The American review of respiratory disease (Am J Respir Crit Care Med )

Publisher: American Thoracic Society; American Lung Association

Description

The AJRCCM focuses on human biology and disease, as well as animal and in vitro studies that contribute to the understanding of pathophysiology and treatment of diseases that affect the respiratory system and critically ill patients.

  • Impact factor
    10.19
  • 5-year impact
    0.00
  • Cited half-life
    0.00
  • Immediacy index
    0.00
  • Eigenfactor
    0.00
  • Article influence
    0.00
  • Website
    American Journal of Respiratory and Critical Care Medicine website
  • Other titles
    American journal of respiratory and critical care medicine, AJRCCM
  • ISSN
    0003-0805
  • OCLC
    29407978
  • Material type
    Periodical, Internet resource
  • Document type
    Journal / Magazine / Newspaper, Internet Resource

Publications in this journal

  • The American review of respiratory disease 05/2014;
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    ABSTRACT: Brain oxygen, CO2 pH and temperature in head injured patients
    The American review of respiratory disease 01/1997; 155:99.
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    ABSTRACT: The accumulation of leukocytes into tissues is a characteristic feature of inflammatory reactions. This process is triggered by chemical signals generated in a tissue in response to an inflammatory stimulus e.g., invading microbes, other foreign organisms, allergens, or damaged tissue cells. The mechanisms involved in neutrophil and eosinophil accumulation in vivo are complex and dependent on an initial interaction between the leukocytes and the microvascular endothelial cells. This response is regulated by the coordinated expression and/or activation of leukocyte and endothelial cell adhesion molecules. The precise mechanisms that control the selective accumulation of eosinophils, as opposed to neutrophils, in certain inflammatory reactions (e.g., in IgE-mediated allergic reactions) remain unclear. This may be explained partly by the generation of eosinophil-specific inflammatory mediators and activation of selective adhesion pathways such as the VLA-4/VCAM-1 interaction. Although the neutrophil and eosinophil have distinct roles in host defense, they have been implicated in the pathogenesis of a number of inflammatory disorders. Thus, a better understanding of the events mediating and regulating neutrophil and eosinophil accumulation in vivo will be of considerable value in the development of therapeutic strategies for inflammatory disease states.
    The American review of respiratory disease 01/1994; 148(6 Pt 2):S60-4.
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    ABSTRACT: Pulmonary function growth rate varies with a child's stage of growth. Since attained pulmonary function reflects the cumulative effects of growth, insults, and repair, rate of growth may be a more sensitive indicator of a child's current pulmonary health status. The sample for analyses included 2,478 white boys and 2,785 white girls followed annually by questionnaire and spirometry. Empirically derived annual growth velocities, peak velocity (Vpk), and age at which peak velocity occurred (Agepk) were determined for height, FVC, FEV1, and FEF25-75 for each child. Mean velocity curves for height, FVC, FEV1, and FEF25-75, stratified by sex and Agepk of height (an indicator for early, middle, or late maturity) were produced as a function of age. The differences between Agepk of FVC, FEV1, and FEF25-75 and Agepk of height (i.e., the lag period) were compared by sex and by the indicator of maturity. Linear regression analyses were performed to investigate associations between Vpk and Agepk of height, as well as between the lag period and Agepk of height. As is generally observed in height growth, there were considerable variations in the age of onset and magnitudes of the adolescent growth spurts of the pulmonary function parameters both between sexes and among children of the same sex. The duration of adolescent growth spurt appeared to be similar for all children, regardless of early, middle, or late maturity. Thus, those who matured earlier had shorter total growth periods than those who matured later. On the other hand, early maturers had greater growth velocities during preadolescence and greater adolescent Vpk than later maturers.(ABSTRACT TRUNCATED AT 250 WORDS)
    The American review of respiratory disease 01/1994; 148(6 Pt 1):1502-8.
