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Ann Thorac Surg 1996;61:1099-1105
© 1996 The Society of Thoracic Surgeons

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Original Article: General Thoracic

Effective 30-Hour Preservation of Canine Lungs With Modified ET-Kyoto Solution

Department of Thoracic Surgery, Chest Disease Research Institute, Kyoto University, Kyoto, Japan

Accepted for publication December 26, 1995.

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Background. With the aim of developing a preservation solution that can preserve donor lungs reliably for a long time, we prepared a modified ET-Kyoto solution by adding N-acetylcysteine, nitroglycerin, and dibutyryl adenosin 3`, 5`-cyclic phosphate to the previously reported ET-Kyoto solution, which contains trehalose, gluconate, and hydroxyethyl starch. In this study, we examined the efficacy of modified ET-Kyoto solution in 30-hour lung preservation.

Methods. Twenty-five pairs of adult mongrel dogs were divided into four groups. Donor lungs were flushed with modified ET-Kyoto solution (n = 9), with ET-Kyoto solution (n = 6), with University of Wisconsin solution group (n = 6), or with ET-Kyoto solution plus the solvents of nitroglycerin (ethanol and propylene glycol) (n = 4), then stored at 4°C for 30 hours. All animals were treated with prostaglandin E₁. Left lungs were transplanted and reperfused for 6 hours.

Results. With respect to arterial oxygen tension, peak inspiratory pressure, and wet-to-dry lung weight ratio, modified ET-Kyoto solution was significantly superior to ET-Kyoto solution. The modified ET-Kyoto solution was significantly superior to University of Wisconsin solution with respect to survival rate, arterial oxygen tension, and wet-to-dry lung weight ratio. Ultrastructural findings supported these results.

Conclusions. These results suggest that modified ET-Kyoto solution is superior to University of Wisconsin solution for 30-hour lung preservation.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
The lack of donors has become a key issue in the field of lung transplantation [1]. The development of effective and highly reliable procedures for lung preservation will allow donor harvest in remote areas and increase the supply of donor lungs. Lungs can be preserved in Euro-Collins solution or in University of Wisconsin (UW) solution for no more than 10 hours [2, 3]. If it were feasible to preserve lungs stably for at least 30 hours, semielective operations would be possible, as can be done with various organs, including the kidneys [4]. Therefore, we thought it necessary to develop a preservation solution that will allow lungs to be preserved stably for at least 30 hours. We reported previously that the nonreducing disaccharide trehalose was more effective than the monosaccharide glucose in preserving canine lungs for 12 hours [5]. Subsequently, we prepared an extracellular-type preservation solution, ET-Kyoto (ET-K) solution, which contains trehalose, gluconate, and hydroxyethyl starch, and found it to be quite effective in 20-hour canine lung storage [6, 7]. However, in our preliminary study, ET-K solution was not so effective for 30 hours, and scanning electron microscopy and transmission electron microscopy showed that cellular damage, with protrusion and vacuolization of pulmonary artery endothelial cells, was largely associated with impaired function of the transplanted lungs. These results led to the hypothesis that protection of the vascular endothelium would be needed for longer-term preservation of the lungs.

Investigators at Columbia University have recently reported that the combined use of N-acetylcysteine (NAC), nitroglycerin, and dibutyryl adenosine 3`,5`-cyclic monophosphate (db-cAMP) was effective in preservation of the heart [8]. N-Acetylcysteine is believed to act as a scavenger for oxygen radicals or a precursor for glutathione, and we have already reported that NAC was effective in repairing ischemia-reperfusion injury after lung transplantation [9]. Nitroglycerin, a precursor molecule for nitric oxide, elevates intracellular nitric oxide/guanosine 3`,5`-cyclic monophosphate levels and dilates the pulmonary artery [10]. Dibutyryl adenosine 3`,5`-cyclic monophosphate is a membrane-permeable cyclic adenosine monophosphate analogue that acts as a vasodilator and protects the vascular endothelium as an intracellular second messenger [11, 12]. These three substances appeared to be useful protectors of the vascular endothelium and were the main objects of our present study. Therefore, we prepared a modified ET-K solution by adding them to the conventional ET-K solution. In this study, we examined the efficacy of modified ET-K solution in 30-hour lung preservation using a canine lung transplantation model.

