Search PubMed⌕ Search

Biomedical subjects

C Picado

Publications and source records attributed to C Picado.

At least 73 records · Page 4Linked to original sources
PubMed1995

Comparative study of the effects of different glucocorticosteroids on eosinophil survival primed by cultured epithelial cell supernatants obtained from nasal mucosa and nasal polyps.

BACKGROUND: Supernatants from epithelial cell cultures enhance eosinophil survival in vitro, this effect being abrogated by previous incubation of eosinophils with glucocorticosteroids. This property has resulted in the development of an in vitro test to compare the potency of these drugs. A comparative study was performed with dexamethasone, methylprednisolone, deflazacort, and budesonide. METHODS: Human epithelial cell conditioned media (HECM) was generated from cultured epithelial cells obtained from healthy nasal mucosa and polyps. Eosinophils isolated from the peripheral blood were incubated with different corticosteroids for one hour before the addition of HECM. The inhibitory potency of the four steroids on the eosinophil survival index was compared using the concentration of steroid causing 50% inhibition (IC50). RESULTS: Eosinophil survival was increased by HECM from both healthy nasal mucosa and polyps. All four steroids blocked HECM-induced eosinophil survival in a dose-dependent manner. On healthy nasal mucosa methylprednisolone was the least potent (IC50 = 536 nM), deflazacort (IC50 = 264 nM) was twice as potent as methylprednisolone, while budesonide and dexamethasone were approximately nine times as potent (both IC50 = 58 nM). When potency was evaluated on the promoting effects of the HECM obtained from nasal polyps, the inhibitory potencies were lower and consequently the IC50 values were higher when compared with HECM generated from healthy nasal mucosa: methylprednisolone (IC50 = 546 nM), deflazacort (IC50 = 390 nM), dexamethasone (IC50 = 76 nM), and budesonide (IC50 = 78 nM). CONCLUSIONS: The potencies of glucocorticosteroids can be compared by evaluating their effects on the survival of eosinophils previously primed by supernatants obtained from epithelial cell culture. The different effects of steroids on eosinophils primed by HECM obtained from healthy nasal mucosa compared with HECM obtained from nasal polyps suggest that polyps might represent more active tissue which is relatively resistant to treatment with corticosteroids.

Administration, Topical↗
PubMed1995

In vitro release of arachidonic acid metabolites, glutathione peroxidase, and oxygen-free radicals from platelets of asthmatic patients with and without aspirin intolerance.

BACKGROUND: An abnormal platelet release of oxygen-free radicals has been described in acetylsalicylic acid (aspirin)-induced asthma, a finding which might suggest the existence of an intrinsic, specific platelet abnormality of arachidonic acid metabolism in these patients. The objective of this study was to evaluate platelet arachidonic acid metabolism in asthmatic patients with or without intolerance to aspirin. METHODS: Thirty subjects distributed into three groups were studied: group 1, 10 healthy subjects; group 2, 10 asthmatic patients with aspirin tolerance; and group 3, 10 aspirin-intolerant asthmatics. Platelets were isolated from blood, preincubated with 3H-arachidonic acid for 30 minutes and then incubated for 10 minutes with platelet activating factor (PAF) and aspirin. Cyclo-oxygenase (thromboxane, PGE2, PGF2 alpha, and HHT) and lipoxygenase (12-HETE) arachidonic acid metabolites were measured by high pressure liquid chromatography. Release of oxygen free radicals after incubation with PAF and aspirin was measured by chemiluminescence. Platelet levels of glutathione peroxidase (GSH-Px) were also measured using spectrophotometry. RESULTS: Platelets from aspirin-intolerant asthmatic patients produced higher quantities of arachidonic acid metabolites than the control group at baseline conditions. This increase was significant only for lipoxygenase products. No differences were found amongst the three groups in the response of arachidonic acid metabolism to PAF and aspirin. Incubation with aspirin but not with PAF caused an increase in oxygen-free radical production in aspirin-intolerant patients whereas in aspirin-tolerant patients PAF, rather than aspirin, was the more potent stimulus for oxygen-free radical production. No differences in GSH-Px levels were found amongst the three groups. CONCