Changes In Lung Weight Research Articles

Long-term effects of pulmonary damage in mice on lung weight, compliance, hydroxyproline content and formation of metastases.

The development of "metastatic" colonies of fibrosarcoma in the lungs of mice after IV injection of a single-cell suspension of tumour cells varied with time after irradiation or administration of bleomycin. Most notably, there was a late radiation-induced enhancement of colony-forming efficiency that coincided with an increase in lung weight and hydroxyproline content and a decrease in compliance. There was no radiation-induced enhancement of "spontaneous" metastases from a mammary carcinoma implanted in the thighs of the animal. The sequence of events after administration of bleomycin was similar to that after irradiation, but the duration of the treatment was different and the temporal relationship between enhanced colony-forming efficiency and changes in lung weight and hydroxyproline content was not as clear cut.

Toxicity of minimal amounts of cadmium to the developing rat lung and pulmonary surfactant

Pregnant rats were injected subcutaneously with 0, 1, 2, 4 or 8 mg cadmium chloride/kg each day during mid-gestation from day 12–15. Dams were sacrified on day 21. The treatment resulted in a dose-related increase in prenatal mortality, and decreases in body weight, lung weight and saturated fatty acid containing lecithin content in the fetus but no change in pulmonary sphingomyelin. Although the lowest dose produced no changes in fetal viability, body weight or lung weight, a significant reduction in the amount of saturated fatty acid containing lecithin occurred. Since saturated fatty acid containing lecithin is a major component of pulmonary surfactant, fetuses from CdCl 2-treated dams may be subject to respiratory distress postnatally.

Effect of Aminophyllin and Dexamethasone on Secretion of Pulmonary Surfactant in Fetal Rabbits

Aminophyllin, dexamethasone, or saline was injected into 27.5-day fetal rabbits 2.5 hr before sacrifice, after which static pressure-volume curves with air were performed. In further similar experiments the lungs were lavaged with physiologic saline which was analysed for total phospholipid content. There were no changes in total lung capacity (TLC) induced with either aminophyllin or dexamethasone. The lungs of fetal rabbits injected with saline retained 44% TLC (+/-3 SE) after deflation to 10 cm H2O trans-pulmonary pressure compared with 48% TLC (+/-3 SE) in those injected with dexamethasone, a difference which was not statistically significant. In contrast, the lungs of fetal rabbits injected with aminophyllin retained 53% TLC (+/-2 SE) after deflation to 10 cm H2O pressure, a significant increase when compared with saline controls (P less than 0.01). There were no changes in lung weight or lung water. These results were interpreted to mean that aminophyllin decreased surface tension and augmented secretion of pulmonary surfactant. This was supported by finding significantly increased total phospholipid recovered in the lung lavage fluid of fetal rabbits injected with aminophyllin, 62 microgram/g dry lung weight (+/-6 SE) compared with 32 microgram/g dry lung weight (+/-3 SE) in saline controls (P less than 0.05). Phospholipid recovered from dexamethasone-injected fetal rabbits was not significantly increased, 38 microgram/g dry lung weight (+/-4 SE).

Pulmonary Pressure-Volume Relationships after Corticotropin (ACTH) and Saline Injections in Fetal Rabbits

ACTH mixed with barium sulfate injected into fetal rabbits on day 24 of a 31-day gestation was associated with increased lung maturity compared with lungs of noninjected controls when assessed by deflation pressure-volume curves and lung weight to body weight ratios measured on day 27. Fetuses injected with saline and barium sulfate also had accelerated (although somewhat less) lung maturation, perhaps from an ACTH-mediated response to stress. The ACTH group LA) maintained the largest lung volumes on deflation, followed by the saline group (B), the ACTH controls (C), and the saline controls (D). Volumes (percentage of total lung capacity) between the two injected groups and their controls (A versus C; B versus D) were significantly different at transthoracic pressures of 15, 10, 7, 4, 0, and -2 cm water (p less than 0.05). Volumes (percentage of total lung capacity) between the ACTH group and the saline group (A versus B) and between the two controls groups (C versus D) were not significantly different. Wet lung weight to body weight ratios were significantly different between the injected groups and their respective controls, between the two injected groups, and between the two control groups.

Effect of hypersensitivity pneumonitis on the pulmonary defense mechanisms of guinea pig lungs.

Many edemagenic and consolidating inflammatory diseases, such as virus pneumonias, of the lung are complicated by bacterial infection. Previous literature has stressed that edema and consolidation may promote bacterial proliferation by interfering with phagocytosis. To test that hypothesis, lung defense mechanisms were studied in guinea pigs with tuberculin-induced hypersensitivity pneumonitis, a noninfectious edemagenic, and consolidating inflammatory disease. Pulmonary bactericidal activity and particle clearance were measured with a mixed aerosol of (32)P-labeled Staphylococcus aureus and(35)S-labeled Proteus mirabilis. Hypersensitivity pneumonitis enhanced the bactericidal activity of the lung but had no effect on particle clearance despite the presence of consolidation and edema. These data indicate that altered host resistance to bacterial infection in acute inflammatory lung diseases can not be attributed to edema, inflammation, consolidation, changes in lung weight, etc., per se and that causes must be sought in functional changes in the bactericidal system of the lung rather than in specific histopathological changes.

Effect of inhaled cigarette smoke on content, release and breakdown of histamine in guinea-pig lung

Daily inhalation of cigarette smoke by guinea pigs for 29 days significantly increased lung weights compared with control animals but did not significantly effect total lung histamine (μg per lung) or 48/80-releasable histamine. However, smoker guinea pigs had significantly reduced lung histamine content when expressed in μg per g lung tissue so that care should be taken when interpreting such data if changes in lung weight occur over periods of such exposures. The in vitro breakdown of histamine by lung tissue was significantly reduced in the smoker group even after compensating for these changes in lung weights.

