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Ann Thorac Surg 1996;62:233-240
© 1996 The Society of Thoracic Surgeons
Center for Experimental Surgery and Anesthesiology, Katholieke Universiteit Leuven, Leuven, Belgium
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Abstract |
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 TopFootnotes Abstract IntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Methods. Adenosine triphosphate (ATP) and hypoxanthine levels were measured postmortem in rabbit lungs comparing deflation (group 1), ventilation with room air (group 2), inflation with room air (group 3), ventilation with oxygen (group 4), ventilation with cooled air (group 5), deflation plus cadaver cooling (group 6), and cooling by pulmonary arterial flush (group 7).
Results. The level of ATP dropped to 25.9% and HYP increased elevenfold at 30 minutes in group 1 but remained constant during 24 hours in group 7. The ATP catabolism beyond 2 hours postmortem appeared less in group 2 compared with group 3 (3.58 ± 1.24 versus 0.39 ± 0.08 µmol/g dry weight for ATP and 3.03 ± 0.49 versus 7.64 ± 0.94 µmol/g dry weight for hypoxanthine at 24 hours, respectively; p < 0.05). Cadaver cooling significantly slowed ATP catabolism. Changes in ATP levels were similar in groups 2, 4, and 5.
Conclusions. These data suggest that in the non-heart-beating cadaver (1) cooling, ventilation, and inflation can delay ATP catabolism; (2) postmortem ventilation but not inflation for more than 2 hours will inhibit further ATP breakdown; (3) ventilation with either oxygen or cooled air is not more beneficial than room air ventilation; and (4) cold flush more than cadaver cooling will prevent ATP depletion.
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Introduction |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Lung transplantation, as other forms of solid organ transplantation, is limited by a scarcity of good donor organs. It is estimated that less than 10% of all available multiorgan donors have lungs suitable for lung transplantation [1]. With continued progress in organ transplantation the demand for transplants, and thus the need for organs, has increased markedly. The result is an increasing waiting time for a suitable organ and augmented risk of premature death of patients listed for lung transplantation.
To alleviate this critical organ shortage, there is a growing interest in increasing the potential donor pool by turning to alternative sources such as the use of living-related donors [2], partial (or lobar) transplants [3, 4], or the use of organs from circulation-arrested cadavers, so called non-heart-beating donors (NHBDs) [5].
In organs from such donors, cellular energy reserves present in the form of adenosine phosphates will become depleted very rapidly even after a short period of ischemia causing tissue and cellular damage. This might result in organ dysfunction jeopardizing the transplanted patient.
In previous studies performed in our laboratory, catabolism of adenine nucleotides was investigated in isolated rabbit lungs extracted after cold pulmonary flush with a crystalloid solution and immersed in saline solution at normothermia (37°C) up to 8 hours. These studies demonstrated that 15 minutes of warm ischemia will result in a significant decrease in adenosine triphosphate (ATP) levels and a concomitant increase in hypoxanthine (HYP) levels as the main catabolite [6, 7]. Inflation during normothermic ischemia resulted in a prolonged high ATP content, and the onset of anaerobic metabolism (reflected by lactate production) was related to the alveolar oxygen concentration during storage [8].
The current study was undertaken to investigate catabolism of adenine nucleotides in lung tissue remaining inside the cadaver left at room temperature after circulatory arrest. It was our aim to compare different methods to delay ATP catabolism and HYP formation in the NHBD.
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Material and Methods |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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): lungs left deflated (group 1 = control NHBD), lungs ventilated with room air (group 2), lungs inflated with room air (group 3), lungs ventilated with 100% O2 (group 4), lungs ventilated with cooled (4°C) room air (group 5), and lungs deflated and topically cooled with ice-cold (1°C) saline solution inside the cadaver submerged in an ice-bath (group 6). To compare catabolism of adenine nucleotides in isolated lungs preserved in the heart-beating donor by immediate flush via the pulmonary artery with a cold (4°C) crystalloid solution followed by ex vivo deflated storage in cold (1°C) saline solution, one more group of animals was added (group 7 = control heart-beating donor).
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Animal Preparation
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).