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    ABSTRACT: Endothelial damage is a hallmark of acute lung injury. Endothelial mediators may increase pulmonary vascular tone and induce pulmonary arterial muscularization, thereby contributing to the pulmonary hypertension seen with acute lung injury. We measured plasma levels and net pulmonary clearance of endothelin-1, a potent endothelium-derived vasoconstrictor peptide and smooth muscle mitogen, in 26 patients with early acute lung injury, the adult respiratory distress syndrome, and pulmonary hypertension. Nineteen had another data collection at clinical improvement or worsening. Control subjects (n = 25) had no pulmonary hypertension or lung injury. Initial mixed venous and systemic arterial plasma endothelin-1 levels were elevated (4.6 +/- 0.6 SEM and 4.9 +/- 0.6 pg/ml, respectively) as compared with control subjects (0.9 +/- 0.1 and 0.6 +/- 0.1 pg/ml). The systemic arterial/venous endothelin-1 ratio was 1.1 +/- 0.1 (0.7 +/- 0.1 in control subjects), indicating a reduction in normal net pulmonary endothelin-1 clearance. With clinical improvement, as compared with clinical worsening, mean plasma endothelin-1 levels, arterial/venous ratio, and pulmonary arterial pressure fell significantly towards normal. Thus, patients with acute lung injury have marked early increases in circulating plasma endothelin-1 levels, associated with abnormal pulmonary endothelin-1 metabolism. These abnormalities reverse in patients who recover. Through its actions, endothelin-1 could contribute to the pulmonary hypertension seen in acute lung injury.
    The American review of respiratory disease 01/1994; 148(6 Pt 1):1646-50.
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    ABSTRACT: Functional residual capacity (FRC), the only lung volume to be assessed routinely in infants, can be measured using plethysmography or gas dilution. Although it is well recognized that both methods yield similar FRC values in healthy adults, gas dilution techniques have consistently produced lower values in healthy infants when compared with plethysmography. However, interpretation of this difference is difficult since data comparing the different techniques within the same infants have rarely been reported. We performed paired measurements of FRC using an automated open-circuit nitrogen washout technique (FRCN2) and whole-body plethysmography (FRCpleth) in 11 healthy infants with a median age of 12 months (range, 2 to 18 months). The mean (SD) FRC was 21.7 (4.0) ml/kg for the N2 washout and 25.6 (4.9) ml/kg for plethysmography. The mean within-subject difference between FRCN2 and FRCpleth was 3.9 (range, -0.3 to 7.2) ml/kg (p = 0.001). Both N2 washout and plethysmography yielded reproducible results, with the mean of the coefficients of variation (CV) being 3.6 and 3.9%, respectively. The results from these paired measurements support previously reported data from separate populations of infants which suggest that gas dilution techniques consistently yield smaller values for FRC than do those measured by plethysmography.
    The American review of respiratory disease 01/1994; 148(6 Pt 1):1496-501.
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    ABSTRACT: The integrin alpha 4 beta 1 and its counter receptor vascular cell adhesion molecule-1 (VCAM-1) mediate well-described cell-cell interactions that are critical for immune function. However, these receptors also mediate cell-cell interactions that are important for skeletal muscle differentiation. We have found that contrasting transcriptional mechanisms control their patterns of expression in the immune system and in muscle. Recent studies indicate that alpha 4 beta 1 and VCAM-1 are also expressed in a number of developing tissues, implying that these receptors have a general role in facilitating cell-cell interactions during development.
    The American review of respiratory disease 01/1994; 148(6 Pt 2):S43-6.
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    ABSTRACT: Several studies have suggested that the TLC after childhood asthma is increased compared wtih that in healthy subjects. The aim of this study was to assess whether TLC is increased after childhood asthma and whether this is associated with an increased growth of the lung during adolescence. During a mean period of 29 months we studied 53 patients and 106 healthy control subjects who were matched for sex, age, and standing height. The patients had had asthma for a mean period of 10 yr. We found that in asthmatics TLC was increased in both sexes by about 7% predicted compared with that in the matched control subjects. The growth of TLC in ml/yr during adolescence was less in patients; this can be accounted for by a delay in pubertal development. When corrected for the delay in growth of stature, growth of TLC in ml/cm in asthmatics was similar to that found in control subjects. These findings support the hypothesis of a developmental change of enhanced lung growth during childhood asthma; they do not support a mechanism with progressive loss of elastic recoil of the lung.
    The American review of respiratory disease 01/1994; 148(6 Pt 1):1484-9.
