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Biomedical subjects

M G Cosio

Publications and source records attributed to M G Cosio.

At least 55 records · Page 3Linked to original sources
PubMed1990

Cellularity of the alveolar walls in smokers and its relation to alveolar destruction. Functional implications.

Inflammatory cells are believed to play an important role in the pathogenesis of emphysema; however, a relationship between presence of cells in the lung parenchyma and its destruction has never been shown. The aim of this study was to quantitate alveolar septal cellularity in smokers' lungs and to investigate its relationship with parenchymal destruction and lung function. The lungs of 23 smokers (SS) undergoing thoracotomy for localized pulmonary lesions were compared with those of eight nonsmokers (NS) and five smokers (AS) who died suddenly of nonrespiratory causes. Pulmonary function tests were performed within 1 wk of surgery in SS. For each subject, we quantitated alveolar wall cells (CELLS), an index of alveolar wall destruction (DI), and the mean linear intercept (Lm). As no significant differences were found between S and AS with regard to these indices, we combined them (Group S) for comparison with NS. Although Lm was not significantly different between S and NS, (0.331 +/- 0.072 versus 0.288 +/- 0.038), CELLS and DI were higher in S than in NS (48 +/- 8 versus 25 +/- 2 cells/mm, p less than 0.001; 47 +/- 20 versus 17 +/- 5, p less than 0.001, respectively). Further, CELLS and DI were significantly correlated (r = 0.799, p less than 0.001). The number of polymorphonuclear cells (PMN) in S can exceed that in NS by as much as 5-fold; however, PMN were inversely correlated with parenchymal destruction (DI) (r = 0.598, p less than 0.01). Thus, smokers' lungs have alveolar septal hypercellularity, possibly inflammatory, and closely related to destruction involving cells other than the PMN.

Aged↗
PubMed1990

Pulmonary denervation in humans. Effects on dyspnea and ventilatory pattern during exercise.

The role of the pulmonary autonomic nerves in the mediation of respiratory sensation is unclear. Pulmonary neurogenic mechanisms may contribute to dyspnea either directly or indirectly via an influence on the pattern of ventilation. Using human heart-lung transplantation as a model of pulmonary denervation, we studied the ventilatory response, respiratory drive (P0.1), and sensation of breathlessness (modified Borg scale) during maximal incremental bicycle exercise. The subjects were four female heart-lung transplant recipients 3 to 9 months post-transplant and 10 age-matched control subjects. The ventilatory response to increasing CO2 output (VCO2) was higher (p less than 0.001) in transplant recipients than in control subjects, such that ventilation at peak exercise was similar in the two groups despite a lower peak VCO2 in transplant recipients. The ratio of tidal volume to inspiratory capacity increased with increasing ventilation in a similar fashion in both groups. Although the respiratory rate increased more quickly in transplant recipients, it was similar at peak ventilation in the two groups. Ventilatory timing and duty cycle at half-peak and peak ventilation were similar in transplant recipients and control subjects. Dyspnea ratings were not different between the two groups at similar levels of ventilation. Dyspnea as a function of P0.1 was also similar in transplant and control groups. These results indicate that pulmonary neurogenic mechanisms play a role in determining the level, but not the pattern, of ventilation during exercise. Furthermore, these pathways do not appear to contribute significantly to the perception of breathlessness in normal humans.

Adult↗
PubMed1989

Effect of saline infusion on body temperature and endurance during heavy exercise.

We tested the hypothesis that volume infusion during strenuous exercise, by expanding blood volume, would allow better skin blood flow and better temperature homeostasis and thereby improve endurance time. Nine males exercised to exhaustion at 84.0 +/- 3.14% (SE) of maximum O2 consumption on a cycle ergometer in a double-blind randomized protocol with either no infusion (control) or an infusion of 0.9% NaCl (mean vol 1,280.3 +/- 107.3 ml). Blood samples and expired gases (breath-by-breath), as well as core and skin temperatures, were analyzed. Plasma volume decreased less during exercise with the infusion at 15 min (-13.7 +/- 1.4% control vs. -5.3 +/- 1.7% infusion, P less than 0.05) and at exhaustion (-13.6 +/- 1.2% vs. -1.3 +/- 2.2%, P less than 0.01). The improved fluid homeostasis was associated with a lower core temperature during exercise (39.0 +/- 0.2 degrees C for control and 38.5 +/- 0.2 degrees C for infusion at exhaustion, P less than 0.01) and lower heart rate (194.1 +/- 3.9 beats/min for control and 186.0 +/- 5.1 beats/min for infusion at exhaustion, P less than 0.05). However, endurance time did not differ between control and infusion (21.96 +/- 3.56 and 20.82 +/- 2.63 min, respectively), and neither did [H+], peak O2 uptake, and CO2 production, end-tidal partial pressure of CO2, blood lactate, or blood pressure. In conclusion, saline infusion increases heat dissipation and lowers core temperature during strenuous exercise but does not influence endurance time.

