PubMed Health⌕ Search

Biomedical subjects

D E Van Raemdonck

Publications and source records attributed to D E Van Raemdonck.

At least 19 recordsLinked to original sources

Macrolides inhibit IL17-induced IL8 and 8-isoprostane release from human airway smooth muscle cells.

Lung transplantation is hampered by bronchiolitis obliterans syndrome (BOS), although recently azithromycin treatment has a published response rate of about 42% in patients with established BOS. We linked this improvement to a reduction in airway neutrophilia and IL8. In the present study, we further investigated the intracellular mechanisms of azithromycin, looking at the possible involvement of mitogen-activated-protein kinases (MAPK) and oxidative stress. Simultaneously, currently used immunosuppressive agents were investigated. Human primary airway smooth muscle cells were stimulated with IL17 and incubated with increasing concentrations of steroids, immunosuppressive agents (tacrolimus, cyclosporine and rapamycin) or macrolides (erythromycin and azithromycin). We measured supernatant IL8 protein, 8-isoprostane and cell lysate MAPK. IL17-induced IL8 production was decreased by both erythromycin and azithromycin. In nonstimulated condition, IL8 production only increased at the highest dose of azithromycin. Dexamethasone failed to attenuate IL8 production, whereas immunosuppressive agents significantly increased IL8 production in both IL17-stimulated and nonstimulated conditions. 8-isoprostane production and MAPK activation proved to be decreased by the macrolides. We conclude that macrolides (but not steroids/immunosuppressive agents) inhibit IL17-induced IL8 production in human primary airway smooth muscle cells via a reduction in MAPK activation and 8-isoprostane production. In BOS patients, these phenomena may explain the anti-inflammatory effects of azithromycin.

Azithromycin↗

The pH of exhaled breath condensate of patients with allograft rejection after lung transplantation.

Endogenous airway acidification, as assessed by the condensate pH, has been implicated in the pathophysiology of inflammatory airway diseases such as cystic fibrosis and asthma. The aim of this study was to investigate the pH of condensate in patients after lung transplantation (LTX). From the cohort of transplanted patients at our center, 83 patients (9 heart-lung transplantation, 48 double-lung transplantation, 26 single-lung transplantation) were recruited and analyzed in a cross-sectional manner: 26 patients were diagnosed with chronic rejection or bronchiolitis obliterans syndrome (BOS), 7 patients were diagnosed with acute rejection (AR) while 50 patients had no evidence of rejection according to the International Society for Heart and Lung Transplantation criteria. The condensate pH was significantly reduced in patients with BOS and AR when compared to patients without rejection and control subjects (5.8 +/- 0.5 and 6.2 +/- 0.4 versus 6.6 +/- 0.4 and 6.5 +/- 0 .4, respectively; p < 0.05). Moreover, there was a significant correlation between condensate pH levels and the BOS grade (r =-0.62; p < 0.01), the FEV(1) (r = 0.39; p < 0.01) and the total cell and neutrophil count in bronchoalveolar lavage fluid (r =-0.39 and r =-0.56, respectively; p < 0.01). Airway acidification occurs in BOS and may directly or indirectly reflect airway inflammation in patients with allograft rejection after LTX. Measuring condensate pH might thus be a new tool for the evaluation of rejection in lung transplant patients.

Adult↗

The role of interleukin-17 during acute rejection after lung transplantation.

Acute rejection (AR) is an important complication that can occur after lung transplantation and constitutes a risk factor for bronchiolitis obliterans syndrome, which is characterised by a neutrophilic airway inflammation. The specific aim of this study was to investigate the role of interleukin (IL)-17, which promotes chemotaxis of neutrophils by inducing IL-8 production, in AR. Cell differentials, mRNA and protein levels were quantified in bronchoalveolar lavages (BALs) taken from patients at 28 and 90 days after lung transplantation. The patient's rejection status was assessed by transbronchial biopsy. An AR was found in nine out of the 26 patients examined, 28 days after transplantation. The number of BAL neutrophils and lymphocytes were increased in these patients. IL-17 mRNA and protein levels in the BAL were increased in patients with AR. Analysis of BAL obtained at day 90 after transplantation, demonstrated that the increase in IL-17 had disappeared, whereas the increase in neutrophils and lymphocytes persisted. These data showed that interleukin-17 is temporarily upregulated in bronchoalveolar lavage during acute rejection. The number of lymphocytes and neutrophils are increased in bronchoalveolar lavage during acute rejection and may persist up to 2 months after acute rejection. These findings suggest that interleukin-17 is important in the pathophysiology of acute lung rejection.

