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At least 883 records · Page 49Linked to original sources
PubMed1998

Expression of ICAM-1, VCAM-1, and LFA-1 in adenocarcinoma of the lung with observations on the expression of these adhesion molecules in non-neoplastic lung tissue.

Intercellular adhesion molecule (ICAM-1), vascular cell adhesion molecule (VCAM-1), and the lymphocyte function-associated antigen (LFA-1) are cell adhesion molecules thought to play an important role in the complex process of airway inflammation and tumor cell growth. The aim of this study was to examine the distribution of ICAM-1, VCAM-1, and LFA-1 in adenocarcinoma of lung and in major cellular compartments of non-neoplastic lung tissue. We examined cellular compartments in tissue from five bronchoalveolar carcinomas, three acinar adenocarcinomas, and one colon cancer metastatic to the lung. The compartments in neoplasms included the tumor cells proper, endothelial cells within the tumor vasculature, tumor stromal cells, and tumor-infiltrating lymphocytes. The compartments in non-neoplastic lung tissue included lung endothelial cells, pulmonary lymphocytes, interstitial fibroblasts, Type II alveolar pneumocytes, and bronchial epithelial cells. ICAM-1 was expressed in tumor cells from all of the nine adenocarcinomas. In contrast, VCAM-1 expression was not identified in tumor cells from any of the nine adenocarcinomas. ICAM-1 was expressed in all cellular compartments of the non-neoplastic lung tissue, whereas VCAM-1 was expressed only in pulmonary lymphocytes and interstitial fibroblastic cells. LFA-1 was uniformly expressed in tumor-infiltrating lymphocytes from each of the nine tumors and all of the lymphocytes in non-neoplastic lung tissue. This study showed major differences in the expression of ICAM-1 and VCAM-1 in tumor cells from pulmonary adenocarcinoma and also provided evidence for a wider distribution of ICAM-1, compared with VCAM-1, in non-neoplastic cellular compartments of the lung. ICAM-1 expression was particularly noticeable in bronchial and alveolar epithelial cells. Upregulation of ICAM-1 in pulmonary adenocarcinoma might foster binding by LFA-1-bearing lymphocytes, with a possible impact on the vulnerability of tumor cells to host defense mechanisms.

Adenocarcinoma↗
PubMed1999

p53 codon 72 polymorphism in Taiwanese lung cancer patients: association with lung cancer susceptibility and prognosis.

An association between the BstUI (Pro/Pro) genotype of the p53 codon 72 polymorphism and lung cancer has been reported previously (X. Jin et al., Carcinogenesis (Lond.), 16: 2205-2208, 1995). However, the genotype distribution of p53 codon 72 polymorphism as well as the association of this polymorphism with lung cancer risk and prognosis remain undefined in the Taiwanese population. Therefore, we investigated the genotype distribution of p53 codon 72 polymorphism in 194 lung cancer patients and 152 noncancer controls. The genotype frequencies in Taiwanese noncancer controls were 0.56 (Arg) and 0.44 (Pro). Chi2 analysis indicated significant differences in genotype distribution of p53 from other reports in Swedish (P < 0.001), Spanish (P < 0.001), Caucasians in the United States (P = 0.002), and African-Americans (P = 0.027). In addition, our data suggest that the Pro allele of the p53 codon 72 polymorphism increased the risk of lung cancer among female Taiwanese. The female patients with genotype Pro/Pro showed a significantly increased odds ratio (3.14; confidence interval, 1.48-6.64; P = 0.003) of having lung adenocarcinoma, compared with normal controls with the other genotypes. Patients with the Pro/Pro genotype had an odds ratio of 2.63 (confidence interval, 1.22-5.68; P = 0.01) higher than those with the other genotypes to be diagnosed with lung cancer at the early ages. We further investigated the association of p53 codon 72 polymorphism with prognosis in 133 lung cancer patients. Patients with the Pro/Pro genotype tended to have poorer prognosis than those with the Arg/Pro genotype (P = 0.05, by the log-rank test). Our data suggested that p53 codon 72 polymorphism may play a role in cancer susceptibility and prognosis in specific classes of lung cancer patients in Taiwan.

