Chronic upper lobe cavitary lung disease may be caused by infections, emphysema, cystic fibrosis, lung cancer, sarcoidosis and rheumatologic syndromes. The diagnostic evaluation includes a complete history, a physical examination, a chest radiograph, and sputum examination and culture. In some cases, computed tomographic scanning and biopsy are required.

Adult↗

PubMed1990

In vivo interleukin-2 activated sheep lung lymph lymphocytes increase ovine vascular endothelial permeability by non-lytic mechanisms.

Therapeutic doses of recombinant interleukin-2 (rIL-2) often result in systemic toxicity consistent with increased vascular permeability. rIL-2 activated lymphocytes (IALs) may produce endothelial dysfunction and have cytolytic potential. However, much of the data on IAL cytotoxicity comes from the use of in vitro activated IALs. Alternatively, rIL-2 may enhance permeability directly or via release of various cytokines by host effector cells. The cytotoxicity of in vivo activated lung lymph lymphocytes has been studied in an ovine model of rIL-2 toxicity. The in vivo IALs had no significant endothelial cytolysis at effector to target ratios of 100:1. However, the in vivo IALs increased endothelial monolayer permeability to albumin, dependent on the concentration of IALs. rIL-2 induced no endothelial cytolysis or permeability alterations at doses of 10(5) and 2 x 10(5) U/ml, respectively. These findings suggest that the acute endothelial dysfunction characteristic of the vascular leak syndrome is not due to rIL-2 directly, but is mediated by in vivo IALs via non-cytolytic mechanisms and/or the release of secondary cytokines in response to rIL-2.

Albumins↗

PubMed1990

Pulmonary hypertensive response to foreign body microemboli.

Pulmonary hypertension and foreign body granulomas are recognized sequelae of chronic intravenous drug abuse. We have recently described the development of transient pulmonary hypertension and increased permeability pulmonary edema after the intravenous injection of crushed, suspended pentazocine tablets in both humans and dogs. To determine the role of vasoactive substances in the development of this transient pulmonary hypertension, we measured pulmonary hemodynamics and accumulation of arachidonic acid metabolites in dogs during the infusion of indomethacin, a cyclooxygenase inhibitor, diethylcarbamazine (DEC), a lipoxygenase inhibitor, and FPL 55712, a receptor antagonist for leukotriene C4/D4 (LTC4/D4). Following the intravenous administration of crushed, suspended pentazocine tablets (3-4 mg/kg of body weight), mean pulmonary artery pressure increased from 14 +/- 2 mmHg to 30 +/- 6 mmHg (p less than 0.05) at 60 secs with a concomitant increase in plasma concentrations of 6-keto-PGF1 alpha from 187 +/- 92 pg/ml to 732 +/- 104 pg/ml and thromboxane B2 from 206 +/- 83 pg/ml to 1362 +/- 117 pg/ml (both p less than 0.05). Indomethacin prevented the increase in both cyclooxygenase metabolites, but had no effect on the pulmonary hypertension. In contrast, DEC had no effect on the increase in cyclooxygenase products, but blocked the pulmonary hypertension. FPL 55712 did not effect either the increase in cyclooxygenase metabolites or the pulmonary hypertension. We conclude that the transient pulmonary hypertension, induced by the intravenous injection of crushed, suspended pentazocine tablets, is not mediated by cyclooxygenase products but may be mediated by lipoxygenase product(s) other than LTC4/D4.

6-Ketoprostaglandin F1 alpha↗

PubMed1990

Relationship between cardiac output and the end-tidal carbon dioxide tension.

STUDY OBJECTIVE: To further define the relationship between cardiac output (CO) and end-tidal carbon dioxide tension (ETCO2) at various levels of systemic flow. DESIGN: Prospective, controlled laboratory investigation. SETTING: Animal laboratory. TYPE OF PARTICIPANTS: Fourteen anesthetized, intubated sheep weighing 23 to 47 kg. INTERVENTIONS: One hundred seventy-two simultaneous measurements of thermodilution CO and ETCO2 were made during controlled arterial hemorrhage. After a 30-minute baseline control period, CO was sampled from approximately 0.6 to more than 8.0 L/min during a 60- to 90-minute period of controlled hemorrhage. MEASUREMENTS: Thermodilution CO; arterial pressure using fluid-filled plastic 14-gauge catheters; ETCO2 using an infrared analyzer. MAIN RESULTS: A plot of CO versus ETCO2 suggested that the relationship was logarithmic rather than linear. Linear regression showed that ETCO2 was significantly related (r = .91; P less than .001) to a logarithmic transformation of the CO. CONCLUSIONS: The relationship between CO and ETCO2 is logarithmic. Decreased presentation of CO2 to the lungs is the major, rate-limiting determinant of the ETCO2 during low flow. As the CO increases during resuscitation from shock or cardiac arrest, respiration becomes the rate-limiting controller of the ETCO2 (after the tissue washout of CO2 has occurred). Under such conditions, the ETCO2 provides useful information about the adequacy of ventilation provided that there is little ventilation/perfusion mismatch.

