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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cigarette smoke can inactivate the alpha-1-proteinase inhibitor (alpha 1PI) by oxidative mechanisms and thus predisposes to the development of pulmonary emphysema. There are differences between the whole smoke and gas phase acting as alpha 1PI inactivators in vitro which suggests that the whole smoke is less oxidizing than the gas phase. Also studies on alpha 1PI oxidative inactivation in the lung of cigarette smokers gave controversial results. The reductive properties of cigarette tar which contains most of smoke nicotine may be some explanation of it. Therefore in this study we have investigated the effect of nicotine (0.4 mumol/l to 4 mmol/l) on the oxidative inactivation of human alpha 1PI by phorbol myristate acetate-activated polymorphonuclear leukocytes (PMNL), chloramine-T (15 mumol/l), hydrogen peroxide (15 mmol/l) and the superoxide radical (O2-.) generating system-xanthine (0.2 mmol/l)-xanthine oxidase (80 U/l). Nicotine at concentrations of greater than 40 mumol/l protected alpha 1PI from stimulated PMNL. The preincubation of PMNL with these concentrations of nicotine did not diminish their ability to inactivate alpha 1PI after stimulation. Nicotine (above 0.4 mumol/l) also protected alpha 1PI from chloramine-T but not from H2O2. The inhibition of O2-.-mediated alpha 1PI inactivation by nicotine was low and was observed only at a concentration of 4 mmol/l. This nicotine concentration did not affect xanthine oxidase activity. It is suggested that cigarettes with low nicotine contents can cause greater oxidative lung injury than their high nicotine counterparts and be a greater risk factor for the development of lung emphysema.
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PMID:Nicotine inhibits alpha-1-proteinase inhibitor inactivation by oxidants derived from human polymorphonuclear leukocytes. 216 36

Human polymorphonuclear leukocytes (PMNL) which are a potential source of proteolytic enzymes and reactive oxidant species contribute to the development of pulmonary emphysema in cigarette smokers. We found that nicotine at concentrations that occur in smokers' plasma enhances human PMNL chemotactic response to zymosan-activated serum (ZAS) and n-formyl-methionyl-leucyl-phenylalanine (FMLP). Maximal increase in chemotactic migration was at nicotine concentration 1 mumol/l. Higher concentrations, above 0.1 mmol/l inhibited PMNL chemotactic response and spontaneous migration. Nicotine also enhanced PMNL influx to the place of inflammation developed in the mouse pleural cavity after injection of ZAS. The number of PMNL found in the pleural cavity was 1.9-fold higher (p less than 0.001, n = 5) when animals were pretreated with 0.15 mg of nicotine. However, this drug itself (concentrations of 0.1 mumol/l to 10 mmol/l) had weak chemotactic activity for PMNL. It seems that the stimulatory action of nicotine on PMNL chemotaxis may be partly responsible for increased PMNL numbers in the lower airways of cigarette smokers and following formation of the elastase/antielastase imbalance in lung tissue.
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PMID:Nicotine increases human polymorphonuclear leukocytes chemotactic response--a possible additional mechanism of lung injury in cigarette smokers. 239 38

Despite major changes in the patterns of cigarette consumption in the United States in the last two decades, cigarette smoking remains a widespread practice. Many studies show a strong association between cigarette smoking and chronic obstructive lung disease, but only recently have mechanisms been elucidated to explain this association, particularly in the case of emphysema. The exact mechanism of chronic bronchitis is less well defined. The mortality rate for lung cancer continues to increase in this country, particularly among women. Compelling evidence associates lung cancer with cigarette smoking, although animal models have not been very successful. Recently, concern has been raised about the effects of passive smoking. There are substantial data available to suggest that passive smoking results in pulmonary infections and abnormal pulmonary function in children of smokers. The data are less clear-cut for pulmonary functional impairment in adults and for lung cancer in the spouses of smokers. Although the concept of "safer" cigarettes has been widely accepted by the American public, these cigarettes may not be as safe as is widely assumed. Clearly, they are far inferior to total smoking cessation. Nevertheless, smoking cessation remains difficult for many Americans, despite a number of methods that have been used to help smokers quit. Nicotine chewing gum, which has recently become available for use in the United States, has shown some efficacy in helping well-motivated, nicotine-dependent smokers quit smoking. Although some inroads have been made into the occurrence of smoking related diseases in the United States, many unnecessary deaths continue to occur.
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PMID:Cigarette smoking and lung disease. 351 99

