Graft damage after a single lung transplantation for pulmonary hypertension in a rat model

The hemodynamic effect and degree of damage in grafts of single lung transplants for pulmonary hypertension were studied in rats with monocrotaline-induced pulmonary hypertension. Inbred male Lewis rats (weight 200–230 g) were divided into two groups. Group 1 (control group,n = 16) underwent isogenic left lung transplantation, while group 2 (n = 15) received an intravenous administration of monocrotaline (80 mg/kg i.v.) and underwent isogenic left single lung transplantation 3 weeks later. Hemodynamic evaluations were performed prior to transplantation, at 1h postoperatively, and on days 3 and 7 after transplantation. Mean pulmonary arterial pressure (mPAP) rapidly declined after transplantation in group 2, from 39.3 ± 8.7 mmHg to 18.5 ±3.0 mmHg 1h after transplantation, and remained stable on day 7 after tranaplantation. No significant difference in the mPAP between the two groups was observed after tranaplantation. The extravascular lung water volume (ELWV: dry/wet ratio) in the right lung of group 2 significantly increased on day 3 (0.86 ± 0.02) (P < 0.01), and subsequently decreased to control levels on day 7 (0.83 ± 0.02). There was no significant difference in the ELWV in the grafted lungs between the two groups (0.84 ± 0.03 vs 0.86 ± 0.04), but there was tendency toward an increase in ELWV in group 2 on days 3 and 7. These data thus demonstrated that a hemodynamic improvement was obtained by single lung transplantation; however the degree of graft damage was remarkable in the pulmonary hypertension group.     

Single lung transplantation in rats with chemically induced pulmonary hypertension.

Physiologic effects of single lung transplantation on pulmonary hypertension were studied in rats with monocrotaline-induced pulmonary hypertension. Inbred rats treated with monocrotaline (40 mg/kg) received a left lung isograft from a normal donor 2 weeks later, when pulmonary hypertension became significant (transplant group; n = 6). These rats and control rats treated with monocrotaline (mediated control group; n = 11) or vehicle alone (normal control group; n = 9) were followed up weekly by metabolic treadmill testing for exercise tolerance and oxygen consumption up to 6 weeks after monocrotaline (4 weeks after transplantation), when all rats underwent hemodynamic and histologic examinations. Whereas maximal oxygen consumption and exercise tolerance consistently deteriorated in the medicated control group of rats, indices in the transplant group stopped deteriorating 2 weeks after lung transplantation and remained at levels similar to those of normal control rats. Severe pulmonary hypertension (68 +/- 19 mm Hg) and right ventricular hypertrophy (right ventricular/left ventricular weight ratio, 0.95 +/- 0.19) were confirmed in medicated control rats in contrast to transplant animals, in which these two indices remained at normal control levels. Whereas left-to-right lung perfusion ratio was constant among rats not receiving transplants (0.69 +/- 0.16), it was significantly elevated (2.27 +/- 0.65; p less than 0.001) in those receiving transplants, suggesting preferential flow through the lung isograft. The results suggest that, in the early phase of pulmonary hypertension, single lung transplantation shifts pulmonary perfusion to the grafted lung, avoiding right ventricular pressure overload and thereby preserving exercise tolerance at a nearly normal level in rats with monocrotaline-induced pulmonary hypertension.     

Single lung transplantation in rats with fatal pulmonary hypertension.

