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Ann Thorac Surg 2000;70:1679-1683
© 2000 The Society of Thoracic Surgeons

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Original articles: general thoracic

Short-term inhaled nitric oxide in canine lung transplantation from non-heart-beating donor

^a Department of Surgery II, Okayama University School of Medicine, Okayama, Japan

Address reprint requests to Dr Date, Department of Surgery II, Okayama University School of Medicine, 2-5-1 Shikata-cho, Okayama 700-8558, Japan
e-mail: hdate{at}nigeka.hospital.okayama-u.ac.jp

	Abstract

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Background. Use of lungs harvested from non-heart-beating donors (NHBDs) would increase the pulmonary donor pool; however, this strategy would have higher risk of early postoperative graft dysfunction due to unavoidable warm ischemic time. We evaluated the effects of short-term inhaled nitric oxide (NO) during reperfusion in canine left single-lung allotransplantation from a non-heart-beating donor.

Methods. The donor dogs were sacrificed without heparinization and left at room temperature for 3 hours. Then, recipient dogs received a left single-lung allotransplantation. After implantation, the right bronchus and pulmonary artery were ligated. In group 1 (n = 6), NO gas was administered continuously at a concentration of 40 parts per million throughout a 6-hour assessment period. In group 2 (n = 6), NO gas was administered for the initial 1 hour during reperfusion. In group 3 (n = 6), nitrogen gas was administered for control.

Results. Groups treated with NO exhibited lower pulmonary vascular resistance, as well as improved survival and oxygenation. There was no significant difference in these parameters between group 1 and group 2. Myeloperoxidase activity was significantly lower in NO-treated groups.

Conclusions. Inhaled NO during reperfusion is beneficial in lung transplantation from non-beating heart donors. The beneficial effect is obtained mainly during the first hour of reperfusion.

	Introduction

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
The most serious impediment to the widespread application of lung transplantation is the relative scarcity of satisfactory pulmonary donors. Use of lungs harvested from non-heart-beating donors (NHBDs) would increase the pulmonary donor pool. The warm ischemic time (WIT) associated with cadaver lung transplantation has been investigated by a number of investigators [1–5].

A WIT of more than 2 hours has resulted in early postoperative graft dysfunction, as manifested by hypoxia and pulmonary hypertension, and has been associated with endothelial dysfunction and polymorphonuclear neutrophil (PMN) activation [6].

Nitric oxide (NO) is believed to be identical to endothelium-dependent relaxing factor [7, 8], a potent vasodilator. In addition, it has been found that NO played a critical role in the maintenance of vascular permeability through attenuation of PMN activation [9, 10] and platelet degradation [8]. A study has shown that inhaled NO continuously improved the oxygenation of canine lung allografts by attenuating ischemia-reperfusion (I-R) injury in the early postoperative period [11]. Ischemia-reperfusion injury starts within a few minutes of reperfusion, and the first hour of reperfusion is the period of higher risk for PMN-induced lung injury [12, 13]. There-fore, we have evaluated the effects of short-term inhaled NO at reperfusion in canine left single-lung allotransplantation from an NHBD.

	Material and methods

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Eighteen weight-matched pairs of adult mongrel dogs (6.5 to 23.0 kg) were used for cadaver left single-lung allotransplantation. The donor dogs were premedicated with an intramuscular injection of ketamine hydrochloride (10 mg/kg) and atropine sulfate (0.02 mg/kg), and anesthetized by an intravenous injection of thiopental sodium (10 mg/kg). Then the donors were sacrificed by an intravenous injection of 20 mL potassium chloride without heparinization. Donor death was determined by cessation of cardiac activity. Each donor was placed in the supine position, and was left at room temperature for 3 hours. After a 3-hour WIT, a double lung block was excised via median sternotomy without flushing, and cooled in cold saline. The left lung was prepared from the double lung block for subsequent transplantation.

The recipient dogs were premedicated in the same manner as the donors, and anesthetized by an intravenous injection of thiopental sodium (5 mg/kg). Each recipient was intubated and ventilated mechanically at 15 breaths/min, a tidal volume of 20 mL/kg, and positive end-expiratory pressure of 5 cm H₂O. Anesthesia was maintained by a 50:50 mixture of nitrous oxide/oxygen and 0.5% halothene. To measure the pulmonary arterial pressure, central venous pressure, and the cardiac output, a Swan-Ganz catheter (Terumo) was placed in the main pulmonary artery through the right femoral vein. A femoral arterial line was inserted for measuring the aortic pressure and for the blood gas analysis. Following thoracotomy in the left fifth intercostal space, a wedge resection of the recipient’s native left lung was taken as a control sample for myeloperoxidase (MPO) activity assay. After left pneumonectomy, the right pulmonary artery and bronchus were mobilized, and taped separately with a silk string for assessment of allograft function after transplantation. Subsequently, a left atrial monitoring line was inserted to measure the left atrial pressure. The left single-lung allotransplantation was performed using standard techniques.

