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PubMed2004

Polymorphisms in genes involved in xenobiotic metabolism and lung cancer risk under the age of 60 years. A pooled study of lung cancer patients in Denmark and Norway.

The genetic susceptibility hypothesis has been used to explain why only a minority of smokers develop lung cancer. Only few studies have studied the role of polymorphisms in phase-I and II metabolizing genes, among young lung cancer patients. We have pooled the individual data of three studies from Denmark and Norway, including 320 patients diagnosed with non-small cell lung cancer at age 59 or below, and 618 age and gender matched controls. A questionnaire was used to determine relevant demographic and lifestyle characteristics, and polymorphisms in following genotypes were determined GSTM1, GSTM3, GSTP1, GSTT1, GPX1, MPO, NQO1 and NAT2. Based on the literature, the alleles of the genotypes were categorised as high- or low-risk alleles. No individual effect of the genotypes was found on the risk of lung cancer. Given a smoking exposure, the presence of high-risk alleles (or phenotypes) was generally found to increase the risk of lung cancer, although the effect modification did not reach statistical significance. A pattern of stronger protective effect was observed in carriers of more than one allele associated with lower risk of lung cancer, and a higher risk of lung cancer in carriers of one or more alleles associated with higher risk of lung cancer, but the results did not reach statistical significance. The effect modification was generally strongest at lower levels of smoking.

Adult↗
PubMedDate not supplied

Quantitative relationship of stress Tc-99m sestamibi lung uptake with resting Tl-201 lung uptake and with indices of left ventricular dysfunction and coronary artery disease.

BACKGROUND: We investigated the relationship of stress technetium 99m sestamibi lung uptake with rest thallium 201 lung uptake and with indices of left ventricular (LV) dysfunction and severity of coronary artery disease (CAD) in patients with known or suspected CAD undergoing stress testing and cardiac catheterization. Stress Tc-99m sestamibi lung uptake and both stress and rest Tl-201 lung uptake are associated with LV dysfunction and extent of CAD. Although the mechanism of lung uptake is thought to be similar for the two isotopes, their physiologic characteristics are different. No direct comparison of lung uptake for the two isotopes has been reported. METHODS AND RESULTS: We evaluated 192 consecutive patients who underwent dual-isotope myocardial perfusion imaging and cardiac catheterization within 30 days. We examined the relationship of stress Tc-99m sestamibi lung-to-heart ratio (LHR) with rest Tl-201 LHR, with indices of myocardial perfusion, and with invasive measures of the severity of LV dysfunction and CAD. Stress Tc-99m sestamibi LHR correlated with rest Tl-201 LHR (r = 0.548, P <.001). Stress Tc-99m sestamibi LHR was positively associated with LV filling pressures and extent of CAD and negatively associated with LV ejection fraction and arterial systolic blood pressure. However, after adjustment for multiple comparisons, stress Tc-99m sestamibi LHR was significantly associated only with LV end-diastolic pressure (r = 0.287, P =.002) and pulmonary capillary wedge pressure (r = 0.337, P <.001). CONCLUSIONS: Increased stress Tc-99m sestamibi LHR correlates with rest Tl-201 LHR in patients with known or suspected CAD. Stress Tc-99m sestamibi lung uptake is also associated with invasively measured LV filling pressures.

Coronary Artery Disease↗
PubMed2002

Lung protection during total cardiopulmonary bypass by isolated lung perfusion: preliminary results of a novel perfusion strategy.

BACKGROUND: The present pilot study was conducted to evaluate the effect of isolated short-term lung perfusion during cardiopulmonary bypass (CPB) on inflammatory response and oxygenation. METHODS: A total of 24 patients undergoing elective cardiac surgery with routine CPB were prospectively assigned to three groups. Group I (n = 7), control subjects receiving neither lung perfusion nor ultrafiltration; group II (n = 9), patients undergoing lung perfusion; and group III (n = 8), patients undergoing lung perfusion plus ultrafiltration. Lung perfusion consisted of single-shot hypothermic pulmonary artery perfusion with oxygenated blood. Proteins indicative of leukocyte activation and lung injury were measured in plasma and bronchoalveolar lavage fluid (BALF). The alveolar-arterial oxygen gradient (A-aDO2) and the oxygenation index (PO2/FiO2) were also determined. RESULTS: Oxygenation values were best preserved in group III, followed by group II. After CPB, elastase-alpha1-proteinase inhibitor complex had increased in plasma in all groups; in BALF it increased in groups I and II, but not in group III. Alpha2-macroglobulin increased significantly in BALF in group I but not in groups II and III. CONCLUSIONS: These preliminary results provide some evidence that single-shot hypothermic lung perfusion with oxygenated blood at the beginning of CPB may have a protective effect on the lungs, especially when combined with ultrafiltration.