Effects of single lung transplantation on fatal pulmonary hypertension were evaluated in rats receiving a lethal dose of monocrotaline. Inbred rats treated with monocrotaline (80 mg/kg) received a left lung isograft at 4 weeks (n = 9) and at 6 weeks (n = 6), when moderate and severe pulmonary hypertension, respectively, had developed. Medicated (n = 12) and nonmedicated rats (n = 12) served as control animals. Each rat was tested weekly with treadmill for exercise tolerance and oxygen consumption during a 10-week period after medication and after they were killed. Medicated control rats lost exercise tolerance and highest oxygen consumption per unit time consistently to the range of resting value (or 45% of nonmedicated control rats), and all died from severe pulmonary vascular occlusive disease with right ventricular hypertrophy before 10 weeks (right ventricular/left ventricular weight ratio of 1.16). All rats receiving a left lung isograft at 4 weeks survived and regained highest oxygen consumption per unit time (87% of nonmedicated control rats), with the lung transplant receiving 65% (nonmedicated control rats, 39%) of cardiac output and milder right ventricular hypertrophy (right ventricular/left ventricular weight ratio of 0.46). Except for one, all rats that received a left lung isograft at 6 weeks tolerated single lung transplantation, but they died soon after reperfusion because of pulmonary edema in the graft that received 58% of cardiac output with right ventricular/left ventricular weight ratio of 0.79. Results of single lung transplantation in rats were dependent on severity of pulmonary hypertension. In rats with moderate pulmonary hypertension, single lung transplantation was successful in reversing exercise intolerance and right ventricular hypertrophy. Single lung transplantation was unsuccessful when pulmonary hypertension was severe in the rat model because increased flow toward the lung transplant resulted in graft pulmonary edema.     

Toxicity of cationic liposome-DNA complex in lung isografts

BACKGROUND: Cationic lipids have been successfully employed as vectors for gene transfer in lung grafts, yet those lipid vectors have potential toxicity. Furthermore, the optimal concentration of cationic lipids for gene transfection to lung grafts has not been determined. We evaluated liposome concentration/toxicity relationships in an in vivo rat lung transplantation model. METHODS: Left lungs were harvested and infused via the pulmonary artery with chloramphenicol acetyl-transferase (CAT)-DNA/lipid 67 (cationic lipid)/dioleoylphosphatidylethanolamine complex (4:1:2 in a final concentration ratio). Donor lungs were allocated into six groups according to lipid 67 concentration: group 1, 0 microM (control); group 2, 10 microM; group 3, 50 microM; group 4, 100 microM; group 5, 250 microM; group 6, 500 microM. Forty-eight hours after orthotopic transplantation, the recipient contralateral right main pulmonary artery and bronchus were ligated. The graft was ventilated with 100% oxygen for 5 min. Arterial blood gas analysis (PaO2, PaCO2), peak airway pressure (PAP), and CAT activity of the grafts were measured. RESULTS: Recipient survival, and PaO2, PAP, and CAT levels correlated with the lipid-DNA complex concentration. The grafts in groups 4-6 were more injured as evidenced by decreased PaO2 and increased PAP levels in comparison to the control group. CAT level was significantly lower in group 2 than in groups 3-6. CONCLUSIONS: The pulmonary toxicity of cationic lipid is dose-dependent. The balance between lung graft function and transgene expression is optimal at a lipid 67 concentration of 50 microM.     

Early Hemodynamic Injury During Donor Brain Death Determines the Severity of Primary Graft Dysfunction after Lung Transplantation

Sympathetic discharge and hypertensive crisis often accompany brain death, causing neurogenic pulmonary edema. Progressive systemic inflammatory response develops, which can injure the lung further. We investigated whether (a) early hemodynamic injury during donor brain death increases reperfusion injury after lung transplantation and (b) delaying lung recovery would augment reperfusion injury further, because of the progressive systemic inflammatory response in the donor. Brain death was induced by intracranial balloon inflation in rats, with or without alpha-adrenergic blockade pretreatment to prevent the hypertensive crisis. Another group of rats had a sham procedure. Lungs were retrieved 15 min after brain death or sham procedure and reperfused using recipient rats. In a fourth group, brain death was induced and the lungs were retrieved 5 h after brain death and reperfused. Postreperfusion, lungs retrieved early from untreated brain-dead donors developed more severe reperfusion injury, as assessed by functional parameters and inflammatory markers, than those from sham or alpha-blockade-treated donors. Lungs retrieved late from brain-dead donors had similar inflammatory markers after reperfusion to those retrieved early, but significantly lower pulmonary vascular resistance. Early hemodynamic damage during donor brain death increases reperfusion injury after lung transplantation. Delaying retrieval may allow the lung to recover from the hemodynamic injury.     