Adolescent↗
PubMed1989

Pressure-volume curves in smokers. Comparison with alpha-1-antitrypsin deficiency.

The diagnosis of emphysema has been associated with changes in the appearance of the pressure-volume (P-V) curve: reduced maximal recoil pressure, increased lung volume, and a shift in the position of the curve to the left. In our clinical practice, we have observed that patients with chronic obstructive lung disease (COPD) commonly had P-V curves with reduced maximal elastic recoil that are difficult to classify according to the classic description of the P-V curve in emphysema. In order to study the variability of P-V curves, we studied 39 cigarette smokers attending a pulmonary clinic (age, 61 +/- 1 yr; smoking history, 45 +/- 3 pack-years; mean +/- SEM) and compared them with 20 patients with alpha-1-antitrypsin deficiency (AATD) (age, 41 +/- 2 yr; 13 smokers with a smoking history of 17 +/- 2 pack-years, and seven nonsmokers). Subjects underwent spirometry, lung volume, and diffusing capacity measurements as well as static deflation P-V curves. To characterize the P-V curves, we used transpulmonary pressure at 90% of TLC (PL90) as a measure of overall recoil and specific compliance (Csp) as a measure of the slope of the initial part of the P-V curve. The curves of non-AATD smokers were classified into three groups: 13 had PL90 greater than or equal to 80% predicted (Group I), 13 had PL90 less than 80% predicted and Csp greater than or equal to 0.08 (Group II), and 13 had PL90 less than 80% predicted and Csp less than 0.08 (Group III).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Reversibility of upper airway obstruction after levodopa therapy in Parkinson's disease.

Serial flow-volume loops obtained in a 66-year-old patient with Parkinson's disease and recurrent episodes of dyspnea revealed a pattern consistent with upper airway obstruction, reversible after oral intake of levodopa. This observation shows that extrapyramidal involvement of the striated upper airway musculature may limit airflow and cause respiratory symptoms. Persistence of flow oscillations on the flow-volume loop contour after reversal of upper airway obstruction and dyspnea should be considered to reflect upper airway dysfunction with possibly serious consequences.

Aged↗
PubMed1989

Mucus hypersecretion and viscoelasticity changes in cigarette-smoking dogs.

Chronic cigarette smoke exposure is well known to cause mucus hypersecretion in experimental animals, but the alterations in mucus rheology have not been described. We studied mucus hypersecretion and viscoelasticity changes in nine tracheostomized beagle dogs exposed to cigarette smoke. The dogs were trained to stand quietly in a harness, and smoke was delivered via a cuffed tracheostomy tube. A 35-cm3 bolus was introduced to the inspiratory line each 20 s, using unfiltered 70-mm cigarettes (20 mg tar, 1.2 mg nicotine). Each dog smoked 10 cigarettes per day over 2.5 h, 5 days per week. Two dogs were exposed for 6 months; 7 dogs were exposed for 10 months. Five dogs served as sham-smoking controls. Mucus was collected twice weekly without drugs by resting a cytology brush on the lower trachea for 2-5 min. The rheological properties of the mucus samples were determined by magnetic rheometry, which yields elasticity and viscosity as a function of frequency. The mucus was also weighed, and the galactose content was determined by phenolsulfuric acid assay. The mucus collection rate served as an index of tracheal mucus flux, and the galactose assay as a marker of mucous glycoprotein content. The tracheal mucus linear velocity (TMV) was determined periodically under xylazine analgesia by observing charcoal particle transport bronchoscopically. Eight of 9 smoking dogs developed mucus hypersecretion (flux greater than 2 X control) versus 1 of 5 controls (p less than .01). TMV did not change significantly in 10 months of exposure. In the first 2-4 months of smoking, the elasticity and viscosity of the mucus both decreased (mean at 4 months = 42% control, p less than .001), as did the galactose content (mean at 4 months = 48% control, p less than .01). At this stage, according to model studies, the mucus should have been more easily clearable by ciliary action. After 6 months, the viscoelasticity returned toward the initial control level, while the galactose content remained low, suggesting an alteration in the nature of the mucous glycoprotein.

