Reversibility of lesions in experimental pulmonary hypertension. Preliminary observations.

Severe pulmonary hypertension with obliterative vascular disease was induced in 13 of 44 dogs subjected to systemic-to-pulmonary artery anastomosis to the left diaphragmatic lobe. In 11 of these, plus 4 with high pressure but normal histology and 4 with normotensive lobes, for a total of 19, reanastomosis to the main pulmonary artery was performed. Only 1 of the histologically abnormal lobes maintained vascular patency; the 5 other dogs with patent reanastomoses had normal vascular histology. Our findings support the reluctance of surgeons to correct cardiac shunts when obstructive vascular disease due to severe pulmonary hypertension is present; in humans pulmonary artery pressure would not drop as much as in our model since the pulmonary vascular resistance of both lungs is high. On the other hand, if a normal lung were transplanted at the same time, the retained abnormal lung would probably lose vascular perfusion.     

Anomalous origin of the right pulmonary artery from the ascending aorta associated with aortopulmonary window.

A rare case of anomalous origin of the right pulmonary artery from the ascending aorta associated with an aortopulmonary window and severe pulmonary hypertension in a 13-year-old girl is reported. The window was closed using a Dacron patch and the continuity between the anomalous vessel and the main pulmonary artery was restored with a tubular Dacron graft. After operation the pulmonary pressure dropped to about one-half of the systemic pressure, and equal perfusion and ventilation of both lungs was demonstrated. Although early recognition and surgical treatment of this condition are mandatory to prevent the onset of irreversible pulmonary vascular disease, the presence of severe pulmonary hypertension did not contraindicate surgical correction in our patient.     

Anomalous Origin of the Right Pulmonary Artery from the Ascending Aorta: A Surgical Case Study in an Adult Patient with "Irreversible" Pulmonary Vascular Disease

Abstract   An adult patient presented with an anomalous right pulmonary artery arising from the ascending aorta with severe unilateral pulmonary vascular disease of the left lung due to a large left-sided patent ductus arteriosus. A stenosis in the right pulmonary artery protected the right pulmonary vasculature. Right ventricular pressure was suprasystemic. After ductal ligation and surgical repair, pulmonary artery pressures fell dramatically. An immediate postoperative angiography confirmed extremely poor perfusion of the left lung. At four-and-a-half years of follow-up, the patient's quality of life had improved dramatically, main pulmonary artery pressure was one-sixth of systemic pressures, and there was vastly improved perfusion of the left lung at this lower perfusion pressure. The calculated pulmonary vascular resistance of the left lung was within normal limits. These findings suggested a significant degree of reversal of pulmonary hypertensive disease in the left lung sustained to 54 months postoperatively.     

Surgical treatment for a 16-year-old girl with anomalous origin of the right pulmonary artery from ascending aorta

Anomalous origin of the right pulmonary artery is a rare congenital malformation and is usually fatal without early surgical correction. A 16-year-old patient, who had received no previous treatment, demonstrated abnormal findings on ECG. On cardiac catheterization, the pressure in the normally arising left pulmonary artery was found to be greater than the systemic level. Bidirectional shunting across a patent ductus was identified and aortography revealed that the right pulmonary artery arose from the posterior wall of the proximal ascending aorta. The presence of severe pulmonary vascular obstructive disease was anticipated and right lung biopsy was performed. The index of pulmonary vascular disease rating was 2.8 and the Heath-Edwards classification was grade 3. Consequently, we considered that corrective right pulmonary circulation could be maintained after correction, and total correction was performed. The postoperative course was uneventful and the pulmonary artery pressure reduced significantly. Discussion focuses on the surgical indications for such infrequent older cases and we conclude that preoperative lung biopsy is useful in identifying severe pulmonary vascular disease and evaluating indications for surgery.     

Venoarterial extracorporeal membrane oxygenation--how safe is it? Evaluation with a new experimental model.