Neutrophils contribute to chronic bronchitis and pulmonary emphysema associated with cigarette smoking. Nicotine was found to be chemotactic for human neutrophils but not monocytes, with a peak activity at approximately 31 micromolar. In lower concentrations (comparable to those in smokers' plasma), nicotine enhanced the response of neutrophils to two chemotactic peptides. In contrast to most other chemoattractants for neutrophils, however, nicotine did not affect degranulation or superoxide production. Nicotine thus may promote inflammation and consequent lung injury in smokers.
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PMID:Nicotine is chemotactic for neutrophils and enhances neutrophil responsiveness to chemotactic peptides. 631 17

Decreased deformability of neutrophils exposed to cigarette smoke is considered a determinant of neutrophil sequestration within the pulmonary microvasculature, which may be a risk for the development of pulmonary emphysema. In this study we examined the effect of nicotine, a major cigarette component, on the reduction in neutrophil deformability, measured as cell filterability, after exposed to cigarette smoke. Neutrophils were exposed to smoke by incubating them in an aqueous solution of smoke extracts. Filterability of neutrophils was studied by a vertical filtration technique by measuring their ability to pass through a micropore membrane and expressed as membrane resistance. There was a negative relationship between membrane resistance after exposure to whole smoke and the nicotine content of the cigarettes tested. Whole smoke increased the membrane resistance less than gas-phase smoke, from which almost all nicotine had been excluded. Addition of nicotine, glutathione, alpha-tocopherol, thymol, and erythrocytes prevented the increase in membrane resistance following gas-phase smoke exposure. Nicotine also protected against an increase in membrane resistance against the effect of chloramine-T and hydrogen peroxide, but it provided no protection from superoxide radical generated from a xanthine-xanthine oxidase mixture of N-formylmethionylleucylphenylalanine. These results suggest that nicotine prevents the reduction in neutrophil filterability, probably by scavenging oxidants present in the cigarette smoke.
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PMID:Nicotine prevents a reduction in neutrophil filterability induced by cigarette smoke exposure. 792 43

The pathogenesis of emphysema is considered to be an imbalance of protease and antiprotease activity in the lower respiratory tract leading to uninhibited degradation of lung interstitium by elastolytic enzymes. An increased amount of the serine protease neutrophil elastase (NE) is though to play a major role in this degradation. Because the expression of NE is limited to neutrophil precursors in the bone marrow, we hypothesized that nicotine, which is readily absorbed from lung and distributed to tissue, including bone marrow, would increase expression of the NE gene and protein. HL-60 cells, a myeloblast/promyelocyte cell line, were cultured in the presence or absence of 0.06 and 0.8 microM nicotine for 5 d. Both concentrations of nicotine caused a 2.4- to 3.3-fold increase, respectively, in NE gene expression over unstimulated cells, and NE protein increased 4.8- to 3.4-fold over unstimulated cells, respectively, similar to our positive control DMSO. Nicotine did not induce upregulation of the NE gene by initiating cell differentiation. Both low and high nicotine concentrations upregulate the NE gene in HL-60 cells leading to increased NE protein concentration per cell suggesting a pathophysiologic mechanism for emphysema.
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PMID:Nicotine enhances expression of the neutrophil elastase gene and protein in a human myeloblast/promyelocyte cell line. 891 74

The aim of this study was thus to determine whether maternal nicotine exposure during gestation and lactation will result in early emphysema in the lungs of the offspring. Female rats received nicotine subcutaneously during gestation and lactation. Nicotine administration commenced 1 day after mating and lasted until weaning on postnatal day 21. The offspring were exposed to nicotine via the placenta and mother's milk only. Lung tissue of the neonates was collected for analysis on postnatal days 14, 21, 35 and 42. The results show that maternal nicotine exposure had no effect on the total alveolar count (Na), mean alveolar volume (Valv), and airspace wall surface area per unit volume of lung tissue (AWUV) of the 14- and 21-day-old rat pups. However, the Na of the 35- and 42-day-old control animals was higher than that of the nicotine exposed animals. The Valv of the 35- and 42-day-old nicotine exposed rat pups was however larger than that of the control animals, whereas the AWUV of the 35- and 42-day-old control animals were bigger than that of the nicotine-exposed animals of the same age. The scanning electron micrographs showed a gradual flattening of the alveoli. It is therefore concluded that maternal nicotine exposure induced changes at gene level that renders the lungs of the offspring more susceptible to emphysema-like lesions.
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PMID:Maternal nicotine exposure during gestation and lactation of rats induce microscopic emphysema in the offspring. 1209 32