Animals↗

PubMed1990

"Mechanical" causes of pulmonary edema.

Explore the source record for details and available documents.

Airway Obstruction↗

PubMed1979

P pulmonale in status asthmaticus.

We studied 129 patients during acute, severe asthmatic attacks. Electrocardiograms showed P pulmonale in 49% of patients who had an arterial carbon dioxide tension (PaCo2) greater than or equal to 45 mm Hg and an arterial pH less than or equal to 7.37, whereas P pulmonale was present in only 2.5% of asthmatics who had a PaCO2 less than or equal to 44 mm Hg and a pH greater than or equal to 7.38 (p less than 0.001). P wave and QRS axes were 79 +/- 8 degrees and 80 +/- 20 degrees, respectively, in the presence of P pulmonale. When P pulmonale disappeared, the P wave and QRS axes shifted significantly to the left (p less than 0.001). Electrocardiographic P pulmonale persisted 12 to 60 hr after correction of hypoxemia, hypercapnia, and acidosis. In 7 patients with P pulmonale and respiratory acidosis, cardiac catheterization demonstrated normal artery pressures (PAPs) measured relative to atmospheric pressure. In 12 of these peak inspiratory pulmonary artery transmural pressures (PATPs) were increased. Since increased right heart transumural pressures could result in chamber distention, these data are consistent with the hypothesis that reversible P pulmonale in status asthmaticus is explainable on the basis of markedly negative tidal pleural pressures and increased right heart transmural pressures.

Adolescent↗

PubMed1979

Adult respiratory distress syndrome secondary to diffuse pulmonary blastomycosis.

We have described diffuse pulmonary blastomycosis in a previously healthy 19-year-old man, which resulted in the adult respiratory distress syndrome (ARDS). Physicians must have a high index of suspicion for treatable causes of ARDS, and the use of open lung biopsy for early diagnosis is stressed.

Adult↗

PubMed1979

Increased alveolar epithelial permeability with acid aspiration: the effects of high-dose steroids.

Using the in vivo, liquid-filled dog lung model, we found that aspriation of acid with a pH of 2.5 or less led to increased alveolar epithelial permeability for albumin (molecular weight, 69,000 daltons; molecular radius, 35 a) and exogenously administered, polydispersed dextrans (molecular weight, 150,000 to 170,000 daltons: approximately molecular radius, 100 a). This increased permeability occurred with a large-volume (3 to 5 ml/kg) or small-volume (1 to 1.5 ml/kg) aspirate and with acid nebulization (1 to 1.5 ml/kg). When animals were either pretreated (30 min before aspiration) or post-treated (30 min after aspiration) with 30 mg of methylprednisolone/kg of body weight, there was no improvement in the increased permeability associated with acid aspiration. We conclude that, acutely, steroids have no effect on the increased alveolar epithelial permeability associated with acid aspiration.

Albumins↗

PubMed1979

Effects of acid aspiration on pulmonary alveolar epithelial membrane permeability.

Employing a modification of the in vivo model of a liquid-filled canine lung, we measured the movement of substances of specific sizes (albumin, 69,000 daltons with a molecular radius of 35 A; and dextran with a molecular weight of 150,000 to 170,000 and an approximate molecular radius of 100 A) from the pulmonary capillary blood to the liquid-filled lung. A solution with a specific pH (1.5 to 4.5) was instilled into the left lung of the animals at a dosage of 3 to 5 ml/kg of body weight. For both albumin and dextran with a molecular weight of 150,000 to 170,000, the time for 50 percent equilibration between the specific substance in the blood and the same substance in the pulmonary liquid decreased significantly with instillation of pulmonary liquid with a pH of 1.5 and 2.5 but did not with a pH of 3.5 or above (P less than 0.05). In addition, since histamine has been implicated as a possible humoral mediator leading to increased permeability of alveolar membranes, the levels of histamine were measured in pulmonary liquids and blood in all groups. Levels of histamine in the pulmonary liquid (but not blood) were significantly higher in animals with instillation of liquids with a pH of 1.5 and 2.5 compared to all other groups.