Immunological unresponsiveness to hepatic allografts in rats. Immunological reactivities of the recipient to donor antigens

Wistar (RT1bv1) rats transplanted orthotopically with ACI (RT1a) livers survive indefinitely without any immunosuppression, while heterotopic heart grafts or skin grafts are rejected acutely in this combination. Levels of alkaline phosphatase after liver allografting remain significantly higher than those found in controls receiving syngeneic grafts. We studied changes in immune responsiveness in rats receiving liver grafts. Local graft-versus-host reactivity was present at all times assayed. Delayed type hypersensitivity reactions were already positive 2 weeks after liver transplantation and increased in strength. Liver graft-bearing rats were subsequently grafted with donor or third-party skin. Third-party skin grafts survived significantly longer on liver-grafted rats than on untreated controls when grafted within the first week after grafting. Donor-type skin grafts survived longer than controls when grafted within the first 4 weeks after liver grafting, although the skin grafts were eventually rejected. Donor-type skin grafted more than 8 weeks after liver grafting was rejected acutely. In an adoptive transfer assay, ACI hearts survived significantly longer in Wistar rats given serum from Wistar donors 2-4 weeks after ACI liver grafts than in untreated controls. On the other hand, spleen cells obtained at any period after liver grafting were not capable of prolonging cardiac allograft survival after transfer to syngeneic recipients. Thus cellular responses to ACI antigen are not changed during the life-span of liver-grafted animals. Evidence suggests that a serum "enhancing" factor protects the donor liver from rejection in the initial period after liver transplantation. The long-term acceptance of liver grafts is discussed.     

Effectiveness of prostaglandin E1 on pulmonary hypertension and right cardiac function induced by single-lung ventilation and hypoventilation.

It is known that prostaglandin E1 (PGE1) is a potent vasodilator and improves red cell deformability. Single lung-ventilation sometimes occurs under lung transplantation, lung cancer surgery and traumatic pneumonectomy, and may result in increased pulmonary resistance, right heart failure and severe hypoxemia. The present experimental study was undertaken to examine the effects of PGE1 on these states induced by single-lung ventilation and hypoventilation. Fourteen pigs weighing 32-33 kg were anesthetized, intubated and ventilated using a respirator and then randomly assigned to two groups, the control group and the PGE1 treated group, 7 pigs each. After median sternotomy to induce severe hypoxemia hypoventilation was induced and then the right hilus pulmonis was cross clamped. Mean blood pressure, mean pulmonary arterial pressure (PAP), pulmonary vessel resistance (PVR), right ventricular stroke work (RVSW) and arterial blood gases (PaO2 and SatO2) were measured at baseline, in the hypoventilation state, and 15 min, 1 hour, and 2 hours after the right hilus pulmonis clamping with hypoventilation. PGE1 (250 microg/20 ml saline) was administered via the central vein starting 15 min after right hilus cross clamping for 1 hour and 45 min in the PGE1 group. PGE1 significantly reduced PAP and PVR, normalized RVSW, and improved PaO2. PGE1 may be useful for the condition of increased pulmonary hypertension during single-lung ventilation and hypoventilation.     

缓激肽β2受体拮抗剂在大鼠肺移植缺血再灌注损伤中的保护作用

目的 探讨缓激肽β2受体拮抗剂（HOE-140）对大鼠移植肺功能的影响以及作用.方法 将纯系SD大鼠随机分为3组,即实验组1、实验组2、对照组.对照组的供肺用低钾右旋糖苷液（LPD液）灌洗,并保存18h,然后行左肺移植,于移植后1d测定对照组的气道峰压（PAP）、静脉血氧分压（PO2）、移植肺湿干重比（W/D）、髓过氧化物酶（MPO）活性.实验组1以及实验组2（加HOE-140干预）的供肺用含特异性不可逆DPPⅣ酶抑制剂（AB192）的LPD液灌洗,并保存18h,然后行左肺移植,分别于移植后1d测定受者的各项肺功能指标,并取相同受体肺部组织做病理学检查. 结果 与对照组比较,各实验组的PAP值降低（P＜0.05）,PO2值升高（P＜0.05）,W/D值降低（P＜0.05）,MPO活性降低（P＜0.05）,差异有统计学意义,病理学结果显示实验组2（HOE-140组）均优于对照组及实验组1.结论 缓激肽β2 受体拮抗剂HOE-140能有效降低肺移植肺缺血再灌注损伤,从而改善移植肺功能.     

