A one-year study of the evolution of elastase-induced emphysema in hamsters

Snider, Gordon L.; Sherter, Carl B.

doi:10.1152/jappl.1977.43.4.721

Cited by 92 publications

(57 citation statements)

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“…As in the present study, an increase in lung volume has been reported in living animals treated with intratracheal elastase (Kaplan et al 1973;Hayes et al 1975;Snider and Sherter 1977;Harkema 1984;Yokoyama et al 1987). However, when elastase was instilled intratracheally to excised lungs no increase in TLC was observed.…”

Section: Discussionsupporting

confidence: 83%

Dose dependency of intratracheal elastase-induced changes in pressure volume curve and morphometry in rat lungs.

Sato

Kato

Takahashi

et al. 1990

Tohoku J. Exp. Med.

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We studied the dose-dependency of the lung pressure-volume curve (n -37) and morphometry (n -30) with intratracheally administered elastase. Four weeks after elastase was instilled at dosages of 20 (EL-20), 40, 80, and 100 U/100 g wt., chord compliance between 50 and 70% of total lung capacity (TLC) (C5o-70) and that between 80 and 100% TLC (C8o-100) Were measured. After a significant initial reduction, the weight of the EL-80 group recovered to the control level, whereas the weight curve of the EL-100 significantly decreased below that of the EL-80. Lung volumes of all the elastase-treated groups were significantly larger than those of control. Air-filled lung volumes monotonously increased when the elastase dose was increased from 20 to 80 U/100 g wt. In contrast lung volume of the EL-100 was significantly lower than that of the EL-80. On the other hand, liquid-filled lung volumes monotonously increased from 20 to 100 U/100 g wt. Cao-ioo was significantly smaller in the EL-100 than in the EL-80. The mean linear intercept increased and alveolar surface area decreased monotonously over the dose range tested. We conclude that there is a critical dose of elastase below which lung volume is increased and above which the increase is suppressed when elastase is administered intratracheally to Wistar rats. pulmonary emphysema ; mean linear intercept ; lung compliance ; alveolar surface area

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Section: Discussionsupporting

confidence: 83%

Dose dependency of intratracheal elastase-induced changes in pressure volume curve and morphometry in rat lungs.

Sato

Kato

Takahashi

et al. 1990

Tohoku J. Exp. Med.

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“…These data corroborate the claim of Fusco et al [4] that emphysema stabilizes at about 40 days. A similar pattern was observed in hamsters after the spraying of papain or pancreatic elastase verifying the significant progression of emphysema between 1 and 2 months after exposure, followed by stabilization of the histologic injury [10]. Other authors have stated that the injury stabilizes in about the third month after the initial exposure to papain [8,9].…”

Section: Commentssupporting

confidence: 73%

Avaliação das alterações morfológicas cardíacas secundárias ao enfisema pulmonar: estudo experimental em ratos

Monteiro

Jatene

Pazetti

et al. 2004

Rev Bras Cir Cardiovasc

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Abstract:Objective: The purpose of this study is to evaluate the occurrence and repercussions of chemically induced pulmonary emphysema and the morphological alterations present in rats' hearts of post-induction and to follow the progression afterwards.Method: Seventy five rats divided into two groups: papain (N=50) and control (N=25), were submitted to intratracheal spraying of papain and saline solution, respectively, and were evaluated. The animals were sacrificed 30, 60, 90, 120 or 180 days post-spraying. Arterial blood gases and cardiac and pulmonary morphometrical analysis were performed.Results: Papain spraying produced alveolar tissue destruction similar to the morphological alterations observed in pulmonary emphysema. The papain group presented mean alveolar diameter higher than controls in all periods evaluated (p<0.05). Right ventricle wall thickness and interventricular septum did not show significant macroscopic alterations until six months after emphysema induction. The right ventricle area presented enlargement 120 days after induction of pulmonary emphysema, with mean area higher than controls at 120 and 180 days (p=0.001). The left ventricle presented significant cavity area decrease 90 days after induction of the pulmonary emphysema, followed by slight wall thickening.Conclusions: The adopted experimental model was efficient to morphologically induce pulmonary emphysema. The presence of pulmonary emphysema did not provoke morphological changes in the right ventricle wall and interventricular septum. The alveolar destruction induced left ventricular hypertrophy and enlargement of the right ventricle.Descriptors: Pulmonary emphysema, chemically induced. Pulmonary emphysema, physiopathology. Papain, pharmacology. Disease models, animal. Heart ventricle, anatomy & histology.Avaliação das alterações morfológicas cardíacas secundárias ao enfisema pulmonar: estudo experimental em ratos Evaluation of the cardiac morphological alterations secondary to the pulmonary emphysema: experimental study in rats 342 MONTEIRO, R ET AL -Evaluation of the cardiac morphological alterations secondary to the pulmonary emphysema: experimental study in rats Braz

