A model of pulmonary atelectasis in rats: activation of alveolar macrophage and cytokine release

1993 ◽  
Vol 264 (3) ◽  
pp. R610-R614 ◽  
Author(s):  
J. M. Kisala ◽  
A. Ayala ◽  
R. N. Stephan ◽  
I. H. Chaudry
Keyword(s):  
Alveolar Macrophages ◽  
Interleukin 1 ◽  
Small Animal ◽  
Small Animal Model ◽  
Main Stem Bronchus ◽  
Pulmonary Atelectasis ◽  
Infection And Inflammation ◽  
Left Main Stem Bronchus ◽  
The Right ◽  
Necrosis Factor

Although atelectasis frequently occurs after surgery and trauma, and such patients have elevated body temperatures, the mechanism of temperature elevation secondary to atelectasis is unknown. Moreover, a small animal model has not been available to study the pathophysiology of pulmonary atelectasis. The purpose of this study, therefore, was to develop a model of pulmonary atelectasis in rats. Because interleukin-1 (IL-1) and tumor necrosis factor (TNF), both potent pyrogens, are produced by macrophages during infection and inflammation, our aim was also to determine whether alveolar macrophages produce IL-1 or TNF in response to atelectasis. Whole-lung atelectasis was produced in rats by ligating the left main stem bronchus while maintaining ventilation of the right lung. After a 1-h period of atelectasis, alveolar macrophages were harvested from the right and left lungs and incubated for 24 h, and the supernatants were assayed for IL-1 and TNF. Both IL-1 and TNF levels of macrophage cultures from the atelectatic lung were significantly increased compared with the control lung. These results suggest that increased IL-1 or TNF production by alveolar macrophages may be responsible for fever caused by atelectasis.

PULMONARY EMPHYSEMA AND OTHER CARDIORESPIRATORY LESIONS AS PART OF THE MARFAN ABIOTROPHY

PEDIATRICS ◽  
1964 ◽  
Vol 33 (3) ◽  
pp. 356-366
Author(s):  
Robert P. Bolande ◽  
Arthur S. Tucker
Keyword(s):  
Connective Tissue ◽  
Left Atrium ◽  
Pulmonary Emphysema ◽  
Left Lung ◽  
Left Main ◽  
Main Stem Bronchus ◽  
Giant Left Atrium ◽  
Left Main Stem Bronchus ◽  
The Right ◽  
Chronic Pulmonary Emphysema

Seven cases of Marfan's syndrome are reviewed clinically, radiologically, and pathologically. Six of the seven cases showed evidence of pulmonary dysaeration: (a) Two of the cases showed compression of the left main-stem bronchus by a giant left atrium with atelectasis of the left lung and compensatory emphysema of the right lung. (b) Two of the cases showed evidence of diffuse chronic pulmonary emphysema. Three cases had bilateral apical bullae. (c) One of the cases developed pneumothorax. The lungs of the children with the Marfan syndrome show precocious maturation of the elastic stroma of the alveolar septae. The pathogenesis of emphysema is discussed in relationship to the Marfan abiotrophy of connective tissue.

Surfactant treatments alter endogenous surfactant metabolism in rabbit lungs

1990 ◽  
Vol 68 (4) ◽  
pp. 1590-1596 ◽  
Author(s):  
S. B. Oetomo ◽  
J. Lewis ◽  
M. Ikegami ◽  
A. H. Jobe
Keyword(s):  
Lower Lobe ◽  
Left Lower Lobe ◽  
Exogenous Surfactant ◽  
Main Stem Bronchus ◽  
Label Incorporation ◽  
Left Main Stem Bronchus ◽  
The Right ◽  
Surfactant Metabolism

The effect of exogenous surfactant on endogenous surfactant metabolism was evaluated using a single-lobe treatment strategy to compare effects of treated with untreated lung within the same rabbit. Natural rabbit surfactant, Survanta, or 0.45% NaCl was injected into the left main stem bronchus by use of a Swan-Ganz catheter. Radio-labeled palmitic acid was then given by intravascular injection at two times after surfactant treatment, and the ratios of label incorporation and secretion in the left lower lobe to label incorporation and secretion in the right lung were compared. The treatment procedure resulted in a reasonably uniform surfactant distribution and did not disrupt lobar pulmonary blood flow. Natural rabbit surfactant increased incorporation of palmitate into saturated phosphatidylcholine (Sat PC) approximately 2-fold (P less than 0.01), and secretion of labeled Sat PC increased approximately 2.5-fold in the surfactant-treated left lower lobe relative to the right lung (P less than 0.01). Although Survanta did not alter incorporation, it did increase secretion but not to the same extent as rabbit surfactant (P less than 0.01). Alteration of endogenous surfactant Sat PC metabolism in vivo by surfactant treatments was different from that which would have been predicted by previous in vitro studies.