Adenocarcinoma↗
PubMed1997

Native lung complications after single lung transplantation for emphysema.

We reviewed the impact of the presence of the native diseased contralateral lung on the outcome after single lung transplantation for emphysema. Twenty consecutive recipients of single lung transplants for emphysema were reviewed for complications related to the native lung. Five patients (25%) suffered major complications arising in the native lung and resulting in serious morbidity and mortality. The timing of onset varied from 1 day to 43 months after transplantation. We conclude that the susceptibility of the native lung to complications such as those described in this report is an additional fact to be considered in choosing the ideal transplant procedure for patients with obstructive lung disease.

Adult↗
PubMed1992

Isolated lung transplantation for end-stage lung disease: a viable therapy.

Since January 1990, we have performed 29 isolated lung transplantations in 28 patients with end-stage lung disease (12 single, 16 bilateral). Recipient diagnoses were: cystic fibrosis (11), chronic obstructive pulmonary disease (6), pulmonary fibrosis (6), eosinophilic granulomatosis (1), postinfectious lung disease (1), adult respiratory distress syndrome (1), and primary pulmonary hypertension (2). There have been four deaths, two in patients with pulmonary fibrosis and two in patients with primary pulmonary hypertension. Four patients have undergone transplantation while on ventilatory support for respiratory failure (2 with cystic fibrosis, 1 having redo lung transplantation with cystic fibrosis, and 1 with adult respiratory distress syndrome); all of these have survived. Six patients required cardiopulmonary bypass, which was associated with increased transfusion requirement. All patients 2 months after discharge have returned to an active life-style, except for 2 patients who currently await retransplantation. Preoperative pulmonary rehabilitation has resulted in significant improvement in exercise performance in all patients. Immunosuppression consists of cyclosporine, azathioprine, and antilymphoblast globulin (University of Minnesota), withholding systemic steroids in the early postoperative period. We have employed bronchial omentopexy in all but four transplants; there has been one partial bronchial dehiscence, two instances of bronchomalacia requiring internal stenting, and one airway stenosis. Cytomegalovirus disease has been seen frequently (15 cases), but has responded well to treatment with ganciclovir. Other complication shave included one drug-related prolonged postoperative ventilation, thrombosis of a left lung after bilateral lung transplantation requiring retransplantation, five episodes of unilateral phrenic nerve palsy after bilateral lung transplantation (4 resolved), and the requirement of massive transfusion (greater than 10 units) in 5 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2000

Regulation of the Hoxa4 and Hoxa5 genes in the embryonic mouse lung by retinoic acid and TGFbeta1: implications for lung development and patterning.

We have previously described a 5; cis-acting retinoic acid response element that is required for a subset of Hoxa4 expression, including the midgestation mouse lung. As both retinoids and Hox genes have been implicated in lung development and patterning, we have examined Hoxa4 expression in the developing mouse lung and extended our work on its regulation. At E12.5, a Hoxa4/lacZ transgene is expressed in the mesenchymal compartment of the lung. Later in development expression is restricted to the proximal mesenchyme and is also observed in smooth muscle cells, subepithelial fibroblasts, and alveolar cells. We show that both Hoxa4 and Hoxa5 are upregulated when cultured in the presence of all-trans retinoic acid. In addition, retinoic acid extends the domain of Hoxa4 and Hoxa5 expression to the periphery of the explants where the distal epithelia are developing. Interestingly, the effect of retinoic acid on Hoxa5 expression was not observed in a Hoxa4 mutant background. In contrast, TGFbeta1 was found to downregulate both Hoxa4 and Hoxa5 expression in cultured lung explants. We also establish that retinoic acid has the effect of proximalizing the mouse lung when cultured in a serum-free medium, as evidenced by reduced expression of the distal marker surfactant protein-C. Lungs from Hoxa4 mutant embryos exhibited a similar response to retinoic acid, suggesting that Hoxa4 alone is not required for the proximalizing effect. Based on their retinoid-dependent expression, we conclude that members of the group 4 and/or group 5 Hox genes are likely to be involved in patterning of the mouse lung. Dev Dyn 2000;217:62-74.

