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Biomedical subjects

Walter A Zin

Publications and source records attributed to Walter A Zin.

13 recordsLinked to original sources
PubMed2003

Evaluation of respiratory mechanics and lung histology in a model of atelectasis.

To develop a reproducible model of atelectasis, 15 mechanically ventilated Wistar rats were wrapped around the thorax/abdomen with a sphygmomanometer. The cuff was inflated to transpulmonary pressures (PL) of -4 cmH2O (group A) and -8 cmH2O (group B) for 5 sec. Group C was not compressed. Airflow, volume, tracheal and oesophageal pressures were registered. Respiratory system (rs), lung (L), and chest wall resistive (DeltaP1), viscoelastic/inhomogeneous pressures (DeltaP2), DeltaPtot (=DeltaP1 + DeltaP2), static (Est) and dynamic (Edyn) elastances, and DeltaE (=Edyn - Est) were determined before and after compression. In A, respiratory mechanics remained unaltered. In B, Est,rs (+99%), Est,L (+111%), DeltaE,rs (+41%), DeltaE,L (+73%), DeltaP1,rs (+45%), DeltaP1,L (+44%), DeltaP2,rs (+41%), DeltaP2,L (+69%), DeltaPtot,rs (+40%), and DeltaPtot,L (+58%) increased after compression. Mean alveolar diameter and bronchiolar lumen decreased in A, and were even smaller in B. In conclusion, chest wall compression with PL of -8 cmH2O yielded a reproducible alveolar collapse, which resulted in increased elastic, resistive and viscoelastic/inhomogeneous pressures.

Animals↗
PubMed2003

Effect of corticosteroid on lung parenchyma remodeling at an early phase of acute lung injury.

In vivo (lung resistive and viscoelastic pressures and static elastance) and in vitro (tissue resistance, elastance, and hysteresivity) respiratory mechanics were analyzed 1 and 30 days after saline (control) or paraquat (P [10 and 25 mg/kg intraperitoneally]) injection in rats. Additionally, P10 and P25 were treated with methylprednisolone (2 mg/kg intravenously) at 1 or 6 hours after acute lung injury (ALI) induction. Collagen and elastic fibers were quantified. Lung resistive and viscoelastic pressures and static elastance were higher in P10 and P25 than in the control. Tissue elastance and resistance augmented from control to P10 (1 and 30 days) and P25. Hysteresivity increased in only P25. Methylprednisolone at 1 or 6 hours attenuated in vivo and in vitro mechanical changes in P25, whereas P10 parameters were similar to the control. Collagen increment was dose and time dependent. Elastic fibers increased in P25 and at 30 days in P10. Corticosteroid prevented collagen increment and avoided elastogenesis. In conclusion, methylprednisolone led to a complete maintenance of in vivo and in vitro respiratory mechanics in mild lesion, whereas it minimized the changes in tissue impedance and extracellular matrix in severe ALI. The beneficial effects of the early use of steroids in ALI remained unaltered at Day 30.

Animals↗
PubMed2003

On the preparation of lung strip for tissue mechanics measurement.

It is widely believed that it is fundamental to degas and/or rinse the lung prior to the measurement of the tissue mechanics, so that the undesirable effects of surfactant and localized gas trapping are eliminated. However, one could hypothesize that these mechanisms are bound to disappear in the in vitro preparation since the small tissue sample remains suspended oscillating in an organ bath. To investigate the real necessity to follow these procedures, dynamic mechanical properties were studied in strips of lungs previously rinsed with saline, degassed by ventilation with 100% O(2), or without any of these prior procedures. Resistance, elastance, hysteresivity, and the amounts of airway, blood vessel, and alveolar wall were computed. There was no difference in either tissue mechanics or morphology among the groups. In conclusion, the time-consuming degassing and rinsing steps are not necessary to adequately prepare lung tissue for in vitro mechanical analysis, and eliminating these steps potentially helps preserving the intact microstructure of the tissue.

Analysis of Variance↗
PubMed2002

Early carbon dioxide challenge test may predict clinical response in panic disorder.

We examined whether responses to the carbon dioxide (CO(2)) challenge test were correlated with clinical response. Thirty-four panic disorder patients participated in a CO(2) test after 1 h, 2 weeks and 6 weeks of treatment with clonazepam (2 mg/day) or placebo. The clonazepam group had significantly fewer panic attacks in response to the CO(2) test and the test may predict clinical response.

Adult↗
PubMed2002

A breath-holding challenge in panic disorder patients, their healthy first-degree relatives, and normal controls.

Our aim was to observe the induction of panic attacks (PA) symptoms by a breath-hold test in panic disorder (PD) patients as the Diagnostic and Statistical Manual for Mental Disorders 4th edition (DSM-IV) and their healthy first-degree relatives. We randomly selected 26 PD patients, 28 healthy first-degree relatives of probands with PD and 25 normal volunteers with no family history of PD. They were induced to breath-hold for as long as possible four times with a two-min interval between them. Anxiety scales were applied before and after the test. Using specific PA criteria, 46.1% (n=12) PD patients, 7.1% (n=2) first-degree relatives and 4.0% (n=1) control subjects had a PA after the test (chi(2)=7.82, df=2, P=0.023). There was no heart rate, anxiety levels or breath-hold time differences among the groups. In this breath hold challenge test PD patients were more sensitive to breath-hold than first-degree relatives and normal volunteers.

Adolescent↗
PubMed2002

Psychiatric disorders in asthmatic outpatients.