Animals↗
PubMed1987

Determinants of respiratory muscle weakness in stable chronic neuromuscular disorders.

In neuromuscular disease, the precise relationship between general and respiratory muscle weakness is at present unclear. That relationship and the influence on respiratory muscle strength of such factors as type and duration of neuromuscular disease, distribution of general muscle weakness, and nutritional status were studied in 30 patients with stable chronic neuromuscular disease not presenting with respiratory symptoms. The degree of general muscle weakness was assessed by clinical examination of the strength of 17 muscle groups, yielding a general muscle strength index. The degree of respiratory muscle weakness was assessed by measuring maximal static inspiratory and expiratory mouth pressures. Maximal inspiratory (mean +/- SD: 68 +/- 28 percent predicted) and expiratory (66 +/- 29 percent predicted) mouth pressures were frequently reduced, but did not correlate with general muscle strength. The ability to estimate the degree of respiratory muscle weakness improved to some extent when the type of neuromuscular disease and the distribution of general muscle weakness were taken into account: thus, maximal expiratory mouth pressure was significantly lower (p less than 0.05) in myopathy than in polyneuropathy, and in proximal than in distal muscle weakness. Duration of neuromuscular disease and nutritional status did not influence respiratory muscle strength. It is concluded that in stable chronic neuromuscular disease, respiratory muscle involvement depends on a complexity of factors, in particular the type of neuromuscular disease and the distribution, rather than the degree, of general muscle weakness. In the individual patient, however, only direct measurement of maximal inspiratory and expiratory mouth pressures allows accurate assessment of respiratory muscle strength. These tests ought to complement neurologic examination.

Adult↗
PubMed1987

Flow-volume loop changes reflecting respiratory muscle weakness in chronic neuromuscular disorders.

In order to identify the changes in pulmonary function and in the flow-volume loop due to respiratory muscle weakness, two groups of 10 nonsmokers with stable, chronic neuromuscular disease but without respiratory symptoms were studied: one without (Group 1) and one with (Group 2) respiratory muscle weakness as assessed by measurement of maximal static inspiratory and expiratory pressures. In Group 1, pulmonary function was normal except for increased ratio of one-second forced expiratory volume to forced vital capacity and forced expiratory flow at 25 to 75 percent forced vital capacity, which may reflect increased elastic lung recoil. Group 2 had mild volume restriction, appropriate for the degree of respiratory muscle weakness, and reduced inspiratory and expiratory flow rates. Pulmonary function was significantly more disturbed in Group 2 than in Group 1, and correlated well with maximal static inspiratory and expiratory pressures. Analysis of the flow-volume loop configuration revealed that four parameters describing effort-dependent portions were significantly related to maximal static inspiratory pressure and maximal static expiratory pressure. These parameters were peak expiratory flow, the slope of the ascending limb of the maximal expiratory curve, a drop of forced expiratory flow near residual volume, and forced inspiratory flow at 50 percent of vital capacity. A flow-volume loop score obtained from these four parameters was significantly higher in Group 2 than in Group 1 (2.8 +/- 1.03 versus 1.1 +/- 1.37; p less than 0.01). A flow-volume loop score of 2 or more had 80 percent specificity and 90 percent sensitivity in predicting respiratory muscle weakness in these patients with chronic neuromuscular disease. These data suggest that sensitive assessment of the flow-volume loop configuration as part of routine pulmonary function testing may help to suspect and identify respiratory muscle weakness.

Chronic Disease↗
PubMed1987

Hyporesponsiveness to aerosolized but not to infused methacholine in cigarette-smoking dogs.