Experimental lung silicosis. Evolution of functional, biochemical, and morphological changes in the rat.

In 57 silicotic and 44 control rats, functional, biochemical, and histological measurements of the lungs were performed during four months of developing silicosis. Pulmonary silicosis was produced by a single intratracheal injection of 50 mg of quartz dust. Among the earliest changes were a significant decrease in arterial oxygen partial pressure, a decrease in lung compliance, and an increase of thoracic gas volume one month after dusting. These were accompanied by corresponding changes in lung weight, in hydroxyprolfne content, and in the histological appearance of the lungs. Four months after dusting the silicotic rate differed significantly in all measured factors from the controls. The picture of fully developed functional, biochemical, and morphological changes In rat silicosis was identical with that described earlier.

Comparative effects of hyperbaric oxygen and pentylenetetrazol on lung weight and non-protein sulfhydryl content of experimental animals

Rats convulsed by hyperbaric oxygen (OHP) or by pentylenetetrazol (PTZ) suffer consolidative lung damage. This effect and its moderation by pretreatment of the animals with protective compounds were quantitated by measuring lung weight and lung non-protein sulfhydryl (NPSH) content; liver NPSH content was also measured. Changes in lung weight were also examined in mice, guinea pigs, and rabbits treated with these two agents. Rats and mice convulsed by either OHP or PTZ suffered a similar degree of lung damage. This effect was absent when exposures did not lead to onset of convulsive seizures. In contrast, guinea pigs and rabbits convulsed by OHP for similar times sustained considerably less lung damage. PTZ-induced convulsions in these two species did not lead to significant increases in lung weight. Rats convulsed with OHP or PTZ had an identical loss of NPSH (44 %) from lung but much less loss (25 %) from liver. The liver NPSH loss was duplicated by non-convulsive OHP treatment, while lung NPSH content was relatively unaffected by such exposures. Starvation for 18 hr depleted liver NPSH levels but led to no greater loss of this component under OHP. Lung weight increases and lung NPSH loss due to PTZ were prevented by prior administration of compounds, (e.g. 5-hydroxytryptamine), known to prevent effects of OHP. The experimental data were contrasted with the results of clinical experience with human patients. The conclusion was reached that the gross aspects of OHP-induced lung damage in animals are probably attributable to some mechanism other than direct oxidative attack upon pulmonary structures.

Toxic effects of intraperitoneal juglone in rats.

SummaryJuglone, administered ip, was found to produce an accumulation of fluid in the abdominal cavity of rats. That the fluid from the circulatory system was accompanied by proteins was suggested by soft clots that formed in the fluid. Changes in hematocrit, plasma proteins, lung weights, and electrolytes suggested that increased capillary permeability resulted from the irritative properties of juglone.

Pulmonary damage due to high pressure oxygen breathing in rats. I. Lung weight, histological and radiological studies.

SUMMARYChanges in lung weights, histology and bronchographic appearances are recorded in rats subjected to oxygen at 60 p.s.i. (gauge) pressure (OHP). Capillary congestion, progressing to alveolar exudation and haemorrhage, was the earliest observable change. The results failed to support a postulate that lung damage due to oxygen poisoning is primarily an atelectasis due to bronchial obstruction. Positive pressure inflation of lungs immediately post mortem, did not reverse oxygen damage. Heparinisation of rats was also without effect on such damage. Exposure of lung tissue in vitro to 100 p.s.i. (gauge) pressure of oxygen for five hours failed to cause changes similar to those observed for OHP lungs exposed in vivo.

Effects of histamine, 5 hydroxytryptamine and epinephrine on pulmonary hemodynamics with particular reference to arterial and venous segment resistances.

Studies were made of the effects of histamine and 5 hydroxytryptamine (5HT) on arterial and venous segmental resistances in the isolated perfused dog lung. The lung was perfused at constant flow while pressures were measured in the pulmonary artery (PA), left atrium (PV) and in either the pulmonary artery wedge position (PAw) or a small pulmonary vein (PVs). Arterial resistance changes were inferred from changes in the PA-PAw pressure drop, and venous resistance from the PAw-PV pressure gradient. Changes in lung weight were recorded continuously. It was found that histamine usually caused a greater increase of the venous resistance than of the arterial resistance, while 5HT usually increased the arterial resistance more than the venous resistance. When the predominant resistance increase was arterial the lung weight fell, but when there was a sizeable increase of the venous resistance the lung weight rose, presumably as a result of increased capillary blood content. The correlation coefficient between the change in lung weight and the change in venous resistance was + .791. Small pulmonary vein pressures rose after administration of epinephrine, norepinephrine, histamine and 5HT. This result gives further proof of constriction of pulmonary veins by these agents.

Effect of gram-negative endotoxin on pulmonary circulation.

Effects of endotoxin on the pulmonary hemodynamics of dogs and cats have been studied in intact animals, open chest animals with and without control of cardiac output by an extracorporeal venous reservoir—pump system, and in isolated perfused continuously weighed lungs. Pulmonary artery pressure increased without a rise in left atrial pressure in all preparations following the injection of endotoxin. Pulmonary artery wedge and small pulmonary vein pressures uniformly increased. Total pulmonary vascular, pulmonary arterial and pulmonary venous resistances were calculated in five perfused lungs. The absolute increase in pulmonary venous resistance was greater than in the arterial resistance in four of the five studies and was relatively greater in every instance. There was a consistent increase in lung weight associated with these hemodynamic changes. Analysis of the determinants of lung weight changes has provided evidence to support the conclusion that the pulmonary vascular response to endotoxin administration is characterized predominantly by constriction of pulmonary venules and/or small veins.