Animals↗
PubMed2000

CGH analysis of radon-induced rat lung tumors indicates similarities with human lung cancers.

Epidemiological studies have shown that inhalation of radon, a radioactive gas, is associated with an increased risk for lung cancer. We have developed a model of radon-induced rat lung tumors to characterize cytogenetic and molecular events involved in radon-induced lung tumorigenesis. Using comparative genomic hybridization (CGH), gains and losses of genetic material were investigated in a series of 13 carcinomas and four adenomas of the lung. Frequent losses occurred at 4q12-21, 5q11-33, and 15q, which are homologous to human chromosome (HSA) bands 7q21-36, 1p31-36/9p21-31, and 13q14.1-14.3/3p14.2, respectively. These regions are frequently (30-80%) deleted in human lung cancer and contain tumor suppressor genes or proto-oncogenes such as MET, CDKN2A/p16/MTS1, CDKN2B/p15/MTS2, FHIT, and RB1 or yet to be identified genes. Frequent gains involved 6, 7q34-qter, and 19q; chromosomes 6 and 7 being homologous to human 2p21-25 and 8q21-24 where the MYCN and MYC oncogenes are located. The genetic similarities between rat and human lung cancer suggest common underlying mechanisms for tumor evolution in both species. Moreover, cytogenetic and molecular genetic analyses of radon-induced rat lung tumors could help to better understand the development and progression of radon-induced lung cancer in man.

Adenoma↗
PubMed2002

PDGF-A/PDGF alpha-receptor signaling is required for lung growth and the formation of alveoli but not for early lung branching morphogenesis.

Platelet-derived growth factors (PDGF) constitute a family of four gene products (PDGF-A-D) acting by means of two receptor tyrosine kinases, PDGFR alpha and beta. Three of the ligands (PDGF-A, -B, and -C) bind to PDGFR alpha with high affinity. Knockout of pdgf-a in mice has demonstrated a role for PDGF-A in the recruitment of smooth muscle cells to the alveolar sacs and their further compartmentalization into alveoli. Although this is a late, postnatal step in lung development, pdgf-a antisense oligonucleotides were previously shown to inhibit epithelial branching in rat lung explants in vitro, which reflects an early embryonic process. These conflicting results may be explained by substitution of genetic loss of pdgf-a by maternal transfer of PDGF-A to the knockout embryo or the presence of other PDGFR alpha agonists (PDGF-B and -C) in vivo, potentially masking an effect of PDGF-A on branching morphogenesis. Alternatively, the administration of pdgf-a antisense oligonucleotides affected other processes than the intended. To discriminate between these opposing possibilities, we have analyzed lung development in pdgfr alpha -/- embryos and lung primordia grown in vitro. Our analysis shows that, while the pdgfr alpha -/- lungs and explanted lung rudiments were smaller than normal, branching morphogenesis appears qualitatively intact and proceeds until at least embryonic day 15.5, generating both prospective conducting and respiratory airways. We conclude that, although PDGF-AA signaling over PDGFR alpha may have direct or indirect roles in overall lung growth, it does not specifically control early branching of the lung epithelium.

Animals↗
PubMed1998

Instillation of allogeneic lung macrophages and dendritic cells cause differential effects on local IFN-gamma production, lymphocytic bronchitis, and vasculitis in recipient murine lungs.