After transplantation, both lungs were ventilated with an inspired oxygen fraction of 1.0 and anesthesia was maintained with an intravenous infusion of thiopental sodium. Following baseline assessment of the hemodynamics and blood gas analysis, the right bronchus and pulmonary artery were ligated. The recipient was observed for 6 hours or until death, during which time the allograft function was measured repeatedly at specific intervals (at 5, 15, and 30 minutes, and at 1, 2, 3, 4, 5, and 6 hours after ligation of the right bronchus and pulmonary artery). If metabolic acidosis occurred, then bicarbonate sodium was injected intravenously. If respiratory acidosis occurred, the respiratory rate of the ventilator was increased to 20 breaths/min temporarily. However, the ventilator was returned to 15 breaths/min before assessment. The allograft was removed at death or at the completion of the 6-hour assessment. Specimens of the part of the left apex were snap frozen in liquid nitrogen until the time of MPO activity assay, performed using the method described by Kraiwsz and colleagues [14]. The rest of the allograft was used to measure the wet-to-dry lung weight ratio (W/D ratio), which was determined by the weight difference between specimens before and after being dried for about 3 weeks in an oven kept at 70 to 90°C.

The dogs were assigned randomly to one of the three groups. In group 1 (n = 6), NO gas was administered continuously at a concentration of 40 parts per million (ppm) before reperfusion throughout the 6-hour assessment period. In group 2 (n = 6), NO gas was administered before reperfusion and continued for the initial 1 hour during reperfusion. Thereafter, nitrogen gas (N₂) was administered in the same manner as NO. In group 3 (n = 6), N₂ was administered in the same manner as NO in group 1, for control. NO gas was administered into the inspiratory limb of the respirator circuit as a mixture of 800 ppm in pure nitrogen. The concentrations of NO and of NO₂ were monitored continuously just proximal to the endotracheal tube using chemiluminescence analyzers. The NO₂ concentration was maintained at under 4 ppm.

Airway edema fluid from the allograft was collected, and the total suction fluid volume for the 6-hour assessment period was measured. Methemoglobin levels were measured at the baseline assessment time and again at 3 hours after the ligation.

Myeloperoxidase is a marker enzyme specific to PMNs, and is used as an indirect measure of tissue PMN activation. Allograft samples were immediately frozen by immersion in dichlorodifluoromethane that had been precooled to the freezing point and stored at -70°C until assay. The quantitative MPO activity was determined as described previously [14]. Briefly, frozen lung tissue (100 mg) was homogenized in 1 mL of 0.5% hexadecyl-trimethyl-ammonium bromide (HTAB), 5 mM EDTA, and 50 mM potassium phosphate (pH 6.2) with a homogenizer. HTAB is a detergent that releases MPO from the primary granules of PMN. The homogenate was centrifuged at 10,000 g for 15 minutes at 4°C. Using the method of Pierce Laboratories [15], the supernatant was subsequently assayed for MPO activity and total soluble protein level.

The MPO activity was measured spectrophotometrically: 10 µL of supernatant was combined with 0.6 mL of Hanks BSA (0.255 g bovine serum albumin added to 100 ml of Hanks solution), 0.5 mL of 100 mM potassium phosphate buffer (pH 6.2), 0.1 mL 0.05% H₂O₂, and 0.1 mL of 1.25 mg/mL o-dianisidine. Color development was stopped by the addition of 0.1 mL of 1% NaN₃ after 5 minutes, or after 20 minutes, at room temperature, respectively. Then, the optical density was measured at 460 nm with a spectrophotometer. The color development from 5 to 20 minutes was linear. Enzyme activity was defined as the amount of MPO that produced an absorbance change of 1.0 optical density unit per minute per milligram of tissue protein at room temperature (OD · min^-1 · mg^-1).

Statistical analysis was performed using analysis of variance. All values are given as the mean ± standard error of the mean. Differences were considered significant at a probability value of less than 0.05. For blood gas analysis and hemodynamics, the statistical analyses were performed up until 120 minutes, because the number of the group 3 recipients became reduced after this time.

All animals received care in compliance with the "Principles of Laboratory Animal Care" formulated by the National Society for Medical Research and the "Guide for the Care and Use of Laboratory Animals" published by the National Institutes of Health (NIH publication No. 86-23, revised 1985).

	Results

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
There was no significant difference among the three groups in donor weight, recipient weight, harvesting time, preparation time, or in implantation time. The total ischemic time was 302.3 ± 8.3 minutes in group 1, 299.0 ± 5.0 minutes in group 2, and 300.3 ± 8.7 minutes in group 3 (p = not significant).

The change in survival rate of the recipients after the ligation of the right bronchus and pulmonary artery is shown in Figure 1. All recipients of groups 1 and 2 survived the 6-hour assessment period. In contrast, only 1 of the 6 recipients of group 3 survived for 6 hours. The 5 nonsurviving recipients in this group died at 130, 150, 210, 252, and at 260 minutes after the ligation, respectively. The survival times in groups 1 and 2 were significantly longer than in group 3: 360 ± 0 minutes and 360 ± 0 minutes versus 227 ± 34 minutes; p < 0.01.

View larger version (17K): [in this window] [in a new window]   Fig 1. Survival rate of the recipients after the ligation of the right bronchus and pulmonary artery. The survival times in groups 1 and 2 were significantly longer than in group 3 (p < 0.01).

The change in arterial oxygen tension (PaO₂) is shown in Figure 2. Throughout the 6-hour assessment period, the PaO₂ levels in groups 1 and 2 were higher than that in group 3 (p < 0.01 0.05). The PaO₂ levels were not significantly different between group 1 and group 2.

View larger version (23K): [in this window] [in a new window]   Fig 2. Change in PaO2. Throughout the 6-hour assessment period, the PaO2 levels in groups 1 and 2 were higher than in group 3. The difference reached statistical significance from 15 to 120 minutes. The PaO2 levels were not significantly different between group 1 and group 2. Baseline assessment (BL) was carried out after reperfusion under ventilation of both lungs. (*p < 0.01, groups 1 and 2 versus group 3.) (PA = pulmonary artery; rt Br = right bronchus.)

View larger version (19K): [in this window] [in a new window]   Fig 3. Change in PaCO2. Throughout the 6-hour assessment period, the PaCO2 levels in groups 1 and 2 were lower than in group 3. The difference reached statistical significance at 120 minutes. (#p < 0.05.) (BL = baseline assessment; PA = pulmonary artery; rt Br = right bronchus.)

View larger version (26K): [in this window] [in a new window]   Fig 4. Change in pulmonary vascular resistance (PVR). The PVRs in groups 1 and 2 at 15 minutes were significantly lower than in group 3. (#p < 0.05.) (BL = baseline assessment; PA = pulmonary artery; rt Br = right bronchus.)

View larger version (22K): [in this window] [in a new window]   Fig 5. Change in aortic pressure (AoP). There was no significant difference among the three groups throughout the 6-hour assessment period. (BL = baseline assessment; PA = pulmonary artery; rt Br = right bronchus.)

View larger version (20K): [in this window] [in a new window]   Fig 6. Change in cardiac output (CO). There was no significant difference among the three groups throughout the 6-hour assessment period. (BL = baseline assessment; PA = pulmonary artery; rt Br = right bronchus.)

View larger version (16K): [in this window] [in a new window]   Fig 7. Myeloperoxidase (MPO) activity in the allograft. The MPO activity was significantly lower in groups 1 and 2 than in group 3 (*p < 0.01), and it was significantly higher in groups 1 and 2 than in control group (#p < 0.01).

	Comment

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Because the scarcity of appropriate pulmonary donors remains a serious problem in lung transplantation, a number of investigators have recently investigated the use of lungs harvested from NHBDs. This approach is premised on the fact that lung cells are able to maintain aerobic metabolism with the oxygen in the alveoli even after the cessation of pulmonary vascular circulation [16]. Using a canine-isolated perfused lung model, Homatas and coworkers [1] demonstrated that lungs harvested at 2 hours or less after death had shown reasonable gas exchange, and that pulmonary edema occurred more frequently beyond 2 hours. Using a canine lung autotransplantation model, Yamazaki and coworkers [2] reported similar results. A study on canine lung allotransplantation from an NHBD was first reported by Egan and coworkers [3] in 1991. In their study, all recipients of a 1-hour cadaver lung survived for an 8-hour assessment period. In contrast, 2 of 5 recipients of a 2-hour cadaver lung survived with excellent gas exchange, and only 1 of 4 recipients of a 4-hour cadaver lung survived with poor gas exchange. Using the same study model, Kayano and coworkers [4] demonstrated that all recipients of a 2-hour cadaver lung survived for a 6-hour assessment period, but only 2 of 6 recipients of a 3-hour cadaver lung survived. Based on these studies, the length of safe WIT appears to be in the vicinity of 2 hours when no treatment is given to the donor or recipient. Several strategies have been developed in an attempt to reduce early allograft dysfunction, including inflation of the graft with 100% oxygen [4], administration of urokinase to the donor lung [5], and administration of oxygen radical scavengers to the recipient [17].

Early severe allograft dysfunction, as manifested by allograft edema, decreased oxygen levels, and pulmonary hypertension, develops in 10% to 20% of lung transplant recipients. It is a recent finding that endothelial dysfunction and PMN activation may play a central role in early graft dysfunction. Nitric oxide is believed to be identical to endothelium-dependent relaxing factor, a potent vasodilator. In addition, NO has been found to play a critical role in the maintenance of vascular permeability through its attenuation of PMN and platelets. Activated PMN produces superoxide, which is known to cause tissue injury [18]. Nitric oxide attenuates PMN activation due to attenuation of CD11b/18-mediated PMN adhesion [6]. Okabayashi and coworkers [11] have demonstrated that inhaled NO continuously improved the oxygenation of the canine lung allograft by attenuating PMN activation in the early postoperative period. Furthermore, the beneficial effects of inhaled NO have been indicated in human lung transplant exercise [19].

The present study was designed to investigate whether inhaled NO at reperfusion attenuated or not I-R injury in lung transplantation from an NHBD. Murakami and coworkers [20] reported that inhaled NO may improve lung function using lung harvested from an NHBD. However, in the Murakami study, the WIT was only 30 minutes and the model used was a rat-isolated perfused model. To develop the concept of lung transplantation from an NHBD, we have used a canine model, and left the donor animals at room temperature for 3 hours after death without any pretreatment such as heparinization.

In addition, it is known that I-R injury starts within a few minutes of reperfusion, and the first hour of reperfusion is the period of higher risk for PMN-induced lung injury [12, 13]. Therefore, we studied the effects of duration of NO treatment by comparing 6-hour inhalation and 1-hour inhalation.

In the present study, inhaled NO resulted in significantly decreased lung edema, as indicated by gas exchange (PaO₂, PaCO₂), W/D ratio, and suction fluid volume from the grafts. A significant reduction in the MPO activity in groups 1 and 2 strongly suggested that the attenuation of I-R injury by inhaled NO was due to inhibiting PMN activation, although the elevated MPO activity in group 3 might be partly derived from a secondary effect of I-R injury. Furthermore, the decrease in PVR in groups 1 and 2, although not as dramatic as the reduction in MPO, indicated that another beneficial effect of inhaled NO might be derived from the vasodilatation of the pulmonary vasculature. The beneficial effects of inhaled NO were similar between groups 1 and 2. In contrast to the findings by Hillman and coworkers [21] obtained in an adult respiratory syndrome model, in which PaO₂ values returned to baseline and rebound pulmonary hypertension was seen when NO was precipitously discontinued, we found that the beneficial effect exerted by 1-hour NO treatment could still be documented 5 hours later. We recognize that there was evidence of ongoing I-R injury in NO-treated groups as well at 6 hours, because MPO in both groups 1 and 2 were significantly higher than the control group. Further study is needed to see if the I-R injury at 6 hours will recover in a longer period of time. Bacha and coworkers [22] reported that short-term inhaled NO given during the first 4 hours of reperfusion after lung transplantation significantly attenuated reperfusion injury, improving graft function as long as 24 hours after operation. I-R injury starts within a few minutes of reperfusion [12], and the first hour of reperfusion is the period of higher risk for PMN-induced lung injury [13]. Our study confirmed that inhaled NO given during the first hour after reperfusion improves lung function by reducing PMN activation and decreasing PVR.

Most organs from NHBDs expected to become available for transplantation will be obtained from individuals who die in accidents or who die suddenly away from a hospital. Under such circumstances, most likely there would be no pretreatment to the donor. It is encouraging to note the beneficial effect of short-term inhaled NO after reperfusion demonstrated in this study, which used NHBDs left at room temperature for 3 hours.

	Acknowledgments

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
We thank Mr Tetsuo Kawakami for technical assistance.

	References

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 

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