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    ABSTRACT: Conventional virgin T cells efficiently and homogeneously recirculate through all secondary lymphoid tissues, but not "extralymphoid" effector sites. In contrast, memory/effector populations are composed of distinct subsets with differential, often tissue-selective, migratory capability to both secondary lymphoid tissues and effector sites. In keeping with these observations, CD45RA(high)/RO(low) virgin T cells in human peripheral blood uniformly express the peripheral lymph node (PLN) homing receptor (HR) L-selectin, and lack the skin-selective HR CLA, whereas among the CD45RA(low)/RO(high) "memory/effector" population, differential expression of these HR yields three predominant subsets: L-selectin+/CLA+, L-selectin+/CLA-, L-selectin-/CLA-. Although these subsets are of approximately equal size in the peripheral blood, the vast majority of T cells obtained from cutaneous chronic inflammatory sites display the L-selectin+/CLA+ phenotype. To investigate the mechanisms responsible for the generation of these memory/effector T-cell subsets, we developed a multiparameter flow cytometric technique that defines a common pathway of postthymic T-cell differentiation in secondary lymphoid tissues: the virgin to memory/effector transition. Our analyses indicate that these HR are differentially regulated during the virgin to memory/effector transition in a tissue-specific fashion. The great majority of memory/effector T cells produced in PLN retain high levels of L-selectin expression, and 50 to 60% upregulate CLA. In contrast, memory/effector T cells produced in appendix and tonsil are generally L-selectin(low), and CLA is upregulated on less than 10% of newly formed memory/effector T cells in appendix and on about 30 to 35% of such cells in tonsil.(ABSTRACT TRUNCATED AT 250 WORDS)
    The American review of respiratory disease 01/1994; 148(6 Pt 2):S47-54.
  • The American review of respiratory disease 01/1994; 150:382.
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    ABSTRACT: Abnormal inspiratory load compensation may be one factor leading to development of obstructive sleep apnea (OSA). Alternatively, abnormalities in ventilatory load compensation may be a consequence of the manifestations of OSA. This investigation was designed to determine if impairment of awake inspiratory load compensation exists in OSA and to determine if abnormalities in this parameter are reversible by nasal CPAP therapy. A new technique for assessment of awake inspiratory load compensation was devised to standardize the degree of ventilatory stimulation applied during load compensation assessment in each subject. This eliminates intersubject differences in degree of ventilatory stimulation during testing, which are inevitable with standard techniques and which have been shown to affect the measurement of load compensation. Inspiratory load compensation was assessed during resting room air ventilation and during steady state CO2 and exercise stimulation titrated to provide similar degrees of ventilatory stimulation in each subject. Impairment of awake inspiratory load compensation was found during all conditions in the patients with moderate to severe OSA studied compared with that in weight-matched control subjects. Normalization of awake inspiratory load compensation was observed after 4 wk of nasal CPAP therapy in five patients. These results indicate that impairment of awake inspiratory load compensation is a reversible consequence rather than a cause of OSA.
    The American review of respiratory disease 01/1994; 148(6 Pt 1):1610-5.
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    ABSTRACT: A multitude of glycoproteins expressed in cellular membranes have been identified by monoclonal antibodies. Besides mediating transient cell/cell contacts, these molecules unequivocally function as receptor structures capable of transmitting signals for cell growth and differentiation. They are the central determinators of local immune responses, and they allow an adjustment of the recirculating immunocompetent cells to their respective local microenvironments. Given that receptor/ligand interactions are characteristic of particular in vivo sites, knowledge of structural and functional features of adhesion receptors can provide new prospects for a more targeted clinical immune intervention.
    The American review of respiratory disease 01/1994; 148(6 Pt 2):S65-9.