Seven beagles were exposed via a tracheostomy to smoke from 10 cigarettes/day, 5 days/wk for 10 months; 2 other dogs were exposed for 6 months only. Four dogs served as sham-exposed control animals. Mucus was collected 2 times/wk prior to and during the exposure period by resting a cytology brush on the lower trachea for 2 to 5 min. At least once prior to and as often as 3 times during exposure, transpulmonary pressure and flow were monitored under anesthesia to determine resistance RL. Two airway responses to methacholine were determined: the infusion response delta Ri, the increment in RL 4 to 6 min after infusion of 4 micrograms/kg/min, and the aerosol response delta Ra, the increment in RL 2 min after aerosolization of 2 mg/ml, the highest common dose reached. Eight of 9 smoking dogs developed persistent mucus hypersecretion. In 5 dogs, tracheal mucus flux increased 5- to 10-fold; in 3 dogs, the increase was 2 to 3 times that of control animals. One of the sham-exposed dogs developed moderate hypersecretion. After 10 months of smoke exposure, delta Ri increased to 2.24 times that of the initial value (+/- 0.47 SE) (n = 7, p less than 0.05), whereas delta Ra decreased to 0.28 times that of the control value (+/- 0.21 SE) (n = 6, p less than 0.02). The difference between aerosol and infusion response, delta Rai = delta Ra - delta Ri, is an index of relative hyporesponsiveness to methacholine aerosol.(ABSTRACT TRUNCATED AT 250 WORDS)

Aerosols↗
PubMed1987

Combination of theophylline and salbutamol for arrhythmias in severe COPD.

We conducted a single-bind placebo controlled study using 24-hour continuous ambulatory electrocardiographic recordings. The arrhythmogenic potential of the combination of salbutamol and theophylline was investigated in 25 ambulatory subjects with severe chronic airflow obstruction (mean age 65 +/- 8 SD, mean FEV1 31 percent +/- 13 SD predicted). Asymptomatic arrhythmias were very prevalent in the study population: 76 percent of the patients had runs of supraventricular tachycardia while 24 percent had runs of ventricular tachycardia. Individual arrhythmia frequency showed greater between-test variability than previously described in non-COPD subjects. The mode of administration of salbutamol may have affected arrhythmia frequency in that subjects using aerosol nebulizers had more ventricular extrasystoles than those using metered dose inhalers. Although the addition of theophylline to salbutamol significantly increased heart rate and supraventricular extrasystoles, there was no statistically significant increase in ventricular arrhythmias.

Aged↗
PubMed1987

Obstructive sleep apnea caused by hemarthrosis-induced micrognathia.

A 42-year-old male hemophiliac with micrognathia caused by temperomandibular hemarthrosis was studied for obstructive sleep apnea and successfully treated without the use of a tracheostomy. Prevention of nocturnal hypoxemia by nasopharyngeal intubation was found to relieve daytime hypersomnolence while he was awaiting corrective jaw surgery. The association of obstructive sleep apnea with micrognathia secondary to hemophilia has not previously been reported to our knowledge.

Adult↗
PubMed1986

Alveolar fenestrae in smokers. Relationship with light microscopic and functional abnormalities.

We studied 12 smokers' lungs with scanning electron microscopy in order to analyze the distribution and size of alveolar fenestrae and their relationship to the average distance between alveolar walls (Lm) and lung function. Alveolar fenestrae in areas near terminal airways (respiratory bronchioles and alveolar ducts) were consistently larger than fenestrae far from airways (alveoli). Fenestrae in near areas increased in size as Lm increased (r = 0.845, p less than 0.001), whereas no correlation between Lm and fenestrae size in far areas was found (r = 0.281, NS). The overall area of fenestrae (near and far) correlated significantly with FEV1 (r = -0.745, p less than 0.01), MMEF (r = -0.752, p less than 0.01), and PL90 (r = -0.804, p less than 0.05). However, when subdivided into near and far, only fenestrae near the small airways showed a significant correlation with function. These findings suggest that in smokers with mild to moderate emphysema, destruction affects preferentially the areas around the terminal airways (near areas), and these changes, although small, might play an important role in the lung function.

Aged↗
PubMed1986

Detection of upper airway muscle involvement in neuromuscular disorders using the flow-volume loop.

Abnormal contours of the flow-volume loop, ie, flow oscillations and inspiratory flow plateaux, have been noted in disorders affecting upper-airway muscular function. In this study, we assessed the incidence and the value of these contours as a test of bulbar and upper-airway muscular involvement in neuromuscular disease. We therefore compared flow-volume loops and pulmonary function test results between ten patients with (group 1) and 20 patients without (group 2) clinically apparent bulbar muscle involvement in neuromuscular disease. An abnormal flow-volume loop occurred significantly more often in group 1 than in group 2 (9/10 or 90 percent vs 3/20 or 15 percent, respectively; p less than 0.001) and predicted bulbar and upper-airway muscle involvement with high sensitivity (90 percent), specificity (85 percent) and efficiency (87 percent). Based on commonly used spirometric criteria, upper-airway obstruction was not more common in group 1 than in group 2 (1/10 vs 2/20); however, all three patients with upper-airway obstruction suggested by these criteria had an abnormal flow-volume loop. Following this study, three patients incurred severe respiratory complications. All three patients had previously shown an abnormal flow-volume loop. We conclude that in patients with neuromuscular disease, involvement of the bulbar and upper-airway muscles is frequently associated with an abnormal contour of the flow-volume loop. Recognition of flow oscillations or flow plateaux on flow-volume loops in these patients seems important, since they may be potential markers of severe respiratory complications.

