory animals" published by the National Institutes of Health (NIH publication 85–23, revised 1985).

Operation and solution
Twelve mongrel dogs, weighing 15 to 20 kg, were randomized into the control group (n = 6) and the antiinflammation group (n = 6). They were anesthetized with pentobarbital sodium (20 mg/kg) and were ventilated with a volume-cycled ventilator. Inspired oxygen concentration was 100%. After median sternotomy and heparinization (300 IU/kg), CPB was established with standard techniques using cannulas placed in the ascending aorta, superior vena cava, and right atrium near the entrance of the inferior vena cava. When the core temperature was cooled to 30°C, the aorta was cross-clamped and the cardioplegic solution was routinely infused. The left pulmonary artery was occluded and the right lung was perfused with protective solution in the antiinflammation group and lactated Ringer’s solution was infused in the control group through a cannula inserted in right pulmonary artery. Both solutions were at 4°C and 40 cm H2O gravity pressure. The initial perfusion was 300 mL and then 150 mL at every 30 minutes. The solution was drained from left atrium through an incision on the atrial septum. Mean systemic pressure was maintained at approximately 50 mm Hg, flow ranged from 1.6 to 2.2 L · min · m-. After aortic cross-clamping and cardioplegic arrest of the heart for 90 minutes, the animals were rewarmed, weaned from CPB, and stabilized for another 90 minutes.

The CPB circuit used in all animals was composed of a bubble oxygenator (XiJing, Corp, Xian, China), Sarns 7000 roller pumps (Sarns Inc, Ann Arbor, MI, USA) primed with crystalloid solution, and a standard arterial filter (XiJing Corp, XiAn, China).

The pulmonary protective solution consisted of glucose (50 g/L), insulin (8 U/L), Na2HPO4 (6.4 g/L), NaH2PO4 (0.6 g/L), KCl (1.5 g/L), mannitol (2.5 g/L), low molecular weight dextran (30 g/L), anisodamine (60 mg/L; Minsheng pharmaceuticals Corp, Hangzhou, China), L-arginine (2.5 g/L; Gibco, Lifetechnologies, Rockville, MD, USA), aprotinin (1,000,000 KIU/L; Trasylol, Bayer, Leverkusen, Germany), at a pH of 7.4 with Na+ 57 mEq/L and K+ 30 mEq/L.

Physiologic measurements and analysis of blood samples
A flow-directed thermodilution catheter (Biosensors International PTE LTD, Singapore) was inserted into the femoral vein and advanced into the main pulmonary artery. Another cannula was placed into the femoral artery. They were connected to a multichannel physiologic recorder (Nihon Kohden Corp; Shinjuku-ku, Tokyo, Japan). Hemodynamic measurements including mean arterial pressure, pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), and thermodilution cardiac output (CO) were obtained before CPB and 5, 30, 60, and 90 minutes after the end of CPB. Pulmonary function indices included PvO2, peak airway pressure, and pulmonary vascular resistance (PVR). Blood samples for PvO2 from right and left superior pulmonary vein were analyzed with a blood gas analyzer (Mallinckrodt Sensor Systems Inc, Ann Arbor, MI).The following formula was used to calculate PVR: . After CPB, the tissue from the left and right lower lungs were obtained, lung sections were stained with hematoxylin and eosin, and the histologic changes were examined under the microscope.

Intraoperative blood samples were collected for determination of white blood cell (WBC) counts and malondialdehyde (MDA) concentration before bypass and 5, 30, 60, and 90 minutes after the clamp was released. Plasma MDA was measured by a thiobarbituric acid-reactive assay. Pulmonary leukosequestration was expressed as the ratio of the right atrial and right pulmonary venous WBC counts.

Changes in WBC counts and plasma MDA were corrected for hemodilution according to the formula: .