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“…1). This phenomenon is well known (Snider and Sherter, 1977) and has raised the possibility that progression of emphysema may relate to the inflammatory process. Hayes and colleagues (Hayes et al, 1975) described a mild infiltration of neutrophils 4 hours after PPE instillation to hamsters, which peaked by 1 day.…”

Section: Discussionmentioning

confidence: 96%

Severity of Elastase-Induced Emphysema Is Decreased in Tumor Necrosis Factor-α and Interleukin-1β Receptor-Deficient Mice

Lucey

Keane

Kuang

et al. 2002

Laboratory Investigation

161

111

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SUMMARY:A single intratracheal dose of porcine pancreatic elastase, which is cleared from the lung by 24 hours, was administered to wild-type, IL-1␤ type 1 receptor-deficient, double TNF-␣ (type 1 and type 2) receptor-deficient, and combined TNF-␣ (type 1 receptor) plus IL-1␤ receptor-deficient mice. The mean linear intercept (Lm) of saline-treated mice was 32(3) m [mean(SE)]. For wild-type elastase-treated mice, Lm was 81(6) m at 21 days versus 52(5) m at 5 days after treatment, indicating that alveolar wall remodeling occurs long after the elastase injury. At 21 days, Lm values were 67(10), 62(3), and 39(5) m in elastase-treated mice deficient in the IL-1␤ receptor, double TNF-␣ receptors, and combined receptors, respectively. The level of apoptosis assessed by a terminal deoxynucleotidyl transferase-catalyzed in situ nick end-labeling assay was increased at 5 days after elastase treatment and was markedly and similarly attenuated in the IL-1␤, the double TNF-␣, and the combined receptor-deficient mice. Our results indicate that inflammatory mediators exacerbate elastase-induced emphysema. We estimate that in the combined TNF-␣ ϩ IL-1␤ receptor-deficient mice, inflammation accounts for about 80% of the emphysema that develops after elastase treatment; decreased apoptosis of lung cells likely contributes to decreased severity of emphysema. (Lab Invest 2002, 82:79 -85). P ulmonary emphysema is defined as abnormal enlargement of respiratory spaces with destruction of the alveolar walls. Experimental evidence supports the concept that alveolar units are damaged when activated macrophages and neutrophils elaborate proteases that degrade elastin and other structural proteins.The proinflammatory cytokines IL-1␤ and TNF-␣ are released during inflammatory reactions induced by infection or injury. These effecter substances have overlapping biologic functions, suggesting that they share some common signal transduction pathways (Dinarello, 1997;Kusano et al, 1998;Ledgerwood et al, 1999;Muegge et al, 1989; O' Neill and Greene, 1998;Stewart and Marsden, 1995).In experimental animals, IL-1␤ stimulates several components of the acute-phase response. The cytokine stimulates the expression of metalloproteinase and other enzymes involved in the degradation of connective tissue proteins (Kusano et al, 1998), and it also stimulates apoptosis (Dinarello, 1998). IL-1␤ utilizes a single signaling receptor to activate two IL-1 receptor-associated kinases (IRAK-1 and IRAK-2), to recruit TNF receptor-associated factor 6 (TRAF6) and activate nuclear factor-B (NF-B) (Cao et al, 1996). Activation of NF-B results in nuclear translocation and alterations in the rate of transcription of certain target genes (Baldwin, 1996;Gilmore, 1999). NF-B also either increases or decreases apoptosis depending on the cell type (Barkett and Gilmore, 1999). IL-1␤ affects gene transcription via several other transacting factors including transcription factor AP-1 proteins and CCAAT-enhancer binding proteins (C/EBP) (Muegge et al, 1989;Osborn et al, 1989).TNF...

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A one-year study of the evolution of elastase-induced emphysema in hamsters

Cited by 92 publications

References 0 publications

Dose dependency of intratracheal elastase-induced changes in pressure volume curve and morphometry in rat lungs.

Dose dependency of intratracheal elastase-induced changes in pressure volume curve and morphometry in rat lungs.

Avaliação das alterações morfológicas cardíacas secundárias ao enfisema pulmonar: estudo experimental em ratos

Severity of Elastase-Induced Emphysema Is Decreased in Tumor Necrosis Factor-α and Interleukin-1β Receptor-Deficient Mice

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