This study was undertaken to find out if about 25% right cardiac output is sufficient for preservation of lung function during prolonged periods of venoarterial extracorporeal membrane oxygenation. Six healthy pigs weighing 57 kg were subjected to 18-hour venoarterial extracorporeal membrane oxygenation. During this period 1200 ml/min venous blood was delivered to the lungs through the pulmonary artery with the help of a separate roller pump and with use of the animal's own right ventricle to generate the pulse. Animals were observed for 6 hours after weaning from the venoarterial extracorporeal membrane oxygenation. At the sixth hour after extracorporeal membrane oxygenation, arterial oxygen tension, venous oxygen tension, lung compliance, and cardiac output had decreased significantly. Pulmonary vascular resistance and pulmonary clearance of technetium 99m-diethylenetriamine pentaacetic acid increased significantly also. The systemic arterial and venous carbon dioxide tensions, pH, and the base excess remained unchanged, as did the blood pressure and the systemic vascular resistance. Histopathology of the lung specimens revealed focal alveolar wall thickening and alveolar capillary congestion. The major portion of the pulmonary parenchyma looked normal. Alterations in pulmonary parameters cited were, to a major extent, explained on the basis of the experimental protocol followed and were believed to be reversible. This study suggests that about 25% of the systemic cardiac output should be diverted into the pulmonary artery for prevention of irreversible physiologic and histopathologic changes in the lungs during 18-hour normothermic venoarterial extracorporeal membrane oxygenation in healthy juvenile pigs.     

Right main bronchus obstruction in a patient intubated with a left double-lumen tube for thoracic aortic surgery

A 29-year-old woman with a tubular thoracic aortic graft prosthesis, placed after repair of a postcoarctation site aneurysm, was reoperated due to fungal infection of the prosthesis. A left thoracotomy was performed and single lung ventilation established through a double lumen tube followed by extracorporeal circulation (ECC), deep hypothermia, and cessation of blood circulation. The venous drainage tube was placed in the right pulmonary artery and arterial return was located in the descending aorta. After replacement of the prosthesis and interruption of ECC, attempts to ventilate the right lung failed. Fiberoptic examination revealed that the carina and tracheal wall completely occluded the opening of the right main bronchus. ECC was interrupted and the left lung was ventilated, but after withdrawal of the tube from the pulmonary artery and repositioning the patient in supine decubitus, oxygenation and right lung ventilation improved. The patient was extubated after 20 hours and discharged home 6 weeks later.     

Long-term extracorporeal membrane oxygenation with minimal ventilatory support: a new paradigm for severe ARDS?

Pulmonary tuberculosis can lead to acute respiratory distress syndrome (ARDS) which is associated with high mortality. We report the case of a patient with pulmonary tuberculosis and severe ARDS (PaO2/FiO2<100 mmHg) who was initially managed with advanced up-to-date treatments (protective ventilation and extracorporeal membrane oxygenation, ECMO) but failed to improve. After a month of failure and the development of bilateral pneumothoraces, we drastically changed our therapeutic strategy: we maximized ECMO support to maintain oxygenation, we greatly reduced ventilation pressures and we left the pneumothoraces undrained. From then on, the patient improved and he eventually survived. This case suggests that ECMO permits large reductions in lung inflation and ventilation to rest the lungs, while maintaining acceptable oxygenation. The combination of ECMO and markedly attenuated ventilation strategy may be effective in cases of severe ARDS.     

Surgical Repair of Hemitruncus: Principles and Techniques

Ten patients have presented at the World Children's Hospital of Melbourne with hemitruncus, a form of truncus arteriosus. Nine of these patients underwent successful one- or two-stage hemodynamic repair. Early repair is carried out to avoid pulmonary vascular disease of the lung directly supplied from the trunk and to recruit as much of the contralateral pulmonary artery vasculature bed as possible is a secondary goal. The repair should be contemplated within the first six months of life to prevent severe pulmonary vasculature obstructive disease. Anatomy that is repairable in one stage is when the left pulmonary artery originates from the trunk and the complete right pulmonary artery supplied by pulmonary collaterals from the arch to the descending aorta. Anatomy requiring two-stage repair occurs when the RPA rises from the trunk and the left PDA rises from the descending aorta or distal aortic notch and either the right or the left lung blood supply is from multiple origins and requires unifocalization. With these anatomical principles and the general meticulous perioperative and postoperative care of the infants, a high degree of success should be obtainable with repair of this hemitruncus.     