Lung allograft rejection is believed to be initiated by donor lung accessory cells, namely macrophages and dendritic cells, interacting with recipient lymphocytes leading to up-regulated Th1 type (IFN-gamma) cellular immunity culminating in graft destruction. The purpose of this study was to determine the individual role of donor lung macrophages and dendritic cells in the rejection response. Utilizing a murine model that reproduces the immunology and histology of acute rejection, C57BL/6 mouse (I-a(b), H-2(b)) lung dendritic cells (DC-enriched lung cells), purified alveolar macrophages (I-a-negative macrophages), or various ratios of I-a-negative macrophages/DC were instilled into BALB/c mouse (I-a(d), H-2(d)) lungs followed by an assessment of local IFN-gamma production and grading of rejection pathology. The data show that DC, and not I-a-negative macrophages, induced IFN-gamma production in recipient lungs. However, the local production of IFN-gamma was not always associated with histological changes characteristic of rejection pathology. In contrast to either cell type alone, instillation of C57BL/6 I-a-negative macrophages and DC, together, were required to induce rejection pathology in BALB/c lungs. In addition, the rejection response was dependent on interactions between donor I-a-negative macrophages and DC.

Animals↗
PubMed1988

Postnatal development of rat lung following retarded fetal lung growth.

Postnatal lung development was examined in rats born with smaller than normal lungs after either prenatal exposure to glucocorticoid or to an inhibitor of collagen synthesis. At birth, treated animals had lower than normal lung weights, lung to body weight ratios, hydroxyproline (HYP) levels, total DNA; and rates of DNA synthesis. Rats exposed to steroid showed a rapid recovery in growth during the normal postnatal cell proliferative phase from 4 to 11 days, though collagen levels did not return to normal until 3 weeks of age. Rats exposed to a prenatal proline analog showed a much slower rise in lung weight and total DNA, and these levels were still much below normal at 2-3 weeks when the cell proliferation phase was completed. Levels of disaturated phosphatidylcholine were significantly below normal up to 11 days, whereas total HYP was significantly reduced and less fibrillar collagen was seen in the lung throughout the study. The results indicate that the smaller but mature lungs at birth after antenatal steroid show a growth rebound and quickly become structurally normal. In contrast, inhibition of fibroblast growth and collagen deposition produces small lungs at birth, which continue to show inhibited growth and development at least up to 3 weeks of age, when the cell division phase is over.

Animals↗
PubMed1994

Differential effects of agents on bronchial and vascular tone and lung weight in the rat isolated perfused lung.

A ventilated perfused model of rat lung is described enabling continuous simultaneous measurement of pulmonary perfusion pressure (PPP), pulmonary inflation pressure (PIP) and lung weight. The preparation was stable for 2h before oedema formation commenced. Phenylephrine injected into the pulmonary artery produced selective increases in PPP (ED50 4.0 +/- 0.7 nmol, n = 5) without affecting airway tone or lung weight. Carbachol under basal perfusion conditions caused bronchoconstriction (ED50 4.25 +/- 0.4 nmol, n = 7) without affecting PPP and lung weight. Bradykinin (BK) caused increases in PPP (ED50 22 +/- 3 nmol, n = 8), lung weight and PIP (ED50 35.6 +/- 3.6 nmol, n = 8). Low doses of BK (25-50 nmol) caused increases in lung weight which were reversible. Higher doses (100-200 pmol) caused irreversible increases in lung weight which albumin-bound dye infusion showed were associated with albumin accumulation. Manipulation of venous outflow pressure revealed that the changes in lung weight induced by BK were potentially explicable as sequelae of vascular hydrostatic pressure changes possibly resulting from venoconstriction. It is concluded that this model is useful for studying drug actions on bronchial tone, pulmonary vasculature tone and vascular permeability.

Analysis of Variance↗
PubMed1977

[The so-called shock lung, a disease of lung parenchyma (author's transl)].

Although the pathogenesis of the so-called shock lung is different, from the clinical point of view the syndrome is uniform. Regarding the morphology microcirculation, vascular permeability and surfactant of the lung in shock lung are discussed. The course of the alterations in lung parenchyma is uniform, independent of the different pathogenesis in a single case. Pathology and disturbtion of lung function are conform. The relation of the so-called shock lung to other diseases of lung parenchyma is discussed and finally a definition of the so-called shock-lung recommended.