Acute Disease↗

Is it bronchiolitis obliterans syndrome or is it chronic rejection: a reappraisal?

Chronic rejection (obliterative bronchiolitis) is the single most important cause of chronic allograft dysfunction and late mortality after lung transplantation. As this condition is difficult to prove using biopsy specimens, a clinical term, bronchiolitis obliterans syndrome (BOS) has been in use for >10 yrs to describe the progressive decrease of pulmonary function. However, before diagnosing a patient as having BOS, based on a sustained and progressive decrease in forced expiratory volume in one second and/or forced mid-expiratory flow between 25-75% of forced vital capacity, different confounding factors have to be eliminated. Treatment of BOS mainly consists of an increase or a change in the immunosuppressive drug regimen, which may lead to more pronounced infectious complications. Recently, two new options have become available to treat patients with BOS, treatment of gastro-oesophageal reflux and azithromycin. In the present paper, the authors give an overview of the current data on these two modalities, which may lead to a restoration of the pulmonary function in some of the patients, illustrating once more the fact that bronchitis obliterans syndrome is not always a manifestation of chronic rejection.

Anti-Bacterial Agents↗

Practical approach to patients presenting with multiple synchronous suspect lung lesions: a reflection on the current TNM classification based on 54 cases with complete follow-up.

OBJECTIVES: To examine the survival after surgical treatment of patients presenting with two synchronous suspect lung lesions, and to reflect on the recent TNM classification, which has upgraded patients with two malignant lung lesions of the same histology into the T4 (both lesions in the same ipsilateral lobe) or M1 (different lobes or lungs) category. METHODS: Retrieval of all consecutive patients with a diagnosis of two synchronous suspect lung lesions in the prospective database of the Leuven Lung Cancer Group in the interval between 1990 and 1994. Analysis of characteristics and survival of all patients, who underwent surgical resection with intention to cure for both lesions. RESULTS: Forty-eight of 54 patients had surgical resection with curative intent. Thirty-five of these proved to have two malignant lesions, in 13 the second lesion was benign. The 5-year survival rate in the patients with two malignant lesions was 33% (95% CI: 17-49). The median survival time was 28 months. Although the number of patients in the subgroups was small, there were no obvious differences between patients with two lesions in the same or in different lobes, if a complete resection could be achieved. CONCLUSIONS: An aggressive surgical approach in carefully selected patients presenting with two suspect pulmonary lesions can be rewarding. Although some degree of upstaging is appropriate in patients with two malignant lung tumours of the same histology, their current stage IIIB or IV classification probably underestimates their prospects for long-term survival after radical resection.

Adult↗

Ischemic preconditioning enhances donor lung preservation in the rabbit.