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    ABSTRACT: Positive end-expiratory pressure (PEEP) commonly decreases cardiac output. The major cause of this is believed to be decreased venous return due to increased right atrial pressure. We hypothesized that when the lungs were hyperinflated they could also restrict venous return by directly compressing the thoracic vena cavae. We measured the longitudinal distribution of pressure in the thoracic vena cavae of 10 dogs on and off 10 mm Hg PEEP, in the supine (S), prone (P), right lateral (RL), and left lateral decubitus (LL) positions. In the superior vena cava (SVC) both on and off PEEP, and in the inferior vena cava (IVC) off PEEP, pressure fell uniformly from the thoracic inlet to the right atrium. However, in the IVC on PEEP, intravascular pressure fell abruptly by up to 5 mm Hg. This pressure drop occurred in a discrete (1 to 2-cm) segment of the IVC, suggesting a localized increased in extravascular surface pressure. When this pressure inflection was present, changes in right atrial pressure had no effect on pressure in the IVC upstream of the inflection, consistent with a "vascular waterfall." These observations were most prominent in the LL, least common in the RL, and variably present in the P and S positions. Occlusion of the right bronchus intermedius prior to PEEP (preventing right lower, middle, and accessory lobe inflation) prevented the appearance of the pressure inflection during PEEP in the LL but not in the S or P positions. We conclude that PEEP impedes venous return partly by direct compression of the IVC, predominantly in positions in which the IVC is non-dependent.(ABSTRACT TRUNCATED AT 250 WORDS)
    The American review of respiratory disease 01/1994; 148(6 Pt 1):1657-64.
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    ABSTRACT: To investigate the importance of the inflammatory response in acute peripheral airway constriction, we measured peripheral airway responses to calcium chelators and acetylcholine in anesthetized Basenji-Greyhound (BG) dogs before, during, and after chronic corticosteroid treatment. A wedged bronchoscope technique was used to measure peripheral airway resistance before and after aerosol challenge with 4% Na2EDTA or acetylcholine (10 micrograms/ml) in contralateral lungs. After the initial measurements, five BG dogs received long-term treatment with methylprednisolone (2 mg/kg/d, subcutaneously), and five dogs were not treated and served as controls. Four weeks of methylprednisolone treatment almost totally abolished responses to Na2EDTA, but responses to acetylcholine did not change significantly. After discontinuing corticosteroid therapy, responses to Na2EDTA returned to levels found before corticosteroid treatment; responses to acetylcholine were significantly enhanced. We conclude that chronic corticosteroid treatment reduces acute response to calcium chelators and that withdrawal of corticosteroid therapy is associated with enhanced cholinergic responsiveness.
    The American review of respiratory disease 01/1994; 148(6 Pt 1):1581-5.
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    ABSTRACT: The integrin receptors on leukocytes are transiently activated by "triggering" molecules that may be other leukocyte membrane structures such as the T-cell receptor complex or small molecules such as PAF, which bind to their own specific receptors. This "inside out" signaling is essential for high affinity integrin/ligand pairing. In the example of LFA-1/ICAM-1, binding is positively supported by Mg2+ but negatively supported by Ca2+. How specific divalent cations affect receptor activation and subsequent ligand binding has still to be fully understood. However, the fact that activation can be mimicked from outside the cell via special anti-LFA-1 monoclonal antibodies such as MEM-83 suggests that activated integrins undergo conformational changes. Further alteration occurs as a result of the interaction of integrin with ligand, and the resulting novel epitopes are named "ligand-induced binding sites." For a brief period of time the integrin/ligand complex is able to transmit signals from "outside in." The transient activation of leukocyte integrins determines that cell-cell adhesion will be short lived and serves the purpose of permitting recycling of effector cells with their targets.
    The American review of respiratory disease 01/1994; 148(6 Pt 2):S55-9.
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    ABSTRACT: Recent studies suggest that cytokines such as recombinant interferon-gamma (rIFN-gamma) may play a role in the treatment of certain respiratory conditions associated with infection and inflammation. This study was designed to determine if rIFN-gamma could be delivered effectively in a group of normal human volunteers. The effectiveness of the inhaled delivery system was demonstrated by the recovery of free IFN-gamma in bronchoalveolar lavage (BAL) fluid and macrophage (M phi) expression of IP-10, an IFN-gamma-inducible molecule, after therapy but not at baseline. IL-1 beta, but not IL-8, gene transcripts also showed evidence for up-regulation after rIFN-gamma therapy. Compared with baseline, inhaled rIFN-gamma did not significantly alter clinical symptom scores, spirometry, morning peak expiratory flow rate (PEFR), or the response to methacholine. Of interest, the evening PEFR increased significantly (p = 0.02), from 568 +/- 36 L/min at baseline to 584 +/- 33 L/min after inhaled rIFN-gamma. Although there was no significant change in total white cell count in BAL fluid, the cellular composition did demonstrate a significant decrease in percentage of alveolar M phi (p = 0.02) and an increase in percentage of lymphocytes (p = 0.02) after rIFN-gamma. There were no histologic differences seen in bronchial biopsy specimens, and there was no evidence for up-regulation of ICAM-1 or HLA-DR expression after rIFN-gamma. We conclude that, in normal persons, rIFN-gamma can be effectively delivered by inhalation. Future trials using inhaled rIFN-gamma appear to be warranted for certain pulmonary diseases.