Adult↗
PubMed1997

EPC-K1 is effective in lung preservation in an ex vivo rabbit lung perfusion model.

BACKGROUND: L-Ascorbic acid 2-[3,4-dihydro-2,5,7,8-tetramethyl-2-(4,8,12-trimethyltridecyl)-2H -1-benzopyran-6yl-hydrogen phosphate] potassium salt (EPC-K1) is a phosphate diester of alpha-tocopherol and ascorbic acid. It has been reported that EPC-K1 inhibits lipid peroxidation and phospholipase A2. We hypothesized that EPC-K1 might enhance lung preservation and reduce the degree of posttransplantation lung dysfunction. METHODS: Eighteen rabbits were divided into three groups, as follows: group 1, no preservation (n = 6); groups 2 (n = 6) and 3 (n = 6), 24 hours of preservation at 8 degrees C. Low-potassium dextran-1% glucose solution was used for flushing and immersion in all groups, but EPC-K1 (0.5 mg/L) was added to the solution used in group 3. After storage the left lung was reperfused with autologous blood and ventilated using a membrane oxygenator in an isolated rabbit lung reperfusion model. The grafts used in the group 1 rabbits were perfused for 5 hours to confirm the reliability of this model, and the grafts used in the group 2 and 3 rabbits were perfused for 2 hours. Pulmonary arterial pressure, airway pressure, blood gas analysis, and the lipid peroxide level of the perfusate were assessed. The lipid peroxide levels of the lung tissue before and after storage and the wet-dry weight ratio of the perfused lung were determined in groups 2 and 3. RESULTS: Superior graft function was noted in group 3 in terms of all indices. The lipid peroxide level in the perfusate and the wet-dry weight ratio were also suppressed in group 3. The lipid peroxide level in the lung tissue did not change during storage in either group. CONCLUSIONS: The administration of EPC-K1 in the flush and preservation solution helps enhance lung graft function and suppresses lipid peroxidation after reperfusion.

Animals↗
PubMed1995

Lung transplantation with cardiopulmonary bypass exaggerates pulmonary vasomotor dysfunction in the transplanted lung.

Pulmonary vascular resistance is significantly increased in the transplanted lung. If cardiopulmonary bypass is required, the transplanted lung is reperfused with activated blood elements, which might exacerbate the reperfusion injury. The purpose of this study was to examine the influence of cardiopulmonary bypass on the following mechanisms of pulmonary vasomotor control in a dog model of autologous lung transplantation: (1) endothelium-dependent cyclic guanosine monophosphate-mediated relaxation (response to acetylcholine), (2) endothelium-independent cyclic guanosine monophosphate-mediated relaxation (response to nitroprusside), and (3) beta-adrenergic cyclic adenosine monophosphate-mediated relaxation (response to isoproterenol). Autologous right lung transplants were performed with (n = 4 dogs) and without (n = 5 dogs) bypass. Lungs were stored in cold saline solution (4 degrees C, 3 hours) before reimplantation. Pulmonary vasomotor control mechanisms were studied in isolated pulmonary arterial rings immediately after harvest and 1 hour after reimplantation. Ten rings were studied in each group at each time. Statistical analysis was by analysis of variance. Without bypass, endothelium-dependent cyclic guanosine monophosphate-mediated relaxation and beta-adrenergic cyclic adenosine monophosphate-mediated relaxation were significantly impaired, although endothelium-independent cyclic guanosine monophosphate-mediated relaxation was not. Use of bypass produced significantly greater impairment of both endothelium-dependent cyclic guanosine monophosphate-mediated relaxation and beta-adrenergic cyclic adenosine monophosphate-mediated relaxation. In addition, use of bypass produced significant dysfunction of endothelium-independent cyclic guanosine monophosphate-mediated relaxation as well. We conclude that using cardiopulmonary bypass to perform lung transplantation greatly exaggerates pulmonary vasomotor dysfunction in the transplanted lung. This dysfunction may contribute to significantly higher pulmonary vascular resistance in the transplanted lung if cardiopulmonary bypass is used.