Protective effect of ventilation on warm ischemic lungs

This study was undertaken to determine whether lung ventilation during warm ischemia provides a protective effect on lung preservation. The mongrel dogs were made left thoracotomy incision. Following a complete dissection of left pulmonary artery and vein, left lung was subjected to room temperature ischemia for 4 hours or 6 hours by clamping vasculature. Left lung was ventilated with oxygen or collapsed during warm ischemic period. The isolated ventilation of left lung was secured by ligation of left main bronchus over Carlens tube. After the ischemic period, blood supply of the left lung was reestablished by unclamping the pulmonary artery and vein. The contralateral pulmonary artery was ligated 10 min later, and blood gas, pulmonary pressure, and pulmonary shunt were monitored for additional 4 hours while left lungs ventilated with oxygen. In lungs collapsed during 4 hour ischemic period, massive pulmonary edema occurred within 30 minutes after reperfusion. Partial oxygen tension was only 63 mmHg at 1 hour after reperfusion. In contrast, lungs ventilated during 4 hours ischemic period did not manifest pulmonary edema, and PaO2 was 407 mmHg at 4 hours after reperfusion. The lungs collapsed during 6 hour ischemic period showed massive edema. When the lung was ventilated, the lung behaved variably but still better than the collapsed lungs. These results suggest that the ventilation of the lung during warm ischemia provide a protective effect.     

Intravital microscopy of pulmonary microcirculation after single lung transplantation in pigs

BACKGROUND: Pulmonary reperfusion injury is a significant risk factor following lung transplantation (LTx). Unfortunately, in vivo observations and quantitative analyses of the pulmonary microcirculation following LTx are technically demanding. METHODS: Pigs, weighing 18 to 22 kg, served as the laboratory animals. The left lung was harvested and preserved using donor aortic vessel segments, the pulmonary artery, and the cuff of the lung veins were extended. After 4 hours of ischemia, the lungs were transplanted by direct connection of the conduits to the left atrial appendage and the left pulmonary artery of the recipient. The lungs were placed extrathoracically and ventilated. The recipient left lung was excluded. With this procedure, mechanical trauma to the lung and moving artefacts were avoided. Intravital microscopic observation became feasible. RESULTS: Following reperfusion, oxygenation of pulmonary venous blood was excellent. However, blood flow distribution was significantly reduced to the transplanted lung compared with the native right recipient lung. Pulmonary vascular resistance was significantly increased, dropping from 3500 to 1000 dynes x s x cm(-5) during reperfusion compared to a value of 500 for the native right lung. The pulmonary microcirculation showed a significant number of no-reflow areas with extremely reduced red blood cell velocities. Greater than 90% of microvessels (<30 microm) showed velocities below 0.1 mm/sec. In conclusion, microvascular injury seems to be a major pathogenic factor for the development reperfusion failure. Quantification of alterations within the microvasculature may shed light on various treatment modalities that reduce perfusion failure.     

The effect of gene transfer with hepatocyte growth factor for pulmonary vascular hypoplasia in neonatal porcine model