OBJECTIVE: Ischemic preconditioning achieved by brief periods of ischemia followed by reperfusion before a prolonged period of ischemia, is well known to reduce myocardial damage. We investigated whether ischemic preconditioning of the lung could also attenuate ischemia-reperfusion injury following pulmonary preservation. METHODS: Transient ischemia of the right lung was achieved in rabbits (n = 4 in each group) by occluding the main bronchus and pulmonary artery, followed by reperfusion according to a protocol that differed between study groups: group 1 (control), 45 min ventilation; group 2, 30 min ventilation, 5 min ischemia and 10 min reperfusion; group 3, three periods of 5 min ischemia and 10 min reperfusion; group 4, five periods of 3 min ischemia and 6 min reperfusion. Donor lungs were then flushed with a crystalloid solution followed by inflated storage at 37 degrees C for 2 h. The function of the right lung was assessed during reperfusion for 2 h with homologous, diluted and deoxygenated blood in an isolated, pressure-limited, and room-air ventilated model. RESULTS: Significant differences (P < 0.0001) were observed between groups 1 and 2 vs. groups 3 and 4 in veno-arterial oxygen pressure gradient (29 +/- 6 and 24 +/- 6 mmHg vs. 124 +/- 24 and 132 +/- 14 mmHg, respectively), and in weight gain (88 +/- 13 and 98 +/- 13% vs. 44 +/- 9 and 29 +/- 3%, respectively) after 1 h of reperfusion, and in wet-to-dry weight ratio (15.5 +/- 1.5 and 14.3 +/- 0.4 vs. 10.1 +/- 1.6 and 9.0 +/- 0.8, respectively) at the end of reperfusion. No significant differences in any of these parameters were observed between group 1 vs. group 2 neither between group 3 vs. group 4. CONCLUSIONS: These data suggest: (1) That 15 min, but not 5 min of transient ischemia prior to pulmonary preservation can significantly reduce edema in the lung graft upon reperfusion, thus improving oxygenation capacity and (2) although not significant, this beneficial effect seems to be slightly better with more repetitive periods of transient ischemia. Further research is warranted to investigate whether ischemic preconditioning in the human organ donor may become a new strategy to protect lung tissue during a planned ischemic event as in pulmonary transplantation.

Animals↗

Alveolar expansion itself but not continuous oxygen supply enhances postmortem preservation of pulmonary grafts.

OBJECTIVE: If lungs could be retrieved for transplant after circulatory arrest, the shortage of donors might be significantly alleviated. Great controversy still exists concerning the optimal mode of preservation of pulmonary grafts in these non-heart-beating donors. METHODS: Graft function was measured in an isolated room air-ventilated rabbit lung model during reperfusion with homologous, diluted (Hb +/- 8.0 g/dl) and deoxygenated (PaO2 +/- 40 mmHg) blood up to 4 h. Five groups of cadavers (n = 4 in each group) were studied: In the control group, lungs were immediately reperfused. In the other groups, cadavers were left at room temperature for 4 h after death with lungs either deflated (group 1), inflated with room air (group 2), or ventilated with room air (group 3) or 100% nitrogen (group 4). RESULTS: After 1 h of reperfusion, significant differences were noted between group 1 and groups 2, 3, and 4 in peak airway pressure (27 +/- 5 cm H2O vs. 15 +/- 1 cm H2O, 17 +/- 2 cm H2O, and 16 +/- 1 cm H2O, respectively; P < 0.05), in weight gain (137 +/- 24 vs. 31 +/- 7, 30 +/- 3, and 30 +/- 2%, respectively; P < 0.05), and in veno-arterial oxygen pressure gradient (9 +/- 5 vs. 95 +/- 13, 96 +/- 7 and 96 +/- 4 mmHg, respectively; P < 0.05). Also, wet-to-dry weight ratio at end of reperfusion was significantly different (10.2 +/- 1.0 vs. 6.0 +/- 0.3. 5.2 +/- 0.3 and 5.4 +/- 0.5, respectively; P < 0.05). No significant differences in any of these parameters were observed between groups 2, 3, and 4. CONCLUSIONS: These data suggest that: (1) pulmonary edema will develop in atelectatic lungs if reperfusion is delayed for 4 h after death; (2) postmortem room air-inflation is as good as ventilation in prolonging warm ischemic tolerance; (3) ventilation with room air is no different from that with nitrogen; (4) therefore, prevention of alveolar collapse appears to be the critical factor in protecting the warm ischemic lung from reperfusion injury independent of continuous oxygen supply.

Animals↗

Vindesine-ifosfamide-platinum (VIP) induction chemotherapy in surgically staged IIIA-N2 non-small-cell lung cancer: a prospective study. Leuven Lung Cancer Group.