Acetylcholine↗
PubMed1996

Inhibition of lung tumor cell growth in vitro and mouse lung tumor formation by lovastatin.

The HMG-CoA reductase inhibitor, lovastatin (LOV), has been reported to inhibit Ras farnesylation and the growth of Ras-transformed cells. Mouse lung tumors and human lung adenocarcinomas often have activating mutations in K-ras alleles. In the present study, we determined whether LOV inhibited the growth in vitro of mouse (C10, E9, LM1, LM2, and 82-132) and human (NCl-H125, H292, H441, H460, and H661) nor-transformed and neoplastically transformed lung epithelial cells and whether growth inhibition was related to cell transformation or K-ras activation. LOV inhibited the growth of mouse and human lung cells, but cell sensitivities were unrelated to neoplastic transformation or K-ras mutation. In addition, we evaluated whether LOV could inhibit the formation of lung adenomas induced by the tobacco-specific nitrosamine, 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in mice. LOV was administered in the diet at 0, 40, 160, or 400 ppm ad libitum to male strain A/J mice beginning 1 week after lung tumor induction with NNK (10 mumol/mouse). Mice were euthanized 6 months later. Enumeration of lung tumors revealed that LOV did not affect tumor incidence or size, but significantly reduced tumor multiplicity in a dose-related manner. These data suggest that LOV can suppress the formation of NNK-induced lung tumors, possibly at an early promotional stage. This suppression does not appear to be related to either the presence of mutated K-ras or to changes in K-ras expression.

Animals↗
PubMed1998

Lack of lung hemorrhage in humans after intraoperative transesophageal echocardiography with ultrasound exposure conditions similar to those causing lung hemorrhage in laboratory animals.

This study investigated the phenomenon of ultrasonically induced lung hemorrhage in humans. Multiple experimental laboratories have shown that diagnostic ultrasound exposure can cause hemorrhage in the lungs of laboratory animals. The left lung of 50 patients (6 women, 44 men, mean age 61 years) was observed directly by the surgeon after routine intraoperative transesophageal echocardiography was performed. From manufacturer specifications the maximum derated intensity in the sound field of the system used was 186 W/cm2, the maximum derated rarefactional acoustic pressure was 2.4 MPa, and the maximum mechanical index was 1.3. The lowest frequency used was 3.5 MHz. This exposure exceeds the threshold found for surface lung hemorrhage seen on gross observation of laboratory animals. No hemorrhage was noted on any lung surface by the surgeon on gross observation. We conclude that clinical transesophageal echocardiography, even at field levels a little greater than the reported thresholds for lung hemorrhage in laboratory animals, did not cause surface lung hemorrhage apparent on gross observation. These negative results support the conclusion that the human lung is not markedly more sensitive to ultrasound exposure than that of other mammals.

Adult↗
PubMed1999

Combined use of prostacyclin and higher perfusate temperatures further enhances the superior lung preservation by Celsior solution in the isolated rat lung.