体外膜肺氧合在肺移植麻醉中的应用

目的 总结肺移植麻醉中体外膜肺氧合(extracorporeal memberane oxygenation,ECMO)辅助的适应证及术中运用ECMO支持的经验.方法 58例终末期肺病患者在麻醉诱导气管插管后,常规给予非术侧单肺通气30 min,监测肺动脉压(PAP)、氧分压(PaO2)、二氧化碳分压(PaCO2)、肺泡气·动脉氧分压差(PA-aO2)和呼吸力学等指标,根据监测指标调节机械通气参数,必要时行手控通气.17例患者分别因肺动脉高压、低氧血症和高碳酸血症而给予ECMO辅助,转流期间维持激活凝血时间(ACT)160秒～200秒,流量控制在1.8 L·m-2·min-1～2.5 L·m-2·min-1.结果 所有患者ECMO转流后PAP及PaCO:下降明显,氧合改善.麻醉伞程生命体征平稳.手术经过顺利.结论 ECMO是肺移植术中肺辅助的有效手段,可提高肺移植手术的麻醉成功率.原发性肺动脉高压、肺纤维化合并肺动脉高压、严重的低氧血症和高碳酸血症是肺移植术中ECMO转流的适应证.     

Significance of biochemical markers in early detection of canine lung allograft rejection

To evaluate the significance of bronchoalveolar lavage fluid, levels of tumor necrosis factor-alpha (TNF), gamma-interferon, interleukin 2, and soluble IL-2 receptor in early detection of canine lung allograft rejection, bronchoalveolar lavages were performed serially in mongrel dogs before and after single lung transplantation. The dogs were divided into three groups. Group 1 (control group) consisted of one in which neither donor nor recipient dogs were treated with cyclosporine. In group 2 (CsA-pretreated group) only donors were treated with CsA orally at a single dose of 20 mg/kg/day for 3 days prior to single lung transplantation. In group 3 only recipients were treated with CsA orally at a single dose of 20 mg/kg/day for a short period of 9 days after single-lung transplantation. Marked elevation was found of TNF, IFN-gamma, IL-2, and IL-2R in BALF obtained from the grafted lungs in group 1 and group 2 dogs. The levels of these markers were significantly higher than those obtained from the normal, native lungs (P less than 0.05). Two of three recipients in group 2 had pneumonia in the native lungs on day 10 after single-lung transplantation. All markers except IFN-gamma in BALF obtained from the infected native lungs were also increased, but the titers were less than those obtained from the grafted lungs at the same time. There were significantly higher levels of TNF, IL-2, and IL-2R present in the BALF of grafted lungs of dogs in group 1 than group 2 (P less than 0.05). In group 3, BALF levels of these markers from the grafted lungs were not significantly different from those of the normal and native lungs during the period of CsA treatment after single-lung transplantation. On various days after discontinuation of CsA treatment, BALF levels of all markers began to rise. Abnormal levels of BALF markers obtained from the grafted lungs heralded the appearance of abnormalities detected by chest x-ray films. Our study suggests that serially measuring BALF levels of TNF, IFN-gamma, IL-2, and IL-2R may serve as a useful means in monitoring the immunologic status of canine lung allografts and in the early detection of lung allograft rejection. The role of BALF IFN-gamma in distinguishing lung allograft rejection from pulmonary infection needs further studies.     

Unilateral donor lung dysfunction does not preclude successful contralateral single lung transplantation.