Animals↗

PubMed1978

Bloody pericardial fluid. The value of blood gas measurements.

Clinically notable pericardial effusions developed in three patients with renal failure. Pericardiocentesis showed hemorrhagic fluid, the source of which was not apparent. Simultaneous determinations of PCO2, PO2, and pH values showed a substantial increase in PCO2 levels and decrease in PO2, pH, and bicarbonate levels in the pericardial compared with the intracardial aspirates. This was true when pericardial fluid PCO2, PO2, and pH values were compared with mixed venous samples. Determination of PO2, PCO2, pH, and bicarbonate values in pericardial aspirates may determine the source of the fluid.

Bicarbonates↗

PubMed1978

The effects of endogenous and exogenous histamine on pulmonary alveolar membrane permeability.

The effects of exogenously administered histamine phosphate (0.1 microgram per kg of body weight per min, or 90 microgram per hour) and endogenous histamine released by intravenous injection of 0.5 mg of Compound 48/80 on alveolar membrane permeability to substances of differing molecular weight (60 to 20,000 daltons) were studied using the in vivo saline-filled dog lung model. The half-time, i.e., the time required for 50 per cent equilibration between tracer substances in the blood compared to the saline-filled lung, was measured at baseline for urea, sucrose, and dextrans of varying molecular weight. The half-time decreased significantly for substances as large as 10,000 daltons after histamine infusion, and 20,000 daltons after injection of Compound 48/80. We conclude that histamine can increase alveolar epithelial permeability for substances of low molecular weight.

Animals↗

PubMed1978

The role of leukocytes in ethchlorvynol-induced pulmonary edema.

Intravenous administration of ethchlorvynol (Placidyl) is known to produce noncardiogenic pulmonary edema in animals and humans. Since intrapulmonary sequestration of leukocytes has been observed to occur following injection of ethchlorvynol, we evaluated the role of these elements of the blood in producing pulmonary edema. In vivo studies in dogs showed intrapulmonary trapping of leukocytes, as evidenced by increasing leukocyte differences between blood from the pulmonary artery and arterial blood. In both animals with normal leukocyte counts and those depleted of leukocytes (less than 500 cells per millimeter), pulmonary edema occurred, as evidenced by increased pulmonary water after injection of ethchlorvynol. Preparations of isolated lung perfused with either whole blood or leukocyte-poor plasma had similar gains in weight following injection of ethchlorvynol, in spite of marked differences in leukocyte counts. We conclude that intrapulmonary sequestered leukocytes do not play a role in ethchlorvynol-induced pulmonary edema.

Animals↗

PubMed1978

Deposits of immunoglobulin and complement in the pulmonary tissue of patients with "heroin lung".

Pulmonary tissues from six patients who died with a clinical diagnosis of "heroin lung" (heroin-induced pulmonary edema) were examined with the light microscope and electron microscope. Immunofluorescent microscopic analysis revealed multifocal granular alveolar septal deposits of IgM in all patients, C3 complement in five patients, IgG in four patients, fibrinogen in three patients, and IgA in two patients. IgM, IgG, IgA, and C3 complement were eluted from the lungs of these addicts with citrate buffer with a low pH. No deposition of albumin was found in any of the specimens. These findings are believed to represent the first report of immune complexes in the alveolar capillary membrane in patients with heroin-induced pulmonary edema. Electron-microscopic studies revealed a proteinaceous plasma-like fluid in the alveolar spaces, thereby confirming the heroin induced pulmonary edema. Mechanisms of transport of edematous fluids from alveolar capillaries to alveolar spaces in lungs from heroin addicts are considered.

Adult↗

PubMed1978

Pulmonary ultrastructure of the late aspects of human paraquat poisoning.

The pulmonary ultrastructure of the late aspects of a case of human paraquat poisoning is investigated and compared with normal human pulmonary ultrastructure. Alveoli in the paraquat patient are numerically reduced in comparison to the control. They are filled with edematous proteinaceous plasma-like fluid containing erythrocytes, macrophages, leukocytes, fibroblast-like cells, platelets, and fibrin. These alveoli are lined by granular pneumocytes. Interstitial areas in the paraquat patient are greatly expanded and there are no alveolar septums. Interstitial areas contain proteinaceous plasma-like material, collagen, fibrin, platelets, mature fibroblasts, plasma cells, many leukocytes, numerous erythrocytes, and capillaries. Capillary permeability seems to be enhanced in the paraquat patient either by vesicles forming transendothelial channels or pores or by disruption of endothelial cells.

Adolescent↗