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Solutions
Solution compositions are shown in Table 1. The modified ET-K solution was produced by mixing NAC, nitroglycerin, and db-cAMP with ET-K solution immediately before pulmonary artery flush. Its pH was maintained at 7.4 with 1 N NaOH. The osmolarity of modified ET-K solution (598 mOsm/L) was elevated mainly by the presence of ethanol and propylene glycol, the solvents of nitroglycerin. In this study, ET-KA solution (osmolarity = 583 mOsm/L) was prepared by adding the ethanol and propylene glycol to ET-K solution for investigation of the effect of the higher osmolarity of modified ET-K solution. The NAC was kindly provided by Eisai Co, Ltd (Tokyo, Japan). Nitroglycerin was purchased from The Green Cross Corporation (Osaka, Japan), and db-cAMP was purchased from Daiichi Pharmaceutical Co, Ltd (Tokyo, Japan). Ethanol was purchased from Ueno Kogaku Inc (Kyoto, Japan), and propylene glycol from Nacalai Tesque Inc (Kyoto, Japan). University of Wisconsin solution (ViaSpan) was purchased from Fujisawa Co, Ltd (Tokyo, Japan). The ET-K solution was prepared in our laboratory.

Donor Operation
Induction and maintenance of anesthesia were performed according to the method reported previously [7]. Ventilatory conditions were maintained as follows: inspired oxygen fraction = 0.5, tidal volume = 20 mL/kg, respiration rate = 15 breaths/min, and positive end-expiratory pressure = 5 cm H₂O. An arterial line (Sur-flow 20G; Terumo Co, Ltd, Japan) was inserted into the right femoral artery, and a Swan-Ganz catheter (7F; Baxter) was inserted into the main pulmonary artery via the right femoral vein. Arterial blood gas analysis, peak airway pressure (PIP), mean pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), cardiac output (CO), systemic blood pressure, and heart rate were measured preoperatively. Pulmonary vessel resistance (PVR) was calculated according to the following equation: PVR = [(PAP-PCWP)/CO] x 80 dyne • s • cm^-5. After a median sternotomy, the azygos vein was ligated and severed, while the superior vena cava, inferior vena cava, aorta, and pulmonary trunk were taped. Heparin (200 units/kg) was injected into the right ventricular outflow tract. An 8-mm catheter was inserted into the pulmonary trunk and fixed with a 3-0 Prolene (Ethicon, Somerville, NJ) purse-string suture. Prostaglandin E₁ (25 µg/kg) was administered by bolus injection via the right ventricular outflow tract. When the systemic blood pressure decreased to less than 40%, the superior vena cava, inferior vena cava, and aorta were divided and the proximal portion of the pulmonary trunk was ligated.

The left atrial appendage was amputated, and the pulmonary artery was flushed with each solution from a height of 50 cm (70 mL/kg). During the pulmonary artery flush, ventilatory conditions were maintained as before. After completion of the pulmonary artery flush, the left atrial appendage was ligated so that the solution would be retained in the pulmonary vascular bed. The donor lung was inflated to its maximal capacity, the trachea was clamped under an inspiratory pressure of 20 cm H₂O, and the heart-lung block was extracted, then immersed in the corresponding preservation solution (1,000 mL) and stored at 4°C for 30 hours.