Single lung transplantation remains limited by a severe shortage of suitable donor lungs. Potential lung donors are often deemed unsuitable because accepted criteria (both lungs clear on the chest roentgenogram, arterial oxygen tension greater than 300 mm Hg with an inspired oxygen fraction of 1.0, a positive end-expiratory pressure of 5 cm H2O, and no purulent secretions) do not distinguish between unilateral and bilateral pulmonary disease. Many adequate single lung grafts may be discarded as a result of contralateral aspiration or pulmonary trauma. We have recently used intraoperative unilateral ventilation and perfusion to assess single lung function in potential donors with contralateral lung disease. In the 11-month period ending October 1, 1990, we performed 18 single lung transplants. In four of these cases (22%), the donor chest roentgenogram or bronchoscopic examination demonstrated significant unilateral lung injury. Donor arterial oxygen tension, (inspired oxygen fraction 1.0; positive end-expiratory pressure 5 cm H2O) was below the accepted level in each case (246 +/- 47 mm Hg, mean +/- standard deviation). Through the sternotomy used for multiple organ harvest, the pulmonary artery to the injured lung was clamped. A double-lumen endotracheal tube or endobronchial balloon occlusion catheter was used to permit ventilation of the uninjured lung alone. A second measurement of arterial oxygen tension (inspired oxygen fraction 1.0; positive end-expiratory pressure 5 cm H2O) revealed excellent unilateral lung function in all four cases (499.5 +/- 43 mm Hg; p less than 0.0004). These single lung grafts (three right, one left) were transplanted uneventfully into four recipients (three with pulmonary fibrosis and one with primary pulmonary hypertension). Lung function early after transplantation was adequate in all patients. Two patients were extubated within 24 hours. There were two late deaths, one caused by rejection and Aspergillus infection and the other caused by cytomegalovirus 6 months after transplantation. Two patients are alive and doing well. We conclude that assessment of unilateral lung function in potential lung donors is indicated in selected cases, may be quickly and easily performed, and may significantly increase the availability of single lung grafts.     

Pulmonary flow-resistance relation in allografts ten days after single lung transplantation in dogs

In order to evaluate the applicability of single lung transplantation as a treatment of pulmonary hypertension, I investigated the relationships between the pulmonary flow and its resistance in allografts ten days after single lung transplantation in dogs. Fourteen dogs underwent single lung transplantation. All dogs received azathioprine (50 mg; given orally) and methylprednisolone sodium succinate (125 mg; given intravenously) every day after operation. Eight dogs survived up to ten days after operation. In the survived recipients and the five healthy dogs, pulmonary flow-resistance relations were investigated. Pulmonary flow was exactly regulated by the pump system, which drained from both cavae and returned to right atrium via azygos vein. The pulmonary artery of native lung or right lung was clamped prior to the measurement. Pulmonary vascular resistance was recorded with the increase of pulmonary flow at the range from 0.3 L/min. to 2.0 L/min. by 0.1 L/min. Lung water was measured by means of Wood's method. Radiographical and pathological examinations were appended. The five allografts received complete studies (successful group) were twice lung water of the healthy lungs (control group) (successful group; 95.6 +/- 16.7 g, control group; 47.8 +/- 7.5 g), and chest roentgenograms of successful group showed mild or moderate consolidation. The other allo-grafts (unsuccessful group), including ones died before investigations, were four times lung water of control group (unsuccessful group; 211.0 +/- 89.6 g), and the chest roentgenograms showed severe consolidation. But any difference was not found in any pulmonary flow between the pulmonary resistance in successful group and in control group. These results show that the allografts, which is under about twice lung water of normal lung, maintains enough pulmonary vascular function, and I concluded that single lung transplantation can be an effective treatment for pulmonary hypertension.     

门静脉和下腔静脉阻断与开放后门静脉高压犬肺动脉和肺组织超微结构改变

目的观察门静脉和下腔静脉阻断与开放后门静脉高压模型犬肺组织与肺动脉的超微结构改变。方法正常家犬18只,随机均分为阴性对照组（仅用于取肺组织和肺动脉标本）、对照组和门静脉高压模型组（采用部分结扎门静脉的方法建立患门静脉高压症犬模型并饲养12周）,进行门静脉、肝上和肝下下腔静脉阻断与开放实验。在术毕后取右下肺动脉和肺组织,应用透射电镜观察其超微结构。结果门静脉和下腔静脉阻断与开放后门静脉高压犬肺组织内皮细胞、Ⅰ型肺泡上皮细胞和Ⅱ型肺泡上皮均出现明显的病理性改变;肺泡隔纤维化明显,胶原纤维增生;肺毛细血管内血栓形成,基膜明显增厚;肺动脉血管内皮细胞损伤明显,部分脱落;肺动脉内皮细胞与中膜间隙明显增宽,内皮下水肿,内皮下胶原纤维增多。结论伴门静脉高压的肝移植犬肺组织和肺动脉的超微结构有明显改变,这可能是肝移植受者围术期出现急性肺高压和急性肺损伤的超微病理学基础之一。     