BACKGROUND: The poor tolerance of the lung to ischemia and reperfusion (IR) still represents one of the limitations in clinically successful lung transplantation. Modified Euro-Collins (EC) is routinely used in lung preservation, but alternative solutions have been developed for improvement of pulmonary preservation. Celsior is an extracellular solution that has significantly reduced the IR-induced pulmonary damage in animal studies. So far, no extensive experimental studies exist concerning the influence of Celsior on pulmonary gas exchange following IR. METHODS: In an extracorporeal rat lung model 10 lungs, each, were preserved with Celsior (CE) and Celsior/prostacyclin (CEPC, 6 microg/100 ml) at 4 degrees and 15 degrees C, each, and compared to low-potassium Euro-Collins (EC-40, 40 mmol/liter potassium). After 2 hours of ischemia lungs were reventilated and reperfused using a roller pump. Oxygenation in terms of oxygen partial tension in the left atrial effluent, pulmonary vascular resistance (PVR), peak inspiratory pressure, and wet/dry ratio were monitored for 50 minutes. Furthermore, edema formation was evaluated by light microscopy. Statistical analysis was performed using ANOVA models. RESULTS: Compared to the EC-40 group, oxygenation was increased and amount of edema was reduced in most Celsior-preserved organs (p<0.032) with exception of the CEPC group at 4 degrees C (p = 0.06). Additional application of prostacyclin did not have any significant effect on oxygenation in the Celsior group. However, after temperature elevation of the CEPC perfusate to 15 degrees C, a superior partial tension of oxygen was observed (p<0.023) in contrast to the 4 degrees C groups CE and CEPC. The lowest PVR was found in the CE 4 degrees C group (p<0.02). CONCLUSIONS: Celsior provides better lung preservation than EC-40 solution. Application of prostacyclin at higher perfusate temperatures results in additional functional improvement. In vivo experiments and ultrastructural analysis are warranted for further evaluation of Celsior in lung preservation.

Animals↗
PubMed2005

Epidural block does not worsen oxygenation during one-lung ventilation for lung resections under isoflurane/nitrous oxide anaesthesia.

BACKGROUND AND OBJECTIVES: The aim of this prospective, randomized, controlled clinical study was to evaluate the effects of thoracic epidural anaesthesia combined with isoflurane/nitrous oxide anaesthesia on intraoperative oxygenation during one-lung ventilation for lung resections. METHODS: Forty patients were randomly allocated to receive general anaesthesia maintained with isoflurane/nitrous oxide (group General, n = 20) or the same anaesthetic combined with thoracic epidural anaesthesia (group Integrated, n = 20). All patients were mechanically ventilated with the same settings (FiO2 = 0.5; VT = 9 mL kg(-1); inspiratory: expiratory time = 1:1; inspiratory pause = 10%). Effects on oxygenation were evaluated by determining the changes in PaO2/FiO2 ratio at 10, 30, 45 and 60 min of one-lung ventilation as compared to values obtained after induction of anaesthesia (supine, two-lung ventilation). RESULTS: The PaO2/FiO2 ratio was decreased in both groups during one-lung ventilation until the end of surgery. No differences were found at any observation time between the groups. Ventilation with 100% oxygen because of SpO2 decrease <92% was required in nine patients of group General (45%) and in eight patients of group Integrated (40%) (P = 0.64). Manual re-inflation of the operated lung was required in one patient of group General only (P = 0.99). Heart rate was lower in group Integrated than in group General throughout the study. No differences between the two groups in mean arterial pressure were observed. CONCLUSIONS: Adding a thoracic epidural block to isoflurane/nitrous oxide anaesthesia during one-lung ventilation for lung resections does not result in clinically relevant detrimental effects on intraoperative oxygenation.

Anesthesia, Epidural↗
PubMed1999

Measurement of lung density by photon transmission for monitoring intravascular and extravascular fluid volume changes in the lungs.

Left ventricular (LV) heart failure increases pulmonary blood volume (PBV) and interstitial fluid volume. Continuous measurements of lung density may be a simple non-invasive method for monitoring of the LV function as the lung density should reflect the changes in the PBV and extravascular lung water. The purpose of the study was to optimize transmission measurements of the lung with a gamma camera and a planar source. Another aim was to assess the possibility of transmission monitoring in normal subjects at rest and during exercise and to compare the results with simultaneous measurements of PBV changes. Transmission measurements were made in a water-filled phantom containing lungs of different density. A gamma camera and a planar 57Co source were used. The coefficient of variation in density determination owing to counting statistics in a lung area was calculated for different energy windows, acquisition times and collimation. Dynamic measurements in normal subjects were carried out in a sitting and a supine position at rest and during exercise. Pulmonary blood volume was monitored simultaneously using 99mTc-labelled red blood cells and the registered blood pool activity was corrected for attenuation. Highest precision in relative density determination was obtained with large energy window and uncollimated source. A precision of 1.0% was obtained with 1 min measuring time. About 10% change in transmission corresponding to a 15% change in density was observed during exercise. Changes in blood pool and lung density covariated. We conclude that lung density changes can be monitored with a high degree of statistical precision in a few minutes and with a low radiation dose of radiation using a gamma camera and a planar source.