Expiratory flow limitation in dogs with regional changes in lung mechanical properties

1988 ◽  
Vol 64 (1) ◽  
pp. 162-173 ◽  
Author(s):  
S. N. Mink ◽  
H. Greville ◽  
A. Gomez ◽  
J. Eng
Keyword(s):  
Mechanical Properties ◽  
Wave Speed ◽  
Main Stem ◽  
Left Main ◽  
Main Stem Bronchus ◽  
Left Main Stem ◽  
In Series ◽  
Left Main Stem Bronchus ◽  
Expiratory Flow ◽  
The Right

We examined maximum expiratory flow (Vmax) in two canine preparations in which regional changes in lung mechanical properties were produced. In one experiment serial bronchial obstructions were made to determine whether flow-limiting sites (choke points, CP) would occur in series. With the right lung tied off, constrictions were placed at the left lower lobar bronchus (LLL) and left main-stem bronchus. On deflation from total lung capacity, the obstructed LLL and nonobstructed left upper lobe (LUL) emptied into the obstructed left main-stem bronchus. Although a CP common to both lobes was identified at the main-stem obstruction, which limited total Vmax, we questioned whether there was also a CP at the lobar obstruction that fixed LLL flow. In that case the rate of LLL emptying would not be dependent on the presence of the common (i.e., central) CP and thus the flow contribution of the LUL. We found that when the LUL was removed, the LLL increased its rate of emptying. Thus a lobar CP did not fix LLL flow and CP did not occur in series. In a second experiment emphysema was produced in the left lung to reduce lung recoil, whereas the right lung was normal. CP were identified at approximately lobar bronchi of each lung, and the lungs were emptied at different rates. A CP common to both lungs was not identified. Our results indicate that in localized lung disease, if flows from the different regions are high enough, then wave speed is reached in proximal airways, and a CP occurs centrally rather than peripherally. On the other hand, if flows are low, then wave speed is reached peripherally and a CP common to all lung regions does not occur.

Protection against oxygen toxicity by tracheal insufflation of endotoxin: role of Mn SOD and alveolar macrophages

1994 ◽  
Vol 266 (1) ◽  
pp. L38-L45 ◽  
Author(s):  
G. Tang ◽  
J. T. Berg ◽  
J. E. White ◽  
P. D. Lumb ◽  
C. Y. Lee ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Alveolar Macrophages ◽  
Tumor Necrosis ◽  
Manganese Superoxide Dismutase ◽  
Interleukin 1 ◽  
Oxygen Toxicity ◽  
Adult Rats ◽  
Manganese Superoxide ◽  
Tracheal Insufflation ◽  
Necrosis Factor

Endotoxin and the cytokines, tumor necrosis factor and interleukin-1, are known to protect adult rats against O2 toxicity. However, whether the effect of endotoxin is mediated through its direct effect on lung cells or through cytokines is not clear. In this study, we demonstrated that endotoxin at a dosage of 5 micrograms/rat (14-20 micrograms/kg) attenuated O2-induced pulmonary injury and markedly prolonged the survival of rats exposed to 100% O2. Endotoxin was more protective when given by intratracheal insufflation or intravenous injection than by intraperitoneal injection. The endotoxin-induced O2 tolerance was associated with a selective enhancement of pulmonary manganese superoxide dismutase, but not Cu,Zn SOD, mRNA. In addition, depletion of 84% rat alveolar macrophages by liposome-encapsulated dichloromethylene diphosphonate, resulted in a marked reduction (86%) of endotoxin-induced release of tumor necrosis factor into the alveolar space. However, endotoxin was still protective in these alveolar macrophage-depleted animals.

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