Recipient Operation
Recipient animals were anesthetized by the procedures described above. An arterial line was inserted into the right femoral artery, and a Swan-Ganz catheter (7F) was inserted preoperatively into the main pulmonary artery via the right femoral vein [5, 13]. Arterial blood gas analysis, PIP, PAP, systemic blood pressure, and heart rate were measured preoperatively. After left pneumonectomy, the preserved left lung was transplanted according to the method reported previously [7, 9]. Briefly, anastomoses were performed in the following order: left atrium, bronchus, and pulmonary artery. At 30 minutes after reperfusion, the tidal volume was reduced to two thirds of the initial tidal volume and the respiratory rate changed from 15 to 20 breaths/min. The right main pulmonary artery and the right main bronchus were ligated. This recipient procedure has been proved to provide no change in any assessments (arterial oxygen tension, peak inspiratory pressure, mean pulmonary artery pressure) after a sham operation (n = 3) in which the right main pulmonary artery and right main bronchus were ligated with no manipulation or transplantation of the left lung.

Assessment
Arterial blood gas analysis, PIP, systemic blood pressure, and heart rate were measured every hour for 6 hours after reperfusion. Six hours after reperfusion, PAP, left atrial pressure, and CO were measured for PVR also, and then the animals were sacrificed. Two segments (ie, S₁ + S₂ and S₉) of the transplanted lung were harvested, weighed, and dried at 70°C for 72 hours, and the wet-to-dry lung weight ratio was then calculated. Furthermore, after 30-hour storage and before transplantation, the S₁ segment of the right lung was resected and examined with scanning electron microscopy.

Statistical Analysis and Animal Care
All values in this article are expressed as mean ± standard error of the mean. Statistical analysis was performed with analysis of variance, and Scheffé's multiple comparison test was used to compare the four groups. Survival rates were calculated by the Kaplan-Meier method, and statistical analysis was performed with the use of a log-rank test. A p value less than 0.05 is considered to be statistically significant.

All animals were treated in accordance with the ``Principles of Laboratory Animal Care'' proposed by the National Society for Medical Research, and in accordance with the ``Guide for the Care and Use of Laboratory Animals'' (NIH publication 85-23, revised 1985) proposed by the National Academy of Science.

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
There were no significant differences among the four experimental groups with regard to cold ischemic times or arterial oxygen tension (PaO₂), PIP, PAP, or PVR in donor or recipient animals.

Survival Rates
All animals in the modified ET-K group (n = 9) and the ET-K group (n = 6) survived for 6 hours after reperfusion, the end of the observation period, whereas 4 of the 6 animals in the UW group died of pulmonary edema 2 to 5 hours after reperfusion. Moreover, in the ET-KA group, 1 of the 4 animals died of pulmonary edema 3 to 4 hours after reperfusion. Survival rates (up to 6 hours after reperfusion) in the modified ET-K, ET-K, and ET-KA groups were significantly greater than that in the UW group (p < 0.01) (Fig 1). Because fewer than 4 animals survived in the UW and ET-KA groups, 4 and 6 hours after reperfusion statistically results were not significant; PaO₂ and PIP values were compared in the four groups up to 3 hours after reperfusion. Four to 6 hours after reperfusion, PaO₂ and PIP values were compared in the modified ET-K and ET-K groups.

View larger version (17K): [in this window] [in a new window]   Fig 1. . Survival rate of recipient animals. (• = modified ET-Kyoto [ET-K] group; = ET-K group; = ET-K plus ethanol and propylene glycol group; = University of Wisconsin [UW] group; *survival rates [up to 6 hours after reperfusion] were significantly higher in the modified ET-K, ET-K, and ET-KA groups than in the UW group; however, there were no significant differences among the modified ET-K, ET-K, and ET-KA groups.)

View larger version (31K): [in this window] [in a new window]   Fig 2. . Arterial oxygen tension of individual donor and transplanted lungs. (ET-K = ET-Kyoto; ET-KA = ET-K plus ethanol and propylene glycol; newET-K = modified ET-K; UW = University of Wisconsin; dead.)