In a previous study, it was shown that maternal nicotine exposure during gestation and lactation interfered with alveolarization and resulted in gradual deterioration of the lung parenchyma, resulting in microscopic emphysema. The aim of this study was thus to investigate the long-term effects of maternal nicotine exposure (1 mg/kg body weight/day, subcutaneous [sc] from the onset of the phase of rapid alveolarization, which occur from postnatal day 4 in rats, on (1) the development of the gas-exchange area of the lungs of the offspring and, (2) whether maternal copper supplementation (1 mg/kg body weight/day, SC) during the same period of time will prevent the effect of maternal nicotine exposure on the development of the neonatal rat lung. Nicotine administration lasted until weaning on postnatal day 21. The day of birth was designated day 0. The offspring were exposed to nicotine via the mother's milk only. The experimental animals received no nicotine or copper after postnatal day 21. The lung tissue of the neonates was collected on postnatal days 14, 21, and 42 and prepared for morphometry. The results obtained show that maternal nicotine exposure had no influence on body weight, chest circumference, crown-rump length, and lung volume, but resulted in bigger alveolar volumes and suppressed alveolarization in the lungs of the offspring. Copper supplementation during this period of lung development reduced the adverse effect of maternal nicotine exposure on neonatal lung development. Even though copper reduced the adverse effects of maternal nicotine exposure during this phase of lung development, it did not prevent the induction of microscopic emphysema.
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PMID:Is maternal copper supplementation during alveolarization protecting the developing rat lung against the adverse effects of maternal nicotine exposure? A morphometric study. 1274 49

THE AIM OF THIS STUDY WAS TO INVESTIGATE THE EFFECT OF MATERNAL NICOTINE EXPOSURE DURING GESTATION AND LACTATION ON: (1) the development of the gas exchange area of the lungs of the offspring; and (2) to determine whether these effects are reversible. Pregnant rats received daily nicotine (subcutaneously 1mgkg(-1) body weight) during gestation and lactation. Nicotine administration started 1 day after mating and lasted until weaning on postnatal day 21. The offspring were exposed to nicotine via the placenta and mother's milk only. The lung tissue of the neonates was collected on postnatal days 14, 21, 35 and 42 and prepared for morphometry. The results obtained show that maternal nicotine exposure resulted in bigger alveolar volumes and suppressed alveolarisation in the lungs of the offspring. Flattening of the alveoli occurred as the animals aged and as a consequence the internal surface area available for gas exchange decreased; a condition that resembles panlobular emphysema. It is unlikely that these effects of maternal nicotine exposure during gestation and lactation on lung development in the offspring was due to a lower birth weight, or a reduction in the period of gestation, or a poor supply of nutrients to the offspring. The changes in the gas-exchange region of the nicotine-exposed rat pups appear to be irreversible.
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PMID:Chronic maternal nicotine exposure during gestation and lactation and the development of the lung parenchyma in the offspring. Response to nicotine withdrawal. 1464 6

A nationwide survey of 776 U.S. residents, divided approximately equally between teenagers and adults, smokers and nonsmokers, assessed public understanding of the illnesses caused by smoking. When respondents were asked what illnesses are caused by smoking, lung cancer was the only illness that could be identified by a clear majority of respondents. Roughly half mentioned emphysema. A much smaller percentage of respondents were able to mention any cardiovascular disease or any kind of cancer other than lung cancer. People also underestimated the death rate from lung cancer and overestimated survival duration. Only a minority realized that emphysema is incurable. Large portions of the sample said they knew only a little about the pain and suffering experienced by individuals with these illnesses. The results demonstrated that even though people recognize that smoking can lead to adverse health consequences, they do not have even a basic understanding of the nature and severity of these consequences.
Nicotine Tob Res 2004 Apr
PMID:Public understanding of the illnesses caused by cigarette smoking. 1520 8


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