Statistical analysis
All values were expressd as mean ± standard error. The data at different time points were analyzed with variance analysis of repeated measures. All analyses were performed using SPSS software for windows (SPSS Inc, Chicago, IL) and differences were considered statistically significant at a probability level of less than 0.05.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 References
 
There was no statistically significant difference between the two groups in peak airway pressure, PVR, gas exchange, or the ratio of right atrial and right pulmonary venous WBC counts and plasma MDA before CPB.

Assessments of lung function
Before CPB, peak airway pressure was 13 ± 1 cm H2O in the control group and 14 ± 1 cm H2O in the antiinflammation group. It increased dramatically in the control group when compared with the antiinflammation group after CPB (Fig 1). Five minutes after CPB, peak airway pressure increased to 24 ± 1 cm H2O in the control group, which was significantly higher than that in the antiinflammation group (17 ± 2 cm H2O, p < 0.01). It increased further to 27 ± 2 cm H2O in the control group by the end of the observation period after CPB, whereas in the antiinflammation group, peak airway pressure increased to 18 ± 1 cm H2O. The differences between groups were significant (p < 0.01).



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  		Fig 1. Peak airway pressure before and after cardiopulmonary bypass (post-CPB). **p < 0.01, antiinflammation group versus control group.

 
Pulmonary vascular resistance increased significantly in the control group than in the antiinflammation group at 5 and 60 minutes after separation from CPB (p < 0.05), and maintained a higher resistance up to 90 minutes after CPB (1,282 ± 62, 1,208 ± 121, 1,269 ± 124, and 1,295 ± 223 dynes · s · cm-5 versus 845 ± 86, 757 ± 112, 852 ± 149, and 949 ± 110 dynes · s · cm-5, respectively (Fig 2).



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  		Fig 2. Pulmonary vascular resistance before and after cardiopulmonary bypass (post-CPB). *p < 0.05, antiinflammation group versus control group.

 
The right PvO2 was higher significantly than the left in the antiinflammation group after CPB (p < 0.05). The right PvO2 in the antiinflammation group was significantly higher than in the control group at 60 minutes after CPB (p < 0.05; Fig 3).



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  		Fig 3. Pulmonary venous oxygen tension of both lungs in two groups before and after cardiopulmonary bypass (post-CPB). *p < 0.05, right lung in antiinflammation group versus right lung in control group. {triangleup} p < 0.05, right lung versus left lung in antiinflammation group.

 
Cell counts and malondialdehyde concentration
The ratio of right atrial and right pulmonary venous blood WBC counts was shown in Table 1. It immediately increased in both groups when CPB was started. After the cross-clamp was released, the ratio increased from 1.14 ± 0.12 to 1.48 ± 0.15 in the control group; it remained at a higher level until 60 minutes after the clamp was removed. In the antiinflammation group, the ratio remained relatively constant near 1.0.


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  		Table 1. White Blood Cell Ratios (right atrial/right pulmonary venous counts)

 
Plasma MDA concentrations from the right pulmonary veins are shown in Table 2. The MDA concentration increased in both groups after the aorta cross-clamp was released, but it increased more in the control group than in the antiinflammation group at 5 minutes and remained at a higher level 90 minutes after the clamp was removed.


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  		Table 2. Plasma Malondialdehyde Concentration (nmol/mL)

 
Tissue analysis
Histologic evaluation of the left lungs in both groups revealed marked intraalveolar edema and abundant intraalveolar neutrophils. The right lung in the control group showed moderate intraalveolar hemorrhage and interstitial vessel congestion (Fig 4). There was preservation of the normal pulmonary parenchyma (Fig 5) in the right lung of the antiinflammation group.



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  		Fig 4. Histologic appearance of the left lung (A) and right lung (B) in the control group (hematoxylin and eosin, x200).

 


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  		Fig 5. Histologic appearance of the right lung taken from an animal in antiinflammation group showing normal lung parenchyma (hematoxylin and eosin, x200).