Pulmonary Vessel Resistance
Pulmonary vessel resistance was measured in the transplanted lungs 6 hours after reperfusion. The value in the modified ET-K group was 3,050.9 ± 756.4 dynes • s • cm^-5, and that in the ET-K group was 3,057.3 ± 847.6 dynes • s • cm^-5. The difference between the two groups was not significant.

Wet-to-Dry Lung Weight Ratio
The wet-to-dry lung weight ratio in the modified ET-K group was 5.1 ± 0.3, significantly less than in the ET-K group (6.8 ± 0.6), UW group (7.7 ± 0.6), and ET-KA group (6.2 ± 0.4) (Fig 3).

View larger version (66K): [in this window] [in a new window]   Fig 3. . Wet-to-dry lung weight ratio of transplanted lungs. (ET-K = ET-Kyoto; ET-KA = ET-K plus ethanol and propylene glycol; newET-K = modified ET-K; UW = University of Wisconsin; *p < 0.01, newET-K group versus ET-K group, UW group, or ET-KA group.

View larger version (792K): [in this window] [in a new window]   Fig 4. . Representative scanning electron micrographs of pulmonary arterial endothelium of preserved lungs: (A) modified ET-Kyoto, (B) University of Wisconsin, (C) ET-Kyoto, (D) ET-Kyoto plus ethanol and propylene glycol. Normal pulmonary arterial endothelial structures were seen in the modified ET-Kyoto group (A). Significant swelling and protrusion of pulmonary arterial endothelial cells were evident in the ET-Kyoto (C) and ET-Kyoto plus ethanol and propylene glycol (D) groups. In the University of Wisconsin group (B), swelling and protrusion of endothelial cells was seen in 5 of 6 animals. (Bars = 5 µm.)

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment References

The higher osmolarity of the modified ET-K solution (598 mOsm/L) was due to ethanol and propylene glycol, the added nitroglycerin solvents. The ET-KA solution, which has a higher osmolarity (583 mOsm/L), similar to that of the modified ET-K solution, failed to provide protection, suggesting that the protective effect of modified ET-K solution on transplanted lungs is not due to its osmolarity. In this study it was not clear how the high osmolarity of the solution affected lung preservation, because ET-KA solution did not show any significant differences from the lower osmolar ET-K solution (366 mOsm/L) but led to a better survival rate than did UW solution (325 mOsm/L).

Of the 6 animals in the UW group, 4 died before completion of the experiment and 2 survived until the experiment was completed, showing a wide individual variation. In this respect, the major findings can be summarized as follows: (1) Levels of PaO₂ in animals that died were lower than those in surviving animals. (2) Transplanted lungs in dead animals showed histologic evidence of severe pulmonary edema. (3) There were no differences in cardiopulmonary function between animals that died and those examined before transplantation. (4) Serum potassium levels did not change after reperfusion. Therefore, the cause of death in these 4 animals appeared to be respiratory failure due to pulmonary edema. Electron microscopic studies revealed that pulmonary artery endothelial cells were swollen and protruded in all 4 animals of the UW group that died, which suggests that ischemia of the pulmonary artery endothelium may have caused lung injury.

There are a number of possible explanations for this variability: (1) The composition of the UW solution had already been altered before it was used in this experiment. It is well known that glutathione, one of the important components of UW solution, is easily oxidized from a reduced form to an oxidized form [4]. Thus, the differences in the ratio of the reduced form/oxidized form resulted in individual variations. (2) The presence of microaggregated crystals in UW solutions has been reported recently [14]. These crystals might act as an embolus, resulting in differences in pulmonary artery flush, because we used the commercial UW solution (ViaSpan). Further studies will be needed to determine the cause of death of animals treated with UW solution.