New Zealand white rabbits weighing 2.5 to 3 kg were premedicated and anesthetized by intramuscular injection with 0.25 mL/kg Imalgene (50 mg/mL ketamine; Rhône Mérieux, Lyon, France) and 0.15 mL/kg Domitor (1 mg/mL medetomidin-chlorhydrate + 1 mg/mL paramethylhydroxybenzoate + 0.2 mg/mL parapropylhydroxybenzoate; Orion Corporation, Farmos, Espoo, Finland). The animals were intubated with a 3.5-mm inner diameter cannula (Mallinckrodt Medical, Athlone, Ireland) via a cervical tracheostomy and the lungs were ventilated using a Harvard rodent ventilator model 683 (Harvard Apparatus, Inc, South Natick, MA) with room air (respiratory rate = 30 breaths/min; tidal volume = 10 mL/kg body weight; positive end-expiratory pressure = 2 cm H2O). Heparin Novo 700 IU/kg (sodium heparin 5,000 IU/mL; Novo Nordisk, Bagsvaerd, Denmark) was administered via a marginal ear vein. Rabbits were sacrificed by intravenous injection with 100 mg/kg Nembutal (60 mg/mL sodium pentobarbital; Abbott Laboratories, North Chicago, IL) resulting in cardiac arrest within 5 seconds and left at room temperature (24°C). In the group of animals with lungs deflated (group 1), the tracheal cannula was disconnected from the ventilator immediately after cardiac arrest. In the group with lungs ventilated (groups 2, 4, and 5), respiration was continued during the time interval with the same minute volume and positive end-expiratory pressure. In the group with lungs inflated (group 3), the tracheal cannula was clamped at end-tidal volume. In the group ventilated with cooled room air (group 5), a long coil of copper tubing submerged in ice was interposed between the ventilator and the tracheal cannula, reducing the temperature of inspiratory room air from 24°C to 4°C at the distal end of the cannula.
Fifteen minutes before the first biopsy, the chest was opened through a median sternotomy. Thymic tissue was excised. Both pleural cavities were opened. The sternal edges were reapproximated after each biopsy using towel clips. In group 6, both pleural cavities were filled once with ice-cold (1°C) saline solution immediately after sacrifice. Thereafter, the animal was completely submerged in an ice-bath preventing direct contact between the ice and the pleural cavity. In the group of animals with lungs preserved by immediate cold pulmonary flush (group 7), both superior caval veins, the inferior caval vein, the ascending aorta, and the main pulmonary artery were encircled by individual ligatures. The main pulmonary artery was cannulated through the right ventricular outflow tract using a 10-gauge cannula (Angiocath; Becton Dickinson Vascular Access, Sandy, UT). The pulmonary artery was isolated from the right ventricle by ligature around the tip of the cannula just distal to the pulmonary valve. The cannula remained in place for subsequent pulmonary flush. The tip of the left atrial appendage was transected to allow free drainage of the flush solution immediately after cardiac arrest. Both lungs were flushed by gravity at 60 cm H2O with 60 mL/kg cold (4°C) modified Krebs-Henseleit solution (composition in millimoles per liter: NaCl, 118; NaHCO3, 25; KCl, 5.6; CaCl2, 2.9; MgCl2, 0.6; NaH2PO4, 1.2; and D-glucose, 11; pH, 7.4; osmolarity, 321 mOsm/L). During the flush, the lungs were continuously ventilated with room air and topically cooled. Thereafter, the heart-lung block was excised and immersed deflated in cold (1°C) saline solution for 24 hours.
The whole procedure was carried out under clean but not sterile conditions.
Lung Biopsies
Small biopsy specimens of peripheral lung tissue were taken at time intervals after circulatory arrest for determination of adenine nucleotides (ATP, adenosine diphosphate [ADP], and adenosine monophosphate [AMP]) and their catabolites (inosine monophosphate, adenosine, inosine, and HYP). The biopsy specimens were immediately cooled in liquid nitrogen, lyophilized overnight, and further stored at -80°C until analysis.
In groups 1, 6, and 7 biopsy specimens were taken before cardiac arrest (preischemic levels). Further biopsy samples in different experimental groups were obtained at time intervals after death as listed in Table 1
. In animals with lungs ventilated or inflated after death (groups 2 through 5), only two biopsy specimens were taken per animal to prevent postbiopsy air leak. The first biopsy specimen was taken from the left lung after one time interval (30, 120, or 480 min). Before this, the hilum of this lung was ligated and the contralateral lung remained inflated (group 3) or ventilated (groups 2, 4, and 5), reducing the tidal volume by half. The second biopsy specimen was taken from the right lung after the next time interval (60, 240, or 1,440 minutes, respectively).
Measurement of Adenosine Nucleotides and Catabolites
The adenine nucleotides and catabolites were measured by high-performance liquid chromatography as previously described [6]. We only focused on ATP, ADP, and AMP degradation and HYP formation as we have previously demonstrated that HYP is the main catabolite from adenine nucleotides in lung tissue, representing 92% of all nucleoside and purine base fraction at 4 hours of warm ischemia [6].