PURPOSE: In the pioneer data from the Memorial-Sloan-Kettering group, preoperative mitomycin-C-vindesine-platinum (MVP) induction chemotherapy in N2-NSCLC was accompanied with substantial pulmonary toxicity. In this study, the efficacy and toxicity of three-drug VIP induction chemotherapy, the pathologic response in resection specimens, the early survival and relapse patterns are examined. PATIENTS AND METHODS: Between June 1995 and March 1997, 39 consecutive patients with pathology proven N2-NSCLC were treated with three cycles of VIP induction, followed by definitive locoregional treatment (resection and mediastinal dissection or radical radiotherapy). Several patients had unfavorable prognostic characteristics with respect to clinical and biological findings, tumor location and bulk of disease. RESULTS: The response rate to chemotherapy was 59% (95% Confidence Interval 34-75). Twenty-three responding patients had radical locoregional treatment: radical radiotherapy in four, resection in 19. Downstaging was present in nine of the 19 resection specimens, with two pathologic complete responses. The median survival time (MST) of all patients is 19 months, with a projected two-year survival of 49%. In patients responsive to chemotherapy who received definitive local treatment, the MST is not yet reached, and the projected two-year survival is 57%. Relapses were mainly distant, with isolated brain relapse as a disturbing finding. The main toxicity's were leukopenia and vomiting, but they were manageable. In contrast with MVP, no severe pulmonary toxicity occurred. CONCLUSIONS: VIP is a suitable induction regimen for N2-NSCLC, demonstrating a good activity and very acceptable toxicity.

Adult↗

Warm ischemic tolerance in collapsed pulmonary grafts is limited to 1 hour.

OBJECTIVE: To determine the length of warm ischemic tolerance in pulmonary grafts from non-heart-beating donors. SUMMARY BACKGROUND DATA: If lungs could be retrieved for transplant after circulatory arrest, the shortage of donors might be significantly alleviated. Great concern, however, exists about the length of tolerable warm ischemia before cold preservation of pulmonary grafts retrieved from such non-heart-beating donors. METHODS: The authors compared the influence of an increasing postmortem interval on graft function in an isolated, room air-ventilated rabbit lung model during blood reperfusion up to 4 hours. Four groups of cadavers (four animals per group) were studied. In group 1, lungs were immediately reperfused. In the other groups, cadavers with lungs deflated were left at room temperature for 1 hour (group 2), 2 hours (group 3), or 4 hours (group 4). RESULTS: Pulmonary vascular resistance was enhanced in all ischemic groups compared with the control group. An increase was noted with longer postmortem intervals in peak airway pressure and in weight gain. A concomitant decline was observed in the venoarterial oxygen pressure gradient caused by progressive edema formation, as reflected by the wet-to-dry weight ratio at the end of reperfusion. CONCLUSIONS: Warm ischemia resulted in increased pulmonary vascular resistance. Graft function in lungs retrieved 1 hour after death was not significantly worse than in nonischemic lungs. Therefore, 60 minutes of warm ischemia with the lung collapsed may be tolerated before cold storage. Further studies are necessary to investigate whether lungs retrieved from non-heart-beating donors will become a realistic alternative for transplant.

Animals↗

Pulmonary cell death in warm ischemic rabbit lung is related to the alveolar oxygen reserve.

BACKGROUND: If lungs could be retrieved for transplantation from non-heart-beating cadavers, the shortage of donors might be significantly alleviated. METHODS: We studied the effect of different postmortem lung conditions on pulmonary cell death. Lungs from 208 New Zealand white rabbits were flushed with trypan blue vital dye solution at intervals after circulatory arrest, fixed, and mounted for histologic examination. Pulmonary cells were judged to be viable on the basis of their ability to exclude trypan blue dye. In the control group, lungs were excised immediately after death and immersed in cold (4 degrees C) saline solution. In the other groups, cadavers were left at room temperature with lungs deflated, ventilated with room air or 100% oxygen or 100% nitrogen, or inflated with room air or 100% oxygen. RESULTS: There was a gradual increase in percentage (mean +/- SEM) of nonviable cells in the control group from 2.5%+/-0.9% (preischemic value) to 18.1%+/-2.8% at 24 hours after death (p < 0.001). In cadavers with lungs deflated, 79.7%+/-2.1% of cells were nonviable at 24 hours after circulatory arrest (p < 0.001 versus control group). In contrast, room air-ventilated cadavers showed only 21.4%+/-2.7% nonviable cells at this interval (p < 0.001 versus deflated group; not significant versus control group). Values in oxygen-ventilated animals were similar. Nitrogen-ventilated cadavers, however, had significantly more nonviable lung cells (73.8%+/-3.2%; p < 0.001 vs room air and oxygen-ventilated group, not significant vs deflated group). Oxygen-inflated lungs showed a parallel decrease in cell viability up to 4 hours after death when compared with room air-inflated cadaveric lungs, but thereafter more cells became nonviable in the latter group (11.1%+/-0.7% vs 19.6%+/-3.2% at 6 hours and 48.7%+/-7.2% vs 75.5%+/-4.6% at 24 hours, respectively; p < 0.01). CONCLUSIONS: Postmortem room air ventilation is as good as oxygen ventilation in delaying pulmonary cell death, and its effect is comparable to cold storage; nitrogen ventilation, however, is ineffective and not different from deflation; oxygen inflation will preserve ischemic cells for longer intervals as opposed to room air inflation. Therefore the alveolar oxygen reserve seems to be the critical factor to protect-the lung parenchyma from warm ischemic damage.