    The American review of respiratory disease 01/1994; 148(6 Pt 1):1677-82.
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    ABSTRACT: To evaluate a possible seasonal change in bronchial responsiveness and the relation of such change to atopy, we administered 2,537 bronchial challenge tests in winter and spring to a dynamic population cohort of children 7 to 10 yr of age. The bronchial challenge test consisted of 10 min of tidal inhalation of an aerosol of ultrasonically nebulized distilled water; the resulting percentage decrease in FEV1 (dFEV1%) was recorded. Atopy was determined on the basis of skin-test positivity (any wheal with a diameter greater than that obtained with a positive control) to seven allergens (cat dander, dog dander, house-dust mite, birch, raygrass, orchard grass, and Alternaria). Greater bronchial responsiveness in winter was independently and significantly predicted by a physician's diagnosis of asthma (difference in dFEV1%, 5.6; 95% confidence intervals [95% CI], 2.8 to 8.5; p = 0.0001) and by shortness of breath (difference in dFEV1%, 4.2; 95% CI, 2.1 to 6.3; p = 0.0001). These factors were also predictive of greater responsiveness in the spring, as was atopy (difference in dFEV1%, 3.2; 95% CI, 1.8 to 4.6; p = 0.0001). Analysis of specific allergens further revealed that reactivity to perennial allergens (house-dust mite, cat dander) was predictive of bronchial responsiveness in both winter and spring. However, the change in responsiveness between seasons was most significantly predicted by allergy to seasonal grass pollen, i.e., ragweed or orchard grass (change in dFEV1%, 2.6; 95% CI, 0.6 to 4.5; p = 0.01). In summary, our study demonstrates increased bronchial responsiveness in spring among children allergic to grass pollen.(ABSTRACT TRUNCATED AT 250 WORDS)
    The American review of respiratory disease 01/1994; 148(6 Pt 1):1460-6.
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    ABSTRACT: To investigate the role of IL-5 in airway hyperreactivity and pulmonary eosinophilia, we used a model of allergic asthma in guinea pigs and a neutralizing monoclonal antibody (TRFK-5) directed against murine IL-5. Sensitized guinea pigs were challenged with 1% ovalbumin (OVA) aerosol and assessed for airway eosinophilia (by bronchoalveolar lavage [BAL] and histologic evaluation of airway tissue) and bronchoconstrictor responsiveness to substance P (SP) (as RL100 and Cdyn40) 24 h later. OVA challenge of sensitized animals caused a significant increase in airway responsiveness to SP, with a 4.9-fold decrease in RL100 and a 4.7-fold decrease in Cdyn40. Accompanying this increased sensitivity to SP was a 9-fold increase in eosinophils recovered in BAL and a 4- to 5-fold increase in eosinophils in intrapulmonary bronchial tissue. Intraperitoneal treatment with 10 mg/kg of the IL-5 antibody 2 h before OVA challenge blocked BAL and lung tissue increases in eosinophils but had no effect on the development of airway sensitivity to SP. In contrast, similar treatment with 30 mg/kg of this antibody blocked OVA-induced increased sensitivity to SP as well as BAL and lung tissue eosinophilia. These data suggest a critical and possibly independent role for IL-5 in allergic airway hyperresponsiveness and the accumulation of eosinophils within the lung of the guinea pig.
    The American review of respiratory disease 01/1994; 148(6 Pt 1):1623-7.
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    ABSTRACT: Using various animal models of toxic or antigenic-induced airway inflammation, we have demonstrated that adhesion molecules play an important role in the recruitment, retention, and site-specific activation of inflammatory cells within the airways. Furthermore, we have shown that cytokines may contribute to inflammatory responses in the airways by enhancing the expression of adhesion molecules on respiratory epithelial cells.
    The American review of respiratory disease 01/1994; 148(6 Pt 2):S83-7.