The level of total adenine nucleotides (TAN) was defined as the sum of ATP + ADP + AMP. Energy charge was calculated as (ATP + 0.5•ADP)/(ATP) + ADP + AMP) [10].
Statistics
Tissue levels of ATP, ADP, AMP, HYP, and TAN are expressed in micromoles per gram of dry weight (µmol/g dw). Data are presented as the mean ± standard error of the mean.
Differences within groups between premortem values and ischemic levels at successive time intervals after death were calculated using one-way analysis of variance with repeated measurements followed by Scheffé's multiple comparison test [11]. Differences between groups at the same postmortem time interval were compared using analysis of variance with factorial analysis (StatView SE+ Graphics [Abacus Concepts Inc, Berkeley, CA] on a Macintosh Performa 630 computer). Values of p less than 0.05 were accepted as significant (Scheffé's test).
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Results |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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. There was a rapid decrease in ATP levels after circulatory arrest from 7.42 ± 0.40 µmol/g dw at 0 minutes (preischemic level) to 1.92 ± 0.44, 0.99 ± 0.11, and 0.80 ± 0.14 µmol/g dw at 30, 60, and 240 minutes, respectively (p < 0.01 starting at 20 minutes versus 0 minutes). Simultaneously, there was a transient increase in levels of ADP (0.97 ± 0.09 µmol/g dw at 0 minutes) and AMP (0.37 ± 0.04 µmol/g dw at 0 minutes) reaching a maximum at 10 min (1.78 ± 0.17 µmol/g dw) and 15 min (2.22 ± 0.55 µmol/g dw) respectively and slowly returning to pre-ischemic levels thereafter (see Table 2). A rapid and constant increase in HYP levels was noted from 0.12 ± 0.05 µmol/g dw at 0 minutes to 2.88 ± 0.27, 3.05 ± 0.56, and 3.60 ± 0.37 µmol/g dw at 60, 120, and 240 minutes, respectively (p < 0.05 starting at 60 minutes versus 0 minutes) (see Fig 1).
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). This indicates that postmortem ventilation (either with room air at 24° or 4°C or with 100% O2), inflation, and topical cooling of the lungs inside the cadaver can slow down catabolism of adenine nucleotides.
In contrast, ATP and HYP levels remained constant during 24 hours in deflated rabbit lungs cooled immediately after cardiac arrest by in situ cold (4°C) pulmonary flush followed by ex vivo storage in cold (1°C) saline solution (group 7 = control heart-beating donor) (Fig 2). Values for ATP and HYP were 7.77 ± 0.30 and 0.09 ± 0.02 µmol/g dw at 0 minutes versus 7.04 ± 0.66 and 0.37 ± 0.08 µmol/g dw at 24 hours, respectively (not significant for ATP at all intervals versus 0 minutes; p < 0.05 for HYP only at 24 hours versus 0 minutes).
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. Inflation with room air significantly delayed ATP levels at 1 hour compared with deflated lungs (group 1) (3.61 ± 0.65 versus 0.99 ± 0.11 µmol/g dw; p < 0.01) and appeared to be better, although not significantly better, than ventilation at this time interval (2.55 ± 0.49 µmol/g dw; not significant versus inflated, p < 0.01 versus deflated). This difference in ATP levels between inflation and ventilation disappeared at 2 hours (3.12 ± 1.44 and 3.51 ± 1.01 µmol/g dw, respectively) but the levels still remained higher in both inflated and ventilated lungs when compared with deflated lungs (1.13 ± 0.20 µmol/g dw). At longer time intervals the ATP level in inflated lungs returned to levels comparable with deflated lungs (1.99 ± 1.01, 1.21 ± 0.38, and 0.39 ± 0.08 µmol/g dw at 4, 8 and 24 hours versus 0.80 ± 0.14 µmol/g dw at 4 hours, respectively). Levels of ATP in ventilated lungs, however, further increased to 4.17 ± 0.83 µmol/g dw at 4 hours and remained at a constant level thereafter (3.17 ± 1.04 and 3.58 ± 1.24 µmol/g dw at 8 and 24 hours, respectively; p < 0.05 versus inflated at 24 hours) (see Fig 3). Energy charge also reincreased in ventilated lungs from 0.55 ± 0.05 at 1 hour to 0.73 ± 0.05 at 4 hours and thereafter remained constant up to 24 hours (0.73 ± 0.04). On the other hand, TAN levels in ventilated lungs remained fairly stable (6.63 ± 0.34, 6.30 ± 0.98 and 5.11 ± 1.45 µmol/g dw at 30 minutes, 4 hours, and 24 hours, respectively; not significant at all intervals versus preischemic levels). This is in sharp contrast with TAN levels in inflated lungs showing a constant decrease up to 24 hours (7.56 ± 0.37, 3.46 ± 1.07, and 1.07 ± 0.19 µmol/g dw at 30 minutes, 4 hours, and 24 hours; p < 0.05 at 2, 4, 8, and 24 hours versus 0 minutes). The differences in TAN levels between group 2 and 3 only were not significant until 24 hours (see Fig 3). The differences observed in HYP levels between ventilated and inflated lungs after 2 hours of warm ischemia are similar to the TAN plot, although this difference became significant at earlier intervals (p < 0.05 at 4, 8, and 24 hours) (see Fig 3).