The modified ET-K solution, devised to suppress pulmonary artery endothelial impairment, contains NAC, nitroglycerin, and db-cAMP. N-Acetylcysteine acts directly as an electrophile and has an antioxidant activity as well as oxygen radical scavenger activity [15]. In addition, NAC provides protection against cellular damage via de novo synthetic pathways for glutathione and cysteine [16]. Nitroglycerin is a precursor molecule for nitric oxide and increases intracellular nitric oxide/guanosine 3`,5`-cyclic monophosphate levels in an in vivo model [10]. Nitric oxide has been reported to dilate the pulmonary arteries to inhibit the elevation of pulmonary vessel resistance and to act as an oxygen scavenger. Dibutyryl adenosine 3`,5`-cyclic monophosphate is a membrane-permeable cyclic adenosine monophosphate analogue that elevates intracellular cyclic adenosine monophosphate levels. Cyclic adenosine monophosphate dilates blood vessels and acts as an intracellular second messenger [11]. It also protects vascular endothelial cells through endothelial barrier function, coagulant properties, and the endothelial cell/leukocyte interactions by controlling vascular smooth muscle tone [12].

Electron microscopic investigations in our study revealed that pulmonary artery endothelial cells were swollen in all 6 animals in the ET-K group, whereas pulmonary artery endothelial cells were almost intact in all 9 animals in the modified ET-K group. The modified ET-K solution was expected to inhibit elevation of PVR mainly by the actions of nitroglycerin and db-cAMP, but there was no significant difference in PVR in the transplanted lungs preserved in the modified ET-K solution and the ET-K solution. These results suggest that the three agents in the modified ET-K solution protected pulmonary artery endothelial cells during storage of the lung and that the effect of modified ET-K solution was mediated not simply through vasodilating actions of nitroglycerin or db-cAMP on the transplanted lung after reperfusion.

In this study, we did not investigate the effectiveness of each of these three substances in lung preservation. Oz and associates [8] reported that the combined use of NAC, nitroglycerin, and db-cAMP was effective in storage of the heart but did not show any effects of NAC alone. However, the effectiveness of NAC in the preservation of the lung cannot be denied, because in their report the concentration of NAC was approximately 1/20 that in our modified ET-K solution. Many possible mechanisms of action of modified ET-K solution can be proposed. First, reduced pulmonary vessel resistance during pulmonary flush due to the activity of nitric oxide produced from nitroglycerin or of db-cAMP might have protected the pulmonary vessel bed from injuries and made it possible to flush the pulmonary vessels uniformly. Second, db-cAMP might have acted as an intracellular second messenger protecting vascular endothelial cells. Moreover, it could be assumed that their interaction helped to protect vascular endothelial cells.

Even though the mechanism is not clear, we have demonstrated definitely that the modified ET-K solution is a consistently excellent preservative solution. In the present study, UW solution was unreliable for 30-hour lung preservation. This finding does not contradict previous reports of excellent results obtained with UW solution in lung preservation for about 24 hours [17, 18]. Therefore, the maximal limit of UW solution appears to be between 24 and 30 hours for the preservation of lungs. In conclusion, we hope that the result of this study will contribute to an increase in the supply of donor lungs and make semielective operations possible in the field of clinical lung transplantation.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Address reprint requests to Dr Wada, Department of Thoracic Surgery, Chest Disease Research Institute, Kyoto University Kawaharacho 53, Shogo-in, Sakyo-ku, Kyoto, Japan 606.

	References

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 

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13. Fukuse T, Hirai T, Yokomise H, et al. Combined therapy with FK-506 and cyclosporine-A for canine lung allotransplantation: immunosuppressive effects and blood trough levels. J Heart Lung Transplant 1993;12:941–7.[Medline]
14. Fischer JH, Jeschkeit S. Effectivity of freshly prepared or refreshed solutions for heart preservation versus commercial EuroCollins, Bretschneider's HTK, or University of Wisconsin solution. Transplantation 1995;59:1259–62.[Medline]
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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Hiromi Wada Toru Bando Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wada, H. Articles by Kosaka, S. Search for Related Content PubMed PubMed Citation Articles by Wada, H. Articles by Kosaka, S.