BACKGROUND: Severe degree of pulmonary vascular hypoplasia remains a major limitation in congenital heart surgery. Considering the potential effect of gene transfer with hepatocyte growth factor to induce the angiogenesis in the lung, we assessed the effects of hepatocyte growth factor gene transfer in neonatal porcine lung with pulmonary vascular hypoplasia to achieve treatment for severe pulmonary vascular hypoplasia. METHODS: The model of pulmonary vascular hypoplasia was introduced with left pulmonary artery banding in piglet lung. After 7 days of pulmonary artery banding, piglets were transfected selectively to the left lung via the left pulmonary artery with a hemagglutinating virus of Japan E vector bearing the cDNA encoding human hepatocyte growth factor (H group) or control vector (C group). RESULTS: Seven days after the transfection, selective angiography of the left pulmonary artery showed the progression of left pulmonary vascular hypoplasia of the left lung in the C group but a significant attenuation of left pulmonary vascular hypoplasia in the H group. A right pulmonary artery occlusion test showed a marked increase in right ventricular systolic pressure in the C group, but this was significantly attenuated in the H group (C: 22.0 +/- 2.9, H: 13.0 +/- 2.7 mm Hg; P < .05). Histologic examination revealed that hepatocyte growth factor gene transfection increased the pulmonary vasculature in the left lung. CONCLUSIONS: Our results demonstrated that gene transfer of hepatocyte growth factor via the pulmonary artery showed the angiogenic effects in porcine model of pulmonary vascular hypoplasia after pulmonary artery banding.     

Hemodynamic unloading leads to regression of pulmonary vascular disease in rats

OBJECTIVE: Treatment options for patients with advanced pulmonary vascular disease caused by a congenital heart defect are still mainly limited to heart-lung transplantation or lung transplantation with repair of the cardiac lesion. Because we have previously shown that the structural changes associated with pulmonary hypertension can be reversed by stress unloading in an organ culture model, we now investigate whether hemodynamic unloading will lead to regression of pulmonary vascular disease in the intact animal. METHODS: Right middle and lower lobectomy and monocrotaline injection were performed in Lewis rats (n = 22) to cause pulmonary vascular disease from a combined hemodynamic and toxic injury. Twenty-eight days later the left lungs were examined (n = 10) or exposed to normal pulmonary artery pressure for an additional 14 (n = 5) or 28 (n = 7) days by transplantation into healthy recipients. Pulmonary artery pressure, ventricular weight, and pulmonary artery morphology were evaluated in each group. RESULTS: Pulmonary hypertension (50 vs 16 mm Hg; P <.001) and right ventricular hypertrophy (right ventricular/left ventricular weight 0.69 vs 0.32; P <.001) associated with pulmonary artery medial hypertrophy (28.2% vs 7.2% wall thickness; P <.001) and muscularization of small pulmonary arteries (92.3% vs 19.4%; P <.001) developed by day 28 (compared with untreated controls). However, transplantation into healthy recipients effectively unloaded the lungs (mean pulmonary artery pressure 17 and 24 mm Hg at 14 and 28 days after transplantation) and resulted in progressive normalization of medial hypertrophy (15.6% and 12.1% at 14 and 28 days) and muscularization (65.1% and 42.2% at 14 and 28 days) relative to nontransplanted controls (P <.005 in each case). CONCLUSIONS: Hemodynamic unloading of lungs with pulmonary vascular disease results in progressive normalization of pulmonary artery structure. These results are the first to provide a rationale for attempting to induce regression of pulmonary vascular disease by pressure unloading of the pulmonary circulation. Methods to mechanically unload the pulmonary circulation should be critically evaluated as a strategy for staged surgical repair of congenital heart defects despite presumed irreversible pulmonary hypertension.     

Anomalous systemic arterial supply to normal basal segment of the left lower lobe; report of a case

A 28-year-old male was referred to our hospital because of hemoptysis. A chest X-ray revealed an increase of vascular marking in the left lower field and a partial defect in the lateral line of the descending thoracic aorta. An aortogram and pulmonary arteriogram showed a large artery arising from the descending thoracic aorta and supplying the left basal segment, which had no normal pulmonary arteries. A bronchoscopy showed no abnormal findings in the bronchial tree. A clinical diagnosis of systemic arterial supply to the basal segment of the left lower lung was made, and a left lower lobectomy and closure of the anomalous systemic artery by video-assisted thoracic surgery (VATS) were successfully performed. Vascular marking of the visceral pleura of left lower basal segment was observed and the anomalous arterial pressure was 84 mmHg, as high as systemic arterial pressure, during the procedure. The histopathological examination revealed normal alveolar structure, and sclerosis and hypertrophy of pulmonary arteries of the lesion (Heath-Edwards V, which means irreversible vascular changes due to pulmonary hypertension). The patient had an uneventful postoperative course and was discharged on postoperative day 8. The VATS procedure is a more useful and less invasive method for cases of systemic arterial supply to the basal segment of the left lower lung than an open thoracotomy.     