It has been reported that the lifetime prevalence of panic disorder in patients with pulmonary disease is higher than epidemiologic estimates of population prevalence. We evaluated the frequency of anxiety disorders in 86 subjects from the Outpatient Asthma Clinic. Psychiatric diagnoses were assessed with the Mini-International Neuropsychiatric Interview 4.4 Version (MINI). Forty-five asthmatic patients (52.3%) reported at least one current anxiety disorder. The frequency of panic disorder with or without agoraphobia was 13.9% (n=12) and that of agoraphobia without panic disorder was 26.8% (n=23). Social anxiety and generalized anxiety disorders occurred in 9.3% (n=8) and 24.4% (n=21) of the sample, respectively. Twenty-nine patients (33.7%) reported a major depressive episode. The psychiatric morbidity of the sample was 61.6% (n=53). Our results tend to support the high morbidity of anxiety disorders, particularly panic/agoraphobic spectrum disorders, in asthmatic outpatients.

Adolescent↗
PubMed2002

Panic disorder and obsessive compulsive disorder in a hyperventilation challenge test.

BACKGROUND: Stress-induced hyperventilation produces symptoms that people are prone to misinterpret as life-threatening if they are unaware of the consequences of overbreathing. Our aim was to observe the induction of panic attacks by a hyperventilation challenge test in a series of panic disorder and obsessive compulsive disorder (OCD) patients (DSM-IV). METHOD: We randomly selected 28 panic disorder patients, 21 OCD patients and 28 normal volunteers. All patients were drug free for a week. They were induced to hyperventilate (30 breaths/min) for 4 min. Anxiety scales were applied before and after the test. RESULTS: A total of 64.3% (n=18) panic disorder patients, 9.5% (n=2) OCD patients and 3.6% (n=1) of control subjects had a panic attack after hyperventilating (chi(2)=3.99, d.f.=2, P=0.026). LIMITATIONS: The hyperventilation challenge test has a low sensitivity for panic disorder. CONCLUSION: In this challenge test the panic disorder patients were more sensitive to hyperventilation than OCD patients and normal volunteers. The induction of panic attacks by voluntary hyperventilation may be an easy test for validating the diagnosis in certain panic disorder patients.

Adult↗
PubMed2002

Comparison of rat and mouse pulmonary tissue mechanical properties and histology.

The present study compares the dynamic mechanical properties and the contents of collagen and elastic fibers (oxytalan + elaunin + fully developed elastic fibers) of mice and rat lung strips. Resistance, elastance (E), and hysteresivity (eta) were obtained during sinusoidal oscillations. The relative amounts of blood vessel, bronchial, and alveolar walls, as well as the mean alveolar diameter were determined. In both species, resistance had a negative and E a positive dependence on frequency, whereas eta remained unchanged. Mice showed higher E and lower eta than rats. Although collagen and elastic fiber contents were similar in both groups, mice had more oxytalan and less elaunin and fully developed elastic fibers than rats. Rats showed less alveolar and more blood vessel walls and higher mean alveolar diameter than mice. In conclusion, mice and rats present distinct tissue mechanical properties, which are accompanied by specific extracellular fiber composition.

Airway Resistance↗
PubMed2002

Apoptosis underlies immunopathogenic mechanisms in acute silicosis.

We investigated immunopathogenic roles for apoptosis in acute murine silicosis. Intratracheal silica instillation induced pulmonary inflammation and enlarged thoracic lymph nodes. Lymphocytes from silica-exposed lymph nodes showed reduced mitogenic responses to T cell receptor (TCR) stimulation, and markedly increased activation-induced cell death, compared with control lymphocytes from saline-exposed lymph nodes. CD4(+) T cell death was mediated by Fas ligand, because CD4(+) T cells from Fas ligand-deficient gld mice did not undergo activation-induced apoptosis. Silica deposition also resulted in increased apoptosis associated with inflammatory infiltrates in lung parenchyma. In vivo treatment with caspase inhibitors reduced neutrophil accumulation, and alleviated inflammation in the lungs of silica-treated mice. These results suggest that silica-induced apoptosis plays an inflammatory role in the lung parenchyma, and creates immunologic abnormalities in regional lymph nodes, with pathogenic implications for the host.

Acute Disease↗
PubMed2002

Carbon dioxide test as an additional clinical measure of treatment response in panic disorder.

OBJECTIVE: We aim to determine if a treatment with a dose of clonazepam--2 mg/day, for 6 weeks, blocks spontaneous panic attacks and the ones induced by the inhalation of 35% carbon dioxide (CO2) in panic disorder (PD) patients. The CO2 challenge-test may be a useful addition tool for measuring the pharmacological response during the initial phase (6 weeks) in the treatment of PD. METHOD: Eighteen PD patients drug free for a week participated in a carbon dioxide challenge test. Fourteen had a panic attack and were openly treated for a 6-week period with clonazepam. At the end of the 6-week period they were submitted again to the CO2 challenge test. RESULTS: After 6 weeks of treatment with clonazepam, 12 of 14 PD patients (85.7%) did not have a panic attack after the CO2 challenge test. Just 2 of 14 patients (14.3%) had a panic attack after the CO2 challenge test. Ten of 14 (71.4%) PD patients had panic free status after clonazepam treatment. The 2 patients who had a panic attack in the sixth week, after the CO2 test, did not have panic free status after the treatment with clonazepam. CONCLUSION: The CO2-test may be a valid tool for testing and predicting the drug response.

Administration, Inhalation↗
PubMed2002

Nocturnal panic attacks.

The panic-respiration connection has been presented with increasing evidences in the literature. We report three panic disorder patients with nocturnal panic attacks with prominent respiratory symptoms, the overlapping of the symptoms with the sleep apnea syndrome and a change of the diurnal panic attacks, from spontaneous to situational pattern. The implication of these findings and awareness to the distinct core of the nocturnal panic attacks symptoms may help to differentiate them from sleep disorders and the search for specific treatment.

Adrenergic Uptake Inhibitors↗