Animals↗
PubMed1984

Lung surfactant and fatty acid composition of lung tissue and lavage of rats fed diets containing different lipids.

Two nutritional models, essential fatty acid (EFA) deficiency and the feeding of saturated vs unsaturated fats, were used to determine the effects of dietary lipids on the fatty acid composition of rat lung and lavage. Semipurified diets containing 7% corn oil, 7% hydrogenated coconut oil (EFA-deficient), 10% butter or 10% safflower oil were fed to dams during lactation and thereafter to their offspring for a total of 24 weeks. Lipids were extracted from the lung lavage and lung tissue and their fatty acid composition was determined. The content of dipalmitoylphosphatidylcholine (DPPC), the main surfactant in the lungs, was also determined. The results show that the levels of DPPC in the lungs of rats fed 10% butter decreased although the decrease in the EFA-deficient rats was greater. Comparing rats fed butter with those fed corn oil, there were also modifications in the fatty acid composition of the total lipids and phospholipids of lung tissue and lavage as well as in phosphatidyl-choline, phosphatidylethanolamine and phosphatidylinositol + phosphatidylserine fractions isolated from the lung tissue. The changes in fatty acid composition were somewhat fewer in rats fed butter then in those fed an EFA-deficient diet. The results suggest that a marginal EFA deficiency produced in rats by long-term feeding of 10% butter may account for the reduction in DPPC levels and in the changes in fatty acid composition in the lung tissue and lavage.

Animals↗
PubMed2004

Clinical utility of co-registered respiratory-gated( 99m)Tc-Technegas/MAA SPECT-CT images in the assessment of regional lung functional impairment in patients with lung cancer.

PURPOSE: The aim of the study was to provide preliminary validation of the utility of co-registered respiratory-gated ventilation/perfusion single-photon emission computed tomography-computed tomography (SPECT-CT) images in the assessment of regional lung functional impairment in patients with lung cancer. METHODS: Twenty untreated and three radiotherapy-treated patients with lung cancer underwent gated( 99m)Tc-Technegas/macroaggregated albumin (MAA) SPECT, using a triple-headed SPECT unit and a respiratory synchroniser. Gated SPECT images were obtained from 1/8 data centered at peak inspiration for each regular respiratory cycle and co-registered with tidal inspiration CT images using an automated three-dimensional registration tool. RESULTS: Gated SPECT images detected 10.2% more ventilation defects (205 vs 186) and 9% more perfusion defects (218 vs 200) compared with ungated images, with a significantly higher lesion-to-normal lung contrast ( P<0.0001). Co-registered gated SPECT-CT images accurately visualised the anatomy of ventilation and/or perfusion defects associated with bronchial and/or vascular involvement by tumours, resulting in changes in surgical planning in two patients with lung cancer. In the three patients who had received radiotherapy, perfusion defects along the radiation field were identified even in the lung areas without abnormal opacities on CT images. In the operated patients, the co-registered gated SPECT-CT images allowed accurate placement of regions of interest over the lung lobes to be resected, yielding a significantly better prediction of postoperative forced expired volume in 1 s (FEV(1)) compared with that predicted without use of these images ( R=0.993 vs R=0.890; P<0.05), with an excellent inter-observer reproducibility. CONCLUSION: Detailed functional-morphological correlation on co-registered gated SPECT-CT images contributes to accurate assessment of regional functional impairment, and may be useful for surgical planning, prediction of postoperative function and assessment of external beam radiotherapy effects in patients with lung cancer.

Administration, Inhalation↗
PubMed2006

Over-expression of PDGF-C using a lung specific promoter results in abnormal lung development.