Animals↗

Extended preservation of ischemic pulmonary graft by postmortem alveolar expansion.

BACKGROUND: If lungs could be retrieved for transplantation from non-heart-beating cadavers, the shortage of donors might be significantly alleviated. METHODS: Peak airway pressure, mean pulmonary artery pressure, pulmonary vascular resistance, and wet to dry weight ratio were measured during delayed hypothermic crystalloid flush in rabbit lungs (n = 6) at successive intervals after death comparing cadavers with lungs left deflated (group 1), inflated with room air (group 2) or 100% oxygen (group 4), or ventilated with room air (group 3), or 100% nitrogen (group 5), or 100% oxygen (group 6). RESULTS: There was a gradual increase in mean pulmonary artery pressure and pulmonary vascular resistance with longer postmortem intervals in all study groups (p = not significant, group 1 versus group 2 versus group 3). There was also a gradual increase in peak airway pressure and wet-to-dry weight ratio over time in all groups, which reflected edema formation during flush (airway pressure, from 14.5 +/- 1.0 cm H2O to 53.7 +/- 12.2 cm H2O, and wet-to-dry weight ratio, from 3.6 +/- 0.1 to 11.5 +/- 1.2, in group 1 at 0 and 6 hours postmortem, respectively; p < 0.05). Compared with group 1, however, the increase in groups 2 and 3 was much slower (airway pressure, 20.9 +/- 0.5 cm H2O and 18.8 +/- 1.2 cm H2O, and wet-to-dry weight ratio, 5.2 +/- 0.3 and 4.6 +/- 0.4 at 6 hours postmortem, respectively; p < 0.05 versus group 1 and p = not significant, group 2 versus group 3). Airway pressure and wet-to-dry weight ratio did not differ between groups 2 and 4 or between groups 3, 5, and 6. CONCLUSIONS: These data suggest that (1) pulmonary edema will develop in atelectatic lungs if hypothermic flush is delayed for 2 hours after death, (2) postmortem inflation is as good as ventilation in prolonging warm ischemic tolerance, (3) inflation with oxygen or ventilation with nitrogen or oxygen is no different from that with room air, and (4) therefore, prevention of alveolar collapse appears to be the critical factor in protecting the lung from warm ischemic damage independent of continued oxygen delivery.

Air↗

Delay of adenosine triphosphate depletion and hypoxanthine formation in rabbit lung after death.

BACKGROUND: If lungs could be retrieved for transplantation from non-heart-beating cadavers, the shortage of donors might be significantly alleviated. 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 mumol/g dry weight for ATP and 3.03 +/- 0.49 versus 7.64 +/- 0.94 mumol/g dry weight for hypoxanthine at 24 hours, respectively; p < 0.05). Cadaver cooling significantly slowed ATP catabolism. Changes in ATP level 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.

Adenosine Diphosphate↗

External cooling of warm ischemic rabbit lungs after death.