Effect of isoflurane on gas exchange and systemic and pulmonary hemodynamics in man during single lung ventilation]

OBJECTIVE. We studied the effect of 1.5% isoflurane end expiratory fraction on arterial oxygenation and on systemic and pulmonary hemodynamics during nonsurgical single lung ventilation. MATERIAL AND METHODS. The study includes 6 patients undergoing surgical thoracotomy. In all cases a double lumen endotracheal tube was inserted and pulmonary ventilation was performed with a FiO2 = 1. Patients were placed on lateral decubitus position. The following variables were measured: mean arterial pressure (MAP), mean pulmonary artery pressure (MPAP), central venous pressure (CVP), capillary pulmonary pressure (CPP), cardiac output (CO), and Qs/Qt. Measurements were taken at three different situations. The first was done under bilateral pulmonary ventilation and intravenous anesthesia with thiopental, fentanyl, and diazepam. The nondependent lung was collapsed by means of a selective ventilation of the dependent lung, and the second series of measurements was done 20 min after intravenous anesthesia. The third block of data was obtained after 15 min of respiratory ventilation with 1.5% isoflurane. RESULTS. Single lung ventilation induced a significant decrease of Pa O2 (379 +/- 96 mmHg vs 208 +/- 93 mmHg) and a significant increase in Qs/Qt (20 +/- 8% vs 30 +/- 10%). However, during isoflurane ventilation there were no significant changes in PaO2 (208 +/- 93 mmHg vs 204 +/- 94 mmHg) nor in Qs/Qt (30 +/- 10 vs 28 +/- 8). Isoflurane elicited a significant decrease of the CO, whereas MPAP, RVS, and PvO2 did not show significant variations. CONCLUSIONS. We conclude that 1.5% isoflurane end expiratory concentrations did not significantly affect pulmonary oxygenation during single lung ventilation.     

The Effects of Intrathoracic Pressure During Continuous Two‐Lung Ventilation for Thoracoscopy on the Cardiorespiratory Parameters in Sevoflurane Anaesthetized Dogs

The cardiopulmonary effects of different levels of carbon dioxide insufflation (3, 5 and 2 mmHg) under two‐lung ventilation were studied in six sevoflurane (1.5 minimum alveolar concentration; MAC) anaesthetized dogs during left‐sided thoracoscopy. An arterial catheter, Swan–Ganz catheter and multianaesthetic gas analyser were used to monitor the cardiopulmonary parameters during the experiment. Baseline data were obtained before intrathoracic pressure elevation and the measurements were repeated at intervals after left lung collapse induced by insufflation with carbon dioxide gas. The intrapleural pressure levels used were 3, 5 and 2 mmHg. Arterial blood pressures, cardiac index, stroke index, left and right ventricular stroke work index, arterial haemoglobin saturation, arterial oxygen tension and systemic vascular resistance decreased significantly during hemithorax insufflation, whereas heart rate, right atrial pressure, mean, systolic and diastolic pulmonary arterial pressure, pulmonary capillary wedge pressure, pulmonary vascular resistance and arterial carbon dioxide tension significantly increased during intrapleural pressure elevation. Although carbon dioxide insufflation into the left hemithorax with an intrapleural pressure of 2–5 mmHg compromises cardiac functioning in 1.5 MAC sevoflurane anaesthetized dogs, it can be an efficacious adjunct for thoracoscopic procedures. Intrathoracic view was satisfactory with an intrapleural pressure of 2 mmHg. Therefore, the intrathoracic pressure rise during thoracoscopy with two‐lung ventilation should be kept as low as possible. Additional insufflation periods should be avoided, since a more rapid and more severe cardiopulmonary depression can occur.     