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compares the effect on ATP catabolism, TAN levels, and HYP formation in deflated lungs of cadaver cooling (group 6) versus cold (4°C) pulmonary flush with Krebs-Henseleit bicarbonate buffer followed by ex vivo cold (1°C) storage (group 7) versus lungs left at room temperature (24°C) (group 1) during 4 hours. Topical cooling of deflated ischemic rabbit lungs inside the cadaver could significantly delay ATP depletion and HYP formation when compared with lungs left at room temperature (5.46 ± 1.32 versus 1.92 ± 0.44 µmol/g dw for ATP [p < 0.05] and 0.36 ± 0.14 versus 1.36 ± 0.19 µmol/g dw for HYP [p < 0.01] at 30 minutes, respectively). However, as expected, cold pulmonary flush was more effective and faster than topical cooling in blocking catabolism of adenine nucleotides after perfusion has stopped (p < 0.05 at 1, 2, and 4 hours for ATP, TAN, and HYP levels in group 6 versus group 7) (see Fig 4).
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Comment |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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The period of inevitable warm ischemia in the NHBD should therefore be kept as short as possible. However, organizing organ retrieval and obtaining family consent for organ donation consumes precious time. During this interval, organs have to be protected against cellular autolysis by preservation already inside the dead body.
Postmortem cardiac massage and continued ventilation of the cadaver until the onset of in situ cold flush through intraarterial catheters [14] or total body cooling on extracorporeal cardiopulmonary bypass [15] can protect the organs from NHBD during this time interval as already clinically demonstrated, albeit so far only in kidney [16] and liver [17] transplantation.
The clinical use of thoracic organs from NHBD is still anecdotal [5]. Nevertheless, transplantation of heart and lungs from NHBD is being investigated in an increasing number of animal experiments during recent years [18–23].
The lung is unique among other solid organs in the way that oxygen can be delivered either through the airway or through its dual (bronchial and pulmonary) arterial circulation. Theoretically, the ventilated alveolar space provides a large oxygen reservoir for continued aerobic metabolism during prolonged storage. Gas exchange is a passive process, and cellular respiration can occur directly across the pulmonary gas interface. The energy requirements in the lung are primarily for the purpose of maintaining cellular integrity. To meet its energy demands, the lung almost exclusively metabolizes glucose [24].
In this study, we wanted to investigate catabolism of adenine nucleotides in lung tissue inside the cadaver left at room temperature after circulatory arrest using high-performance liquid chromatography. It was our aim to compare different methods to delay ATP catabolism and HYP formation in a rabbit model of NHBD. In a previous study from our laboratory, we already demonstrated a rapid decline in ATP content in normothermic deflated lungs (from a preischemic value [±standard deviation] of 9.42 ± 0.58 to 5.17 ± 0.86 µmol/g dw at 15 minutes and further to 3.42 ± 0.24 µmol/g dw at 30 minutes of normothermic ischemia) [6]. In the present study, ATP levels (±standard error of the mean) were lower both at 0 and 30 minutes of ischemia (7.42 ± 0.4 and 1.92 ± 0.44 µmol/g dw, respectively). In the previous study, however, lungs were ventilated and flushed with 60 mL/kg cold (4°C) Krebs-Henseleit bicarbonate buffer solution to remove all blood elements. The first lung biopsy specimen (preischemic value) was taken at the end of the flush (±2 minutes after the onset). Thereafter, the lungs were extracted and immersed deflated in saline solution at 37°C. A lung tissue temperature of 37°C was obtained after 5 minutes. In the present study, warm ischemia in deflated lungs started immediately after cardiac arrest. This difference in technique might explain the overall lower ATP levels in this study.
In a recent study, Bishop and colleagues [25] investigated the effect of in vivo pulmonary artery occlusion on ATP catabolism. They were able to demonstrate that combined pulmonary artery occlusion and lung collapse resulted in decreased ATP levels at 24 hours. This ATP decline was not observed in rabbits with either pulmonary artery occlusion or lung collapse alone, demonstrating that both ischemia and hypoxia are required for ATP depletion. The persistence of normal ATP content at 4 hours in rabbit lungs after combined pulmonary artery occlusion and lung collapse was attributed to the intact anastomotic bronchial circulation in vivo providing oxygen and substances for continued aerobic lung metabolism during a short period.