BACKGROUND: If lungs could be retrieved for transplantation after circulatory arrest, the shortage of donors might be significantly alleviated. However, in such non-heart-beating donors, there is great concern that even a short period of warm ischemia will be deleterious for lung tissue, jeopardizing the transplant recipient. It was the purpose of this study to look for the efficacy of different methods of lung cooling inside a cadaver after circulatory arrest. METHODS: New Zealand white rabbits were sacrificed with an intravenous overdose of pentobarbital and left at room temperature. Subcutaneous, rectal, lung core, lung surface, and endobronchial temperatures were measured at intervals after death. Cooling of the lung during ischemia differed between groups (n = 6 in each group): lungs left deflated at room temperature (24 degrees C) (group 1 = control non-heart-beating donors), lungs ventilated with cooled (4 degrees C) room air (group 2), lungs left deflated plus topical cooling (1 degree C) of both the cadaver and its lungs (group 3), and lungs flushed in situ immediately after circulatory arrest with a cold (4 degrees C) crystalloid solution followed by ex vivo deflated storage in cold (1 degree C) saline solution (group 4 = control heart-beating donors). RESULTS: There was a slow decline in lung core, lung surface, and endobronchial temperatures toward room temperature in group 1 (1.5 degrees +/- 0.0 degree C/h, 1.8 degrees +/- 0.2 degree C/h, and 1.9 degrees +/- 0.1 degree C/h, respectively). In contrast, all three lung temperatures immediately ( < 5 minutes) dropped to less than 10 degrees C in group 4. Hypothermic ventilation (group 2) decreased endobronchial temperature (p < 0.05 at 30 minutes) but not lung surface, rectal, or subcutaneous temperature when compared with group 1. Cooling rate for lung surface and endobronchial temperatures during the first 4 hours after death was faster (p < 0.01) in group 3 (6.6 degrees +/- 0.3 degree C/h and 6.1 degrees +/- 0.2 degree C/h, respectively) when compared with group 2 (2.5 degrees +/- 0.3 degree C/h and 3.9 degrees +/- 0.1 degree C/h, respectively), but slower (p < 0.001) when compared with group 4 (9.2 degrees +/- 0.1 degree C/h and 8.7 degrees +/- 0.1 degree C/h, respectively). CONCLUSIONS: These data demonstrate that in the non-heart-beating donor, (1) in situ cold flush will result in immediate cooling of the lung, (2) ventilation with cooled air will only accelerate the decline in endobronchial temperature but has no effect on lung surface temperature, and (3) topical cooling of the cadaver is more efficacious in decreasing lung temperature than hypothermic ventilation.

Animals↗

Effect of inflation on adenosine triphosphate catabolism and lactate production during normothermic lung ischemia.

Although few biochemical data comparing adenosine triphosphate (ATP) catabolism or lactate production in isolated deflated versus inflated lung tissue are available, most transplant centers preserve their donor lungs inflated. We measured ATP level (using high-performance liquid chromatography), energy charge, and lactate level during 2 hours of normothermic ischemia in deflated lung tissue (n = 6), in lung tissue inflated with room air (n = 6), and in lung tissue inflated with 100% oxygen (n = 6). To determine the onset of anaerobic metabolism in lung tissue inflated with 100% O2, ATP and lactate levels were measured in another group (n = 6) during 8 hours of normothermic ischemia. Rabbit lungs were flushed in situ with a modified Krebs-Henseleit solution (60 mL/kg). They were isolated and immersed in 0.9% NaCl at 37 degrees C. In deflated lung tissue, ATP level (control value, 9.4 +/- 0.58 mumol/g dry wt) decreased and lactate level (control value, 5.6 +/- 1.16 mumol/g dry wt) increased after 15 minutes of ischemia (ATP, 5.2 +/- 0.86 mumol/g dry wt; lactate, 13.3 +/- 1.58 mumol/g dry wt). When the lung was stored inflated with room air, ATP breakdown and increase of lactate concentration only occurred after 90 minutes of normothermic ischemia (at 60 minutes: ATP, 8.0 +/- 0.58 mumol/g dry wt; lactate, 6.3 +/- 1.1 mumol/g dry wt). In lungs stored inflated with 100% O2, ATP breakdown and lactate accumulation only occurred after 5 hours of normothermic ischemia (at 4 hours: ATP, 8.1 +/- 0.74 mumol/g dry wt; lactate, 5.9 +/- 1.28 mumol/g dry wt).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

Thoracoscopic surgery: the Belgian experience.