Adult↗
PubMed1986

Upper airway dysfunction detected by respiratory flow oscillations.

In 3 patients with chronic respiratory symptoms, we identified rapid flow oscillations on flow-time and flow-volume recordings, corresponding to fluttering of lax but otherwise normal-appearing upper airway structures at cinefluoroscopy and fiberoptic endoscopy. This entity of upper airway dysfunction was responsible for, or at least contributed to, the respiratory symptoms as evidenced by dramatic relief of dyspnea following tracheostomy in one patient, and significant improvement of flow rates following helium breathing in the other 2 patients. We suggest that identification of flow oscillations on flow recordings, in particular flow-volume loops, should lead to investigation of the upper airway. When fluttering is the only abnormality observed, it should not be disregarded, but rather considered as possibly contributing to airflow limitation.

Adult↗
PubMed1985

Destructive index: a measurement of lung parenchymal destruction in smokers.

Destruction of alveolar walls is considered by most observers to be the most important part in the definition of emphysema, yet it has never been precisely defined and quantitated. We therefore attempted to devise a reliable microscopic technique to quantitate alveolar destruction that would be both sensitive to disease and easy to perform. Using a point-count system, we obtained an index of parenchymal destruction that represents the percentage of destroyed space as a fraction of the total alveolar and duct space. We have called this measurement the destructive index (DI). In the lungs of 8 nonsmokers and 23 smokers, we quantitated the DI and compared it with the mean linear intercept (Lm) and with pulmonary function in smokers. Although Lm was not significantly different in the 2 groups, significant differences between the DI of smokers and nonsmokers (p less than 0.005) were found. In addition, the DI correlated with FEV1(-0.43, p less than 0.05), MMEF (r = -0.44, p less than 0.05), and recoil pressure at 90% TLC (r = -0.61, p less than 0.05) in smokers. These findings suggest that the destructive component of emphysema can be easily quantitated microscopically, occurs in smokers before dimensional changes are evident (i.e., increased Lm), and influences lung function. Therefore, the quantitation of this destruction (DI) could add greatly to the microscopic definition of emphysema, complementing the information given by the dimensional component of emphysema (Lm).

Aged↗
PubMed1985

Loss of alveolar attachments in smokers. A morphometric correlate of lung function impairment.

We studied post-mortem 9 nonsmokers' lungs and 9 smokers' lungs as well as 14 surgical smokers' lungs to examine the possible relationship of the number of alveolar attachments with airways inflammation and with lung function. Alveolar attachments are the alveolar walls radially attached to the small airways, and any discontinuity or rupture of these alveolar walls was considered abnormal. Normal and abnormal attachments were counted in nonsmokers and smokers and expressed as number of attachments, distance between attachments, and percentage of abnormal attachments. Although internal small airways diameter and mean linear intercept were not significantly different between smokers of either group and nonsmokers, significant differences in number of attachments (p less than 0.001), distance between attachments (p less than 0.01), and percentage of abnormal attachments (p less than 0.01) were found. The 3 indexes of alveolar attachments correlated significantly with the score for airways inflammation and with the elastic recoil pressure in smokers. No significant correlation with any other lung function test was found. We conclude that smokers have fewer alveolar attachments than do nonsmokers, and that the loss of alveolar attachments represents an early stage in the destruction of lung parenchyma, and is probably linked to inflammation of the small airways. Because of the strategic situation of this lesion, it could be responsible in part for the loss of elastic recoil seen in the initial stages of chronic obstructive pulmonary disease.

Aged↗
PubMed1985

Respiratory muscle dysfunction after herpes zoster.

We report an unusual neurologic complication of herpes zoster. After thoracic herpes zoster, our patient complained of severe shortness of breath as a result of myoclonus of the abdominal muscles as documented by electromyography. The myoclonus resulted in repetitive interruption of expiratory air flow, resulting in shortness of breath and a staccato speech. This case demonstrates the need to evaluate the function of all the respiratory muscles in a patient complaining of dyspnea.

Abdominal Muscles↗