Sildenafil for pulmonary hypertension after heart transplantation

Patients with increased pulmonary vascular resistance may experience acute pulmonary hypertension after heart transplantation. Pulmonary vasodilator drugs usually are delivered by the intravenous or the endotracheal route during acute pulmonary hypertensive crisis. Oral pulmonary vasodilators have a potential role in less acutely ill patients with increased pulmonary artery pressure after heart transplantation. We describe the 1st successful post-operative use of oral sildenafil for pulmonary vasodilation in a patient after heart transplantation.     

Secondary pulmonary hypertension does not adversely affect outcome after single lung transplantation

OBJECTIVE: Primary and secondary pulmonary hypertension have been associated with poor outcomes after single lung transplantation. Some groups advocate double lung transplantation and the routine use of cardiopulmonary bypass during transplantation in this population. However, the optimal procedure for these patients remains controversial. The goal of our study was to determine the safety of single lung transplantation without cardiopulmonary bypass in patients with secondary pulmonary hypertension. METHODS: We retrospectively reviewed 76 consecutive patients with pulmonary parenchymal disease who underwent single lung transplantation from 1992 to 1998. Recipients were stratified according to preoperative mean pulmonary artery pressure. Secondary pulmonary hypertension was defined as parenchymal lung disease with a preoperative mean pulmonary artery pressure of 30 mm Hg or more. Patients with primary pulmonary hypertension or Eisenmenger's syndrome were excluded from analysis. RESULTS: Eighteen of 76 patients had secondary pulmonary hypertension. No patient with secondary pulmonary hypertension required cardiopulmonary bypass, whereas 1 patient without pulmonary hypertension required bypass. After the operation, no significant differences were seen in lung injury as measured by chest radiograph score and PaO(2)/FIO(2) ratio, the requirement for inhaled nitric oxide, the length of mechanical ventilation, the intensive care unit or hospital length of stay, and 30-day survival. There were no differences in the forced expiratory volume in 1 second or 6-minute walk at 1 year, or the incidence of rejection, infection, or bronchiolitis obliterans syndrome greater than grade 2. Survival at 1, 2, and 4 years after transplantation was 86%, 79%, and 65%, respectively, in the low pulmonary artery pressure group and 81%, 81%, and 61%, respectively, in the group with secondary pulmonary hypertension (P >.2). CONCLUSION: We found that patients with pulmonary parenchymal disease and concomitant secondary pulmonary hypertension had successful outcomes as measured by early and late allograft function and appear to have acceptable long-term survival after single lung transplantation. Our results do not support the routine use of cardiopulmonary bypass or double lung transplantation for patients with this disorder.     

体外循环下单肺移植一例的体会与教训

目的 总结体外循环下单肺移植的经验和教训。方法 在体外循环下给１例终末期双肺纤维化患者施行左侧单肺移植术,供肺采用Ｅｕｒｏ－Ｃｏｌｌｉｎｓ液灌洗,管道吻合时间为５５ｍｉｎ。术后联合应用环孢素Ａ、激素及硫唑嘌呤进行免疫抑制治疗。结果 移植肺术后即刻发挥功能,术后第１、２ｄ因出血致心脏压塞,２次剖胸止血,第３、７ｄ发生急性排斥反应,第９ｄ死于急性排斥反应。结论 肺移植术后应注重出血及急性排斥反应的监测     