PDGF isoforms are a family of polypeptides that bind to cell surface receptors and induce fibroblast proliferation and chemotaxis. PDGF-A and -B chain isoforms have previously been shown to be involved in murine lung development. A new PDGF polypeptide, PDGF-C, was recently recognized and differs from the PDGF-A and -B isoforms in that it requires proteolytic cleavage before it can bind and activate the PDGF alpha receptor. In these studies PDGF-C was over-expressed during embryogenesis using the lung specific surfactant protein C promoter. PDGF-C transgenic pups died from respiratory insufficiency within minutes following birth. At E18.5, nontransgenic lungs exhibited lung morphology consistent with the saccular stage of lung development. In contrast, E18.5 transgenic lungs retained many features of the canalicular stage of lung development and had abundant numbers of large poorly differentiated mesenchymal cells. These results suggest that PDGF-C is activated during lung development and is a potent growth factor for mesenchymal cells in vivo.

Animals↗
PubMed1995

Obliterative bronchiolitis after lung and heart-lung transplantation.

Obliterative bronchiolitis (OB) has emerged as the main cause of morbidity and mortality in the long-term follow-up after lung and heart-lung transplantation. The pathogenesis of OB is multifactorial, with acute rejection and cytomegalovirus infection being the main risk factors for the development of OB. The final common pathway of all inciting events seems to be an alloimmune injury, with subsequent release of immunologic mediators and production of growth factors leading to luminal obliteration and fibrous scarring of the small airways. Analyzing the 14 years of experience in 163 patients at Stanford University, we found a current incidence of bronchiolitis obliterans syndrome or histologically proven OB within the first 3 years after lung and heart-lung transplantation of 36.3%, with an overall prevalence of 58.1% after heart-lung and 51.4% after lung transplantation. Both pulmonary function indices (forced expiratory flow between 25% and 75% of forced vital capacity and forced expiratory volume in 1 second) and transbronchial biopsies have proven helpful in diagnosing bronchiolitis obliterans syndrome or OB at an early stage. Early diagnosis of OB and improved management have achieved survival rates in patients with OB after 1, 3, 5, and 10 years of 83%, 66%, 46%, and 22%, compared with 86%, 83%, 67%, and 67% in patients without OB. Recently, different experimental models have been developed to investigate the cellular and molecular events leading to OB and to evaluate new treatment strategies for this complication, which currently limits the long-term success of heart-lung and lung transplantation.

Bronchiolitis Obliterans↗
PubMed1983

Lactate dehydrogenase isoenzymes in hamster lung lavage fluid after lung injury.

Lactate Dehydrogenase Isoenzymes in Hamster Lung Lavage Fluid after Lung Injury. Beck, B. D., Gerson, B., Feldman, H. A., and Brain, J. D. (1983). Toxicol. Appl. Pharmacol. 71, 59-71. Lactate dehydrogenase (LD) levels and isoenzyme patterns were determined in the cell-free supernatant fractions of lung lavage fluid from hamsters exposed to alpha-quartz, iron oxide, Triton X-100, 100% O2, or 200 ppm SO2. The isoenzyme patterns were compared to those derived from hamster lung homogenates, serum, polymorphonuclear neutrophils (PMNs), pulmonary macrophages, and red blood cells. The isoenzyme patterns from alpha-quartz- and iron oxide-exposed animals resembled each other and were similar to that of PMNs. In contrast, the pattern seen after Triton X-100 exposure was similar to those of whole lung homogenates and of red blood cells. A 96-hr exposure to 100% O2 yielded an LD isoenzyme pattern in lung lavage fluid similar to that of serum. Exposure to SO2 did not alter LD levels, showing that upper airways damage is not reflected by changes in LD in lung lavage fluid. We conclude that LD isoenzyme patterns of lung lavage fluid can be used to differentiate among types of pulmonary injury and may help identify the sites of injury.

Animals↗
PubMed1994

Risk of late recurrence and/or second lung cancer after treatment of patients with small cell lung cancer (SCLC).