Blood Volume↗
PubMed2001

Topographic analysis of K- ras mutations in histologically normal lung tissues and tumours of lung cancer patients.

Mutations in the K- ras gene are very common in lung tumours and are implicated in the development of lung cancer, but the timing of their occurrence remains poorly understood. We investigated K- ras mutations in cell samples microdissected by laser capture microscopy at multiple sites from lung tissue sections representing tumour tissue and matched histologically normal tissue obtained from 48 lung cancer patients. K- ras mutations were detected in cell samples from 10 of 38 (26.3%) lung adenocarcinomas and in none of the histologically normal or tumour cell samples taken from 10 lung squamous cell carcinomas. Of the K- ras mutation-positive adenocarcinomas, in 4 cases a mutation was found in only the tumour tissue, in 1 case a mutation was found only in the histologically normal tissue, and in 5 cases mutations were found in both the tumour tissue and histologically normal tissue. Among these 5 cases, 2 had identical mutations in both the tumour tissue and histologically normal tissue, 2 had 1 mutation in the tumour tissue and 2 mutations in the histologically normal tissue, 1 of which was identical to the mutation found in the tumour, and 1 case had 2 codon 12 mutations in tumour tissue and 2 mutations, in codons 9 and 11, in histologically normal tissue. These results showed that K- ras mutations are frequent in histologically normal cells taken from outside lung adenocarcinomas and suggest that some of these mutations may represent early events which could pave the way of lung carcinogenesis.

Adenocarcinoma↗
PubMed1991

Mediation of lung metastasis of murine melanomas by a lung-specific endothelial cell adhesion molecule.

Organ-specific adhesion molecules expressed by vascular endothelial cells have been implicated in the arrest of blood-borne cancer cells in selective, secondary sites. A lung-specific endothelial cell adhesion molecule (Lu-ECAM-1) localized on endothelia of distinct branches of lung blood vessels has been purified by immunoaffinity chromatography from detergent extracts of lung matrix-modulated endothelial cells using monoclonal antibody (mAb) 6D3. It has a molecular mass of 90 kDa and promotes the selective attachment of lung-metastatic B16 melanoma cells. Corresponding with their metastatic performance, B16-F10 tumor cells selected for higher lung colonization bind to Lu-ECAM-1 in significantly higher numbers than their low lung metastatic counterpart B16-F0. Binding of B16-F0 and B16-F10 is reduced with mAb 6D3 to slightly lower levels than B16-F0 bound to Lu-ECAM-1. mAb 6D3 injected into C57BL/6 mice 1 hr prior to an i.v. challenge with B16-F10 causes a 90% reduction in the number of lung colonies compared with animals injected with control mAb (6D8 or 3C6). Lu-ECAM-1 neither binds nor effects metastasis of other lung-colonizing tumor cells (e.g., KLN205). Thus, site-specific metastasis of tumor cells is regulated by similar mechanisms as the homing of lymphocytes--namely, by the ability of blood-borne cancer cells to recognize and adhere to distinct endothelial cell adhesion molecules.

Animals↗
PubMedDate not supplied

Redox regulation of lung development and perinatal lung epithelial function.

Throughout gestation, low oxygen tensions are a dominant feature of the fetal environment and so may be important in sustaining a normal pattern of lung morphogenesis until the moment of birth. As breathing begins, the equilibration of the lung lumen to postnatal PO2 evokes a series of physiologic and morphogenic maturation events that are partially reversible by hypoxia. In this review, we discuss the experimental evidence that fetal and perinatal oxygen tensions differently influence lung morphogenesis through oxygen- and redox-responsive signaling pathways and identify five loci at which this regulation may occur: (I) proliferation of undifferentiated lung mesenchyme as governed by hypoxia-regulated transcription factors (HIF-1alpha, C/EBPbeta); (II) transient production of reactive oxygen species (ROS) and nuclear oxidation of the perinatal lung epithelium; (III) nuclear transport and oxidation of thioredoxin in hand with the acute activation of nuclear factor- kappaB (NF-kappaB); (IV) ROS-evoked chronic rise in intracellular glutathione and thioredoxin redox buffering capacity; and (V) NF-kappaB-dependent increase in transepithelial Na+ transport and lung lumenal fluid clearance. Although not exhaustive, this analysis leads us to the conclusion that redox events that occur in the lung during gestation, parturition, and the early neonatal period may dramatically influence the expression of genes and physiological events that are crucial to the successful transition from fetal to postnatal lung maturation.