We compared ATP breakdown and TAN levels in room-air-ventilated (group 2) versus inflated (group 3) lungs and found that ATP breakdown was less in inflated lungs during the first hour but thereafter a further decline was observed only in inflated lungs. The differences, however, between these groups were not statistically significant until 24 hours. The fact that both TAN and HYP levels in group 2 remained fairly constant between 1 and 4 hours and the fact that ATP levels and energy charge reincreased during this same time interval suggests that ATP is regenerated from AMP and ADP by oxidative phosphorylation during postmortem oxygen ventilation. In contrast, TAN levels further decreased and HYP levels increased in group 3. This suggests that oxygen supply in nonperfused lungs inflated with room air is not sufficient for continued aerobic metabolism. In one of our previous studies [8], we already demonstrated that inflation with 100% O2 could prolong this period of preserved high-energy phosphate levels up to 4 hours before the onset of anaerobic metabolism as reflected by the formation of lactate. Identical observations were made by Akashi and associates [26] in rat lungs. The data observed in this study also confirm the findings in recent work by D'Armini and co-authors [27] in cadaveric rat lung. They nicely demonstrated that O2 ventilation of the nonperfused lung preserved adenine nucleotides and this correlated well with light microscopic pulmonary cell viability quantified by pulmonary artery infusion with trypan blue vital dye [27]. Ventilation with N2, however, was not associated with maintenance of ATP and TAN levels or with prolonged lung viability. This study suggests that not ventilation itself but continued oxygen supply is important to maintain aerobic metabolism and prevent cellular damage.
The biochemical data in our present study as well as in all the previously mentioned studies support the experimental findings in canine models that the duration of tolerable lung ischemia may be prolonged if the lungs remain ventilated or inflated during the ischemic interval [13, 19, 28].
We also investigated the effect of cooling on ATP metabolism. Both cadaver cooling (group 6) and cold pulmonary flush (group 7) will significantly delay ATP depletion, TAN degradation, and HYP formation when compared with lungs left at room temperature. As expected, cold pulmonary flush is more effective and faster than cadaver cooling in blocking ATP catabolism after cessation of circulation (p < 0.05 at 1, 2, and 4 hours for ATP, TAN, and HYP levels comparing group 6 versus group 7) (see Fig 4). These results are in accordance with the findings of Date and colleagues [29], who found that ATP levels in lungs inflated with 100% oxygen were stable for 18 hours after cold (4° or 10°C) pulmonary flush with low-potassium dextran and immersion in the same solution. The ATP level was significantly worse at 18 hours after preservation at 22°C [29]. Omote and associates [30] compared ATP concentrations in deflated rat lungs preserved in three different cold flush and storage solutions. Adenosine triphosphate content at 24 hours was significantly greater after preservation with University of Wisconsin solution when compared with Euro-Collins solution or low-potassium dextran.
We have found no significant difference in ATP and TAN levels between postmortem ventilation with either room air at 24°C (group 2), 100% O2 (group 4), or cooled (4°C) room air (group 5). In a companion study, we could not demonstrate a decline in lung temperature through ventilation with cooled air [9]. Therefore, we did not expect any more benefit from cooled air ventilation in delaying ATP breakdown. Levels of HYP at 24 hours differed significantly when comparing lungs ventilated with room air versus 100% oxygen. The ideal O2 concentration that should be administered to lung grafts during storage remains an open question [28].
From this study, we can conclude that in the NHBD (1) cooling, ventilation, and inflation can slow down ATP catabolism; (2) 24-hour postmortem ventilation but not inflation can inhibit further ATP breakdown and HYP formation beyond 2 hours of warm ischemia; (3) ventilation with either 100% O2 or cooled (4°C) air is not more beneficial than ventilation with room air; and (4) cold (4°C) crystalloid flush will immediately prevent ATP depletion and is more effective than cadaver cooling. Further studies are necessary to investigate whether lungs from human NHBDs will become a realistic alternative to expand the pulmonary donor pool.
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Acknowledgments |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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We thank André Berghen, Peter Lemmens, Magda Mathijs, and Kanigula Mubagwa, MD, for expert technical and secretarial assistance.
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Footnotes |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Address reprint requests to Dr Van Raemdonck, Department of Thoracic Surgery, University Hospital Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium (E-mail: Dirk.VanRaemdonck{at}uz.kuleuven.ac.be).
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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