The aim of this study was to illustrate some difficulties in distinguishing late recurrence of small cell lung cancer (SCLC), from second primary lung cancer. Three-hundred fourteen SCLC patients were observed at the Institute of Tuberculosis and Chest Diseases in Warsaw, during the period 1976-1985. All patients were treated with chemotherapy and 125 were also treated with radiotherapy on the tumour and mediastinum. Nineteen patients (6%) survived 3 years. This group consisted of eight females (9%) and 11 males (5%). In all of them a complete remission was obtained. In six patients from this group no progression of lung cancer was observed. Four of them are still living, 7.9-16.2 years after the start of treatment. Two patients died of heart infarct. In the remaining 13 patients, progression of SCLC or development of new cancer was noted in the course of observation. In seven of them, histological proof of the character of progression was obtained. In four cases non-small cell lung cancer (NSCLC) was diagnosed after 3-11 years of observation. In one of them SCLC metastases in the liver were unexpectedly found in the autopsy, although adenocarcinoma in the lung diagnosed during bronchoscopy was also confirmed in the autopsy. In three cases SCLC was diagnosed. In one case, 2.7 years from the beginning of treatment, only SCLC metastases were found during laparoscopy. SCLC was found in two other cases after a 7-year cancer-free period. In one of those patients, a new lesion was found in the other lung while the second patient developed a new lesion exactly in the place of the former cancer. In six other patients no histological proof of the character of progression was obtained. Two of the six are still living, 8.2 and 15.1 years later. In the first of these two, a new lesion developed very early in the course of treatment in the same place as the primary tumour and it was regarded as the progression of SCLC. In the second patient, who probably had NSCLC the lesion developed in the contralateral lung after 12.5 years of remission and disappeared after radiotherapy. Four patients died of cancer after 3.2-6.4 years of observation. The cumulative risk of a second primary lung cancer after a 3-year survival period oscillated in our SCLC patients between 4% and 6% for every patient/year of observation. It was concluded that prognosis in SCLC patients is still doubtful, nevertheless, some patients made a complete recovery.

Adult↗
PubMed2004

Lung perfusion with protective solution relieves lung injury in corrections of Tetralogy of Fallot.

BACKGROUND: The aim of this study was to evaluate the protective effect of pulmonary perfusion with hypothermic protective solution on lung function after cardiopulmonary bypass in corrections of Tetralogy of Fallot. METHODS: Sixty-four consecutive children with Tetralogy of Fallot were randomly divided into a control group (n = 30) and a protective group (n = 34). Hypothermic protective solution was infused to the main pulmonary artery in the protective group. Hemodynamics and lung functions were monitored. Concentrations of malondialdehyde, tumor necrosis factor-alpha, von Willebrand factor, and endothelin in plasma were measured. The interleukin-6 and interleukin-8 levels in bronchoalveolar lavage fluid were also determined. Lung biopsy specimens were obtained after weaning from cardiopulmonary bypass. RESULTS: Oxygenation values (oxygen index and alveolar-arterial O(2) gradient) were better preserved in the protective group than in the control group. The time of mechanical ventilation and length of intensive care unit stay were shorter in the protective group compared with the control group. The tumor necrosis factor-alpha and malondialdehyde levels in plasma increased in both groups after operations, and the rising extents were lower in the protective group than in the control group. The von Willebrand factor and endothelin levels in plasma increased more significantly in the control group than in the protective group. The concentrations of interleukin-6 and interleukin-8 in bronchoalveolar lavage fluid were lower in the protective group than in the control group. The examination of histopathology demonstrated capillary hyperemia and hemorrhage, intra-alveolar edema, leukocytes accumulation, mitochondria swelling and vacuolation, and gas-blood barrier broadening in the control group, whereas there were no significant changes in the protective group. The intercellular adhesion molecule-1 expression on lung vascular endothelial cells was stronger in the control group. CONCLUSIONS: Lung perfusion with hypothermic protective solution during cardiopulmonary bypass relieved lung injury in corrections of Tetralogy of Fallot. The inhibition of lung vascular endothelial cell injury may be the major mechanism of relieving cardiopulmonary bypass-induced lung injury.

Bronchoalveolar Lavage Fluid↗