Animals↗
PubMed2004

Lung cancer and internal lung doses among plutonium workers at the Rocky Flats Plant: a case-control study.

The authors conducted a nested case-control study of the association between lung cancer mortality and cumulative internal lung doses among a cohort of workers employed at the Rocky Flats Plant in Colorado from 1951 to 1989. Cases (n = 180) were individually matched with controls (n = 720) on age, sex, and birth year. Annual doses to the lung from plutonium, americium, and uranium isotopes were calculated for each worker with an internal dosimetry model. Lung cancer risk was elevated among workers with cumulative internal lung doses of more than 400 mSv in several different analytical models. The dose-response relation was not consistent at high doses. Restricting analysis to those employed for 15-25 years produced a statistically significant linear trend with dose (chi-square = 67.2, p < 0.001), suggesting a strong healthy worker survivor effect. The association between age at first internal lung dose and lung cancer mortality was statistically significant (odds ratio = 1.05, 95% confidence interval: 1.01, 1.10). No associations were found between lung cancer mortality and cumulative external penetrating radiation dose or cumulative exposures to asbestos, beryllium, hexavalent chromium, or nickel.

Adult↗
PubMed2000

Hypermethylation of the p16 (Ink4a) promoter in B6C3F1 mouse primary lung adenocarcinomas and mouse lung cell lines.

Primary lung tumors from B6C3F1 mice and mouse lung cell lines were examined to investigate the role of transcriptional silencing of the p16 (Ink4a) tumor suppressor gene by DNA hypermethylation during mouse lung carcinogenesis. Hypermethylation (>/=50% methylation at two or more of the CpG sites examined) of the p16 (Ink4a) promoter region was detected in DNA from 12 of 17 (70%) of the B6C3F1 primary mouse lung adenocarcinomas examined, whereas hypermethylation was not detected in normal B6C3F1, C57BL/6 and C3H/He mouse lung tissues. Immunohistochemistry performed on the B6C3F1 lung adenocarcinomas revealed heterogeneous expression of the p16 protein within and among the tumors. Laser capture microdissection was employed to collect cells from immunostained sections of four tumors displaying areas of relatively high and low p16 expression. The methylation status of the microdissected samples was assessed by sodium bisulfite genomic sequencing. The pattern of p16 expression correlated inversely with the DNA methylation pattern at promoter CpG sites in nine of 11 (82%) of the microdissected areas displaying variable p16 expression. To provide further evidence that hypermethylation is involved in the loss of p16 (Ink4a) gene expression, three mouse lung tumor cell lines (C10, sp6c and CMT64) displaying complete methylation at seven promoter CpG sites and no p16 (Ink4a) expression were treated with the demethylating agent, 5-aza-2'-deoxycytidine. Re-expression of p16 (Ink4a) and partial demethylation of the p16 (Ink4a) promoter were observed in two cell lines (C10 and sp6c) following treatment. These are the first reported studies to provide strong evidence that DNA methylation is a mechanism for p16 inactivation in mouse lung tumors.

Adenocarcinoma↗
PubMed1999

A case of long-term survival with stage IV small cell lung cancer and early-stage central-type squamous cell lung cancer treated by photodynamic therapy.