 

   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
References
 
Lung injury after CPB is a problem of concern. This is particularly severe in neonatal patients and those who suffered from complex cardiac defects. The mechanisms of CPB-induced lung injury are multifactorial including ischemia–reperfusion and whole body inflammatory response [1, 14]. During CPB, systemic venous blood is transferred to extracorporeal circuits, the lungs are not cooled further, and the temperature is relatively high. The metabolism of the lung tissue is still active and oxygen consumption is high. When blood perfusion resumes, there is a further ischemic reperfusion injury from the oxygen free radicals, calcium paradox, and abnormal energy metabolism [8, 15, 16].

In our study (to determine the effect of hypothermia on lung tissue), we designed the model so that the right lung in the control group was perfused with 4°C lactated Ringer’s solution whereas the left lung was not perfused during bypass. The histologic examination from the left lung showed a diffuse intraalveolar edema, hemorrhage, and abundant neutrophils, whereas the right lung had less pathologic changes. It revealed that perfusion of the hypothermic solution could decrease lung temperature effectively by way of the pulmonary microcirculation system and increase the antihypoxemic ability of the lung tissue.

It has been well documented that the inflammatory response resulting from CPB leads to lung injury. This inflammatory response includes activation of neutrophils, platelets, and endothelium, as well as complement, kinin, and other systems [17–20]. Neutrophil activation, adhesion, and diapedesis play important roles in the lung damage after CPB. Earlier studies have shown that during and after CPB, the neutrophil surface adherence receptors CD11/CD18 are upregulated [21]. They recognize endothelial ligands such as intercellular adhesion molecules 1 and 2, and then bind to them, resulting in neutrophil sequestration in the lung. Another study [22] demonstrated that neutrophil deformability decrease in the pulmonary capillary segments is another major cause for sequestration. On the basis of these studies, we postulated inhibiting adhesion with endothelium and increasing the deformability could prevent neutrophil sequestration in the lung and block the damaging process.

In this study, our antiinflammatory solution consisted of anisodamine, aprotinin, and L-arginine. In experimental studies, anisodamine appears efficacious in inhibiting granulocyte and platelet aggregation [23]. Aprotinin is a nonspecific serine protease inhibitor. Recent studies have shown its antiinflammatory actions by several possible mechanisms: (1) increasing neutrophil deformability, (2) inhibiting fibrinolysis, (3) direct dilating effect on preconstricted vasculature, (4) inhibiting the expression and activity of adhesion molecules on the neutrophils and endothlium, and (5) inhibiting the release of cytotoxic products [13, 22, 24–26]. L-Arginine is an amino acid precursor of nitric oxide that acts as a endothelial-derived relaxing factor that dilates the microvasculature, neutralizes superoxide radicals, and reduces neutrophil interaction with the endothelium [27–29]. It has been shown that L-arginine could preserve endothelial function and promote metabolic recovery in the ischemic myocardium by increasing the coronary blood flow [30]. Therefore, we added L-arginine to our solution. In the present study, we found that the WBC ratio increased immediately at the beginning of CPB. It illustrated that the neutrophils had been sequestrated before the heart arrested. After the heart was arrested during CPB, the lung infusing solution could reduce inflammatory response and provide energy sources. Furthermore, the neutrophils adhering to the endothelium may be washed out by mechanical force. Our experiment showed that the antiinflammation group had lower peak airway pressure and pulmonary vascular resistance, higher right PvO2, and less pathologic changes in the pulmonary parenchyma. The WBC ratio and MDA concentration also did not increase dramatically. These results suggested that the lung function was well protected from CPB-induced injury with this solution.

In conclusion, with the use of the experimental model of right pulmonary artery perfusion with a protective solution, we demonstrated that higher temperature and inflammatory responses in lung tissue during CPB were two major causes of lung injury; furthermore, infusing a hypothermic protective solution into the lungs during CPB could reduce the CPB-induced lung injury.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

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Accepted for publication November 5, 1999.




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