A new model for assessment of lung preservation

No completely satisfactory experimental model exists to compare different techniques of preservation currently used in the distant procurement of a lung allograft. A canine model of left lung transplantation is described in which an inflatable cuff is placed around each pulmonary artery. Each cuff is connected to a subcutaneous reservoir, which allows alternate occlusion of either pulmonary artery. Functional assessment of lung function is made during ventilation of both lungs and after a 10-minute period of perfusion to the native lung alone and then to the transplanted lung alone. Systemic and pulmonary artery pressures are recorded continuously, and measurement of arterial blood gases and oxygen uptake are made immediately after the operation and again at 3 days. The animal is then put to death and the lungs are excised and weighed. Five dogs underwent transplantation of the donor lung immediately after excision (mean ischemic time = 55 +/- 7 minutes). Similar values for oxygen tension and oxygen uptake were obtained postoperatively for the right lung (oxygen tension = 420 mm Hg, oxygen uptake = 101 ml/min) and the left lung (oxygen tension = 368 mm Hg, oxygen uptake = 108 ml/min). However, carbon dioxide tension was elevated (right lung = 41 mm Hg, left lung = 52 mm Hg). Mean pulmonary artery pressure increased during allograft perfusion (right lung = 14 mm Hg, left lung = 24 mm Hg), although systemic blood pressure was unchanged. Similar results were observed at 3 days. The mean weight of the native lung was 101 +/- 2 gm and that of the transplanted lung, 128 +/- 6 gm. This model achieves consistent survival and allows serial observations of the functional adequacy of an allograft compared with a normal contralateral lung.     

Inhalation administration of nitric oxide during selective pulmonary ventilation decreases the intrapulmonary shunt]

OBJECTIVE: To assess the effects of inhaled nitric oxide (NO) on oxygenation and hemodynamics in patients undergoing lung resection surgery during one-lung ventilation (OPV). PATIENTS AND METHODS: Prospective study of 16 patients aged 62 +/- 10 years scheduled for chest surgery under combined general and epidural anesthesia. During ventilation of only one lung, NO was administered for 15 minutes. Arterial blood and mixed venous blood samples were taken for analysis of blood gases and the calculation of intrapulmonary shunt. Pulmonary and systemic hemodynamic variables were also recorded using a Swan-Ganz catheter at three times: baseline (ventilation of both lungs), OLV, and with OLV plus NO (OLV NO). RESULTS: The most relevant data consisted of a significant decrease in shunt after start of NO inhalation in comparison with the level during OLV (31.1 +/- 0.5% versus 36 +/- 0.6%; p < 0.05). Arterial oxygen pressure decreased significantly during OLV and increased after start of NO (118.9 +/- 53.6 versus 155.4 +/- 78.5 mmHg; p < 0.05). Mean pulmonary artery pressure, pulmonary and systemic vascular resistances, and cardiac index did not change with inhalation of NO. CONCLUSIONS: Inhalational administration of NO during OLV significantly improves arterial oxygenation and decreases intrapulmonary shunt during OLV, without causing hemodynamic or systemic effects.     

Long-term fate of lung autografts charged with providing total pulmonary function. I. Light and electron microscopic studies.

Two groups of dogs underwent light and electron microscopic examination of both lungs up to five years after left lung autotransplantation. In one group of four dogs that had undergone ligation of the right pulmonary artery at the time of left lung autotransplantation, no generalized or consistent lesions were present in the transplant except for slight distension of net capillaries and slight capillary basement membrane thickening. Aside from theseminor changes which were probably of no functional significance, most areas of lung examined up to five years after transplantation were normal. In the second group of four dogs that did not have contralateral pulmonary artery ligation at the time of left lung autotransplantation, no consistent abnormality was present in either the transplanted left or nontransplanted right lung. In three animals in this group, widespread normal areas were present bilaterally up to five years after transplantation. One animal in this group had focal changes consistent with chronic pulmonary disease in both of its lungs. Thus, transplanted lungs do not necessarily develop significant late pathologic lesions.     