Despite the already wide experience with video-assisted techniques in laparoscopic surgery, video-assisted thoracic surgery only recently came to be developed. This is clearly seen in a survey reflecting the experience among Belgian surgeons. A majority of the surgeons (63%) had limited experience (1 to 5 interventions), and only 28.5% had fairly considerable (between 11 and 20 interventions) or considerable (more than 20 interventions) experience. The majority of interventions performed were the treatment of pneumothorax, lung biopsies, wedge resections, and intrathoracic staging procedures, accounting for 209 (70%) of the 296 interventions collected in this survey. The remaining interventions display a wide variety of different thoracic procedures including lobectomy (4) and esophagectomy (20) for carcinoma. The overall technical success rate was 91% in this survey. Our own experience with 71 interventions or attempts reflects the same evolution with an overall technical success rate in 85% (60 patients). Pneumothorax was the most frequently performed intervention (35 patients), with a technical success rate of 94.5% (32 patients). Recurrences requiring further treatment occurred in 5 of the 32 patients (14.3%). All recurrences occurred before endostaplers were available, after which there were no failures in 12 consecutive cases. Other procedures successfully performed were lung biopsy/wedge resection (6), lung cancer staging procedures (3), lobectomy (1), hemothorax (3), chest wall neurinoma (2), sympathectomy (5), dorsal mediastinal neurinoma (1), thymectomy (1), esophagectomy (3), benign esophageal tumor enucleation (2), and Belsey Mark IV antireflux procedure (1). Furthermore, special emphasis was given to the development of video-assisted mediastinoscopy, which greatly facilitates teaching and interpreting this operation. Endoscopic myotomy using endostaplers was performed in 2 patients with Zenker's diverticulum. From our experience, however, it becomes clear that thoracoscopic approaches do not always result in a distinct benefit for the patient, as these procedures are more time consuming and usually require one-lung ventilation (probably the cause of the only fatal outcome in this series: a lung biopsy in an 85-year-old patient). In conclusion, video-assisted thoracic and thoracoscopic surgery is a new surgical modality offering new perspectives. However, careful patient selection and the same expertise as in open procedures are essential in determining the final outcome of each procedure.

Adult↗

Primary immotile oesophagus in young patients.

Since 1984 we have identified 14 patients under the age of 45 years with severe, unexplained loss of oesophageal motility. The ages at presentation ranged from 20 to 42 years and nine were female. Barium swallow was normal in eight patients and showed minor abnormalities in six. Twenty-four hour pH studies were normal in all patients and the only endoscopic abnormality was minimal oesophagitis in three. Upper oesophageal sphincter resting pressures and cervical motility were normal except in one patient. Motility in the body of the oesophagus was severely reduced in all patients with a mean peristaltic amplitude of 10 mmHg. Lower oesophageal sphincter resting pressures were reduced in 11 patients and normal in three, with incomplete sphincter relaxation in three. All patients have been followed up for a minimum of 3 years without progression of their symptoms or the development of a secondary cause. Six patients have undergone repeat manometry and pH studies with no changes. We conclude that there is a group of young patients who appear to undergo severe primary loss of oesophageal motility for reasons that have not yet been identified. It is important to identify these patients so that inappropriate surgery can be avoided.

Adult↗

Surgical treatment for higher stage non-small cell lung cancer.

Locally advanced lung cancer (stage IIIa, IIIb) in which the primary tumor is proximal (T3) or has invaded adjacent structures (T3) or organs (T4) or in which mediastinal lymph nodes are involved (N2, N3) worsens the prognosis significantly. However, in stage IIIa (T3 or N2), when surgical treatment results in total removal of the primary tumor and involved lymph nodes, there still is a reasonable chance for ultimate cure. On the other hand, total excision can be very rarely performed in T4 or N3 tumors. Therefore, this group (stage IIIb) usually indicates unresectability. Disseminated lung cancer with distant metastasis (stage IV) is still considered to be incurable. Nevertheless, solitary metastatic sites (M1), especially brain, have been treated on occasion by resection of the primary tumor and removal of the solitary metastasis. This appears to improve median survival and does yield 5-year survival in selected patients. The results after surgical treatment in these patients with higher stage lung cancer reported over the last 10 years are reviewed.

Carcinoma, Non-Small-Cell Lung↗