Hyperinflation during lung preservation and increased reperfusion injury

BACKGROUND: Reperfusion injury after lung transplantation remains a perplexing and unpredictable problem. Most surgeons preserve the lung inflated, but the amount of inflation that should be used is not well documented. Therefore, we studied the effect of high inflation during organ preservation on lung function during reperfusion. Our hypothesis is that donor lung hyperinflation during storage contributes to early allograft dysfunction during reperfusion. METHODS: To test our hypothesis we used an isolated, blood-perfused, ventilated rabbit lung model. Group I lungs (control) underwent immediate reperfusion after harvest. Group II lungs (low-inflation, maintained at 6 mmHg airway pressure) and group III lungs (high-inflation, maintained at 20 mmHg airway pressure) were stored for 4 h in 4 degrees C Euro-Collins solution after harvest. All lungs were then reperfused with whole blood for 1 h, and measurements of arterial oxygenation (PO2, mmHg), pulmonary artery pressure (PAP, mmHg), peak inspiratory pressure (PIP, cm H2O), and wet-to-dry weight ratio (WTD) were obtained. RESULTS: Throughout the 1 h reperfusion period group III lungs had significantly lower oxygenation compared to groups I and II. In addition, throughout reperfusion, group III lungs showed significantly higher PAP and PIP compared to group II. WTD did not differ significantly between groups, however, there was a trend toward increased edema in group III. CONCLUSIONS: These results indicate that high inflation during cold storage results in acute pulmonary dysfunction. Careful monitoring of airway inflation pressure during storage, especially to prevent hyperinflation, should be maintained in the current practice for lung transplantation.     

Inhaled nitric oxide does not alter pulmonary or cardiac effects of fat embolism in dogs after cemented arthroplasty

PURPOSE: We examined the effect of inhaled nitric oxide (NO) on the acute pulmonary hypertension and right ventricular (RV) dilation after fat embolism. METHODS: A bilateral cemented arthroplasty (BCA), created fat embolism in 20 dogs. In Part A, 12 dogs were randomized to an NO group (n=6, inhaled NO 40 ppm before BCA and throughout the study) or a control group (n=6). In Part B, a third group of dogs (n=8) were given NO 20-40 ppm 2-3 min after BCA when pulmonary artery pressure (PAP) increased. Transesophageal echocardiography (TEE) and invasive hemodynamic monitoring evaluated the hemodynamic response to BCA. Postmortem, quantitative morphometry was used to estimate the number of fat emboli and diameter of lung vessel occluded by fat. RESULTS: Part A: The increase in PAP in the NO group (16 +/- 1 to 34 +/- 9 mmHg) within three minutes of BCA was not different from that in the control group (14 +/- 4 to 35 +/- 9 mmHg). Within three minutes of BCA, TEE demonstrated RV dilation in all groups (P < 0.05) but there was no difference in the change in RV area in the NO and control groups. When NO was given after BCA, no difference in PAP or RV dilation was noted from that in the control group. There were no differences, at post mortem, between the groups in the diameter of lung vessel occluded by fat CONCLUSION: Whether given before the embolic insult or two to three minutes after the onset of pulmonary hypertension, inhaled NO did not attenuate the acute pulmonary hypertension or RV dilation after cemented arthroplasty.     

65例肺移植手术的临床分析

目的探讨肺移植术中供者肺的获取和术中可能遇到的特殊情况处理,以提高肺移植手术的成功率。方法65例重症呼吸衰竭,其中长期依赖呼吸机9例;病种包括肺气肿23例,肺纤维化24例,矽肺5例,肺结核2例,肺淋巴管平滑肌瘤病1例,室间隔缺损合并艾森曼格综合征4例,支气管肺囊肿4例,弥漫性细支气管炎1例和原发性肺动脉高压1例。行单肺移植术47例,双肺移植术18例。回顾性总结肺移植手术的临床经验,特别是手术中遇到的特殊情况的处理经验。结果64例供肺均获取成功。肺移植术后住院死亡11例（16.9%）,其中原发性移植肺失功3例,严重感染6例,急性排斥反应1例,肺梗死1例。术后发生并发症9例,包括术后渗血多二次开胸止血3例,肺动脉狭窄二次手术重新吻合纠正1例,支气管吻合口狭窄3例;肺梗死2例,其中1例肺叶梗死患者二次开胸手术切除。随访54例,随访时间1.0~5.6年,1年生存率达72.3%（47/65）,大部分患者生活质量良好,肺功能有极大的改善。结论提高供肺获取和受者肺移植手术技术有助于降低肺移植手术后的早期死亡率。