The present report is on a 67-year-old man with stage IV small cell lung cancer and early-stage centrally located squamous cell cancer of the lung. He was diagnosed as small cell lung cancer with multiple metastasis to the ipsilateral lung and was found to have a central-type early-stage squamous cell cancer by bronchoscope. After obtaining a complete response to the small cell lung cancer with chemotherapy and radiotherapy, photodynamic therapy was applied to the squamous cell carcinoma, resulting in complete disappearance of the tumor. Recurrence of small cell cancer occurred at the ipsilateral lung and this patient died of small cell cancer 8 years after initiation of treatment. Post mortem examination confirmed complete disappearance of squamous cell cancer treated by photodynamic therapy. This is a rare case of long-term survival with stage IV small cell lung cancer and early-stage central-type squamous cell lung cancer successfully treated by photodynamic therapy.

Aged↗
PubMed2001

Attenuation of lung inflammation by adrenergic agonists in murine acute lung injury.

BACKGROUND: Acute lung injury leading to a systemic inflammatory response greatly increases mortality in critically ill patients. Cardiovascular management of these patients frequently involves beta-adrenergic agonists. These agents may alter the inflammatory response. Therefore, the authors tested the hypothesis that beta-adrenergic agonists alter the pulmonary inflammatory response during acute lung injury in mice. METHODS: Five-week-old CD-1 mice received continuous infusions of 10 microg x kg(-1) x min(-1) dobutamine, 6 microg x kg(-1) x min(-1) dopexamine, or vehicle via intraperitoneal mini osmotic pumps, followed immediately by intratracheal instillation of approximately 2 microg/kg endotoxin (or phosphate-buffered saline control). Six hours later the mice were killed, and lung lavage was performed. Interleukin-6 and -10 concentrations in lung homogenates were measured using enzyme-linked immunosorbent assay. Interleukin-6 and macrophage inflammatory protein-2 mRNA was measured using reverse-transcription polymerase chain reaction. RESULTS: Interleukin-6 protein and mRNA significantly increased after intratracheal endotoxin (P < 0.001), and the fraction of neutrophils in lung lavage fluid increased in endotoxin-treated (41 +/- 25%) versus control mice (2 +/- 4%, P < 0.05). Treatment of endotoxic mice with dobutamine significantly decreased interleukin-6 protein (P < 0.05) and mRNA (P < 0.05) expression. Dopexamine had similar but less pronounced effects. Dobutamine decreased interleukin-10 expression, whereas dopexamine did not. In endotoxemic mice, both dobutamine and dopexamine decreased induction of macrophage inflammatory protein-2 mRNA (P < 0.05) and reduced the fraction of neutrophils in lung lavage fluid (P < 0.05). CONCLUSIONS: In endotoxin-induced acute lung injury, beta-adrenergic agonists can significantly decrease proinflammatory cytokine expression, decrease induction of chemokine mRNA, and decrease the resultant neutrophil infiltrate in the lung.

Acute Disease↗
PubMed2002

Does hypertension increase mortality risk from lung cancer? A prospective cohort study on smoking, hypertension and lung cancer risk among Korean men.

OBJECTIVE: To examine the effects of hypertension on lung cancer prospectively and to determine the interactive effect of hypertension and smoking on lung cancer risk. DESIGN: A prospective cohort study. PARTICIPANTS: The cohort comprised 452,645 Korean men, aged 35-64 years, who received health insurance from the Korea Medical Insurance Corporation and who had biennial medical evaluations in 1992 and 1994. METHODS: Multivariate Cox proportional hazard models were tested, controlling for age, smoking status, exercise, body mass index, alcohol use, diabetes and serum cholesterol concentration. MAIN OUTCOME MEASURE: Deaths from lung cancer. RESULTS: At baseline, 261 080 persons (58.3%) were identified as current cigarette smokers. Between 1995 and 1999, 883 deaths from lung cancer (44.8/100,000 person-years) occurred. An initial finding indicated that hypertension increased the mortality risk of lung cancer [risk ratio (RR) 1.3, 95% confidence interval (CI) 1.1-1.5]. However, after stratification for smoking status, the risk ratio was increased only for current smokers (RR 1.4, 95% CI 1.2-1.6). When the interaction term was included in the multivariate model, there was a significant interactive effect of hypertension with current smoking (RR 1.8, 95% CI 1.0-3.1) on the risk of death from lung cancer, whereas the effect of hypertension itself did not attain significance. CONCLUSION: Hypertension was not an independent risk factor in lung cancer-related deaths, but it increased the modest risk of lung cancer death among current smokers.

Adult↗