Oxygen Attenuates Atelectasis-induced Injury in the In Vivo Rat Lung

Background: Atelectasis results in impaired compliance and gas exchange and, in extreme cases, increased microvascular permeability, pulmonary hypertension, and right ventricular dysfunction. It is not known whether such atelectasis-induced lung injury is due to the direct mechanical effects of lung volume reduction and alveolar collapse or due to the associated regional lung hypoxia. The authors hypothesized that addition of supplemental oxygen to an atelectasis-prone ventilation strategy would attenuate the pulmonary vascular effects and reduce the local levels of vasoconstrictor eicosanoids.

Methods: In series 1, anesthetized, atelectasis-prone mechanically ventilated rats were randomly assigned to one of six groups based on the inspired oxygen concentration and ventilated without recruitment. Series 2 was performed to determine the cardiac and pulmonary vascular effects of 21% versus 100% inspired oxygen. In series 3, computed tomography scans were performed after ventilation with a recruitment strategy (21% O2) or no recruitment strategy (21% O2 or 100% O2). In series 4, functional residual capacity was measured in animals where the gas was 21% or 100% O2.

Results: The partial pressure of arterial oxygen increased with increasing inspired oxygen, but the alveolar-arterial oxygenation gradient was also greater with higher inspired oxygen. Ventilation with 21% O2 (but not with 100% O2) was associated with progressive pulmonary vascular impedance and increased pulmonary vascular permeability. Prostaglandin F2[alpha] was increased by mechanical ventilation, especially without supplemental oxygen. Computed tomography scans demonstrated no atelectasis in recruited lungs, and atelectasis in nonrecruited lungs that was greater with supplemental oxygen. Increased atelectasis with 100% O2 (vs. 21% O2) was demonstrated by measurement of functional residual capacity.     

Lung retrieval from non-heart beating cadavers with the use of a rat lung transplant model.

BACKGROUND: Lungs retrieved from cadavers after death and circulatory arrest may alleviate the critical shortage of lungs for transplant. We report a rat lung transplantation model that allows serial measurement of arterial blood gases after left single lung transplantation from non-heart beating donors. METHODS: Twelve Sprague-Dawley rats underwent left lung transplantation with a vascular cuff technique. Donor rats were anesthetized with intraperitoneal injection of pentobarbital, heparinized, intubated via tracheotomy, and then killed with pentobarbital. Lungs were retrieved immediately or after 2 hours of oxygen ventilation after death (tidal volume 1 mL/100 g, rate 40/min FIO2 = 1.0, positive end-expiratory pressure 5 cm H2O). Recipient rats were anesthetized, intubated, and ventilated. The carotid artery and jugular vein were cannulated for arterial blood gases and infusion of Ringer's lactate (4 mL/h). Anesthesia was maintained with halothane 0.2%, and recipient arterial blood gases were measured at 4 and 6 hours after lung transplantation after snaring the right pulmonary artery for 5 minutes. Animals were put to death 6 hours after lung transplantation, and portions of transplanted lungs were frozen in liquid nitrogen and assayed for wet/dry ratio, myeloperoxidase as a measure of neutrophil infiltration, and conjugated dienes as a measure of free radical-mediated lipid peroxidation. RESULTS: Arterial PO2 and wet/dry ratio were not significantly different in recipients of non-heart beating donor lungs retrieved immediately after death or after 2 hours of oxygen ventilation. Significant neutrophil infiltration was observed in recipients of non-heart beating donor lungs retrieved 2 hours after death from oxygen-ventilated donors. CONCLUSIONS: Strategies to ameliorate reperfusion injury may allow for successful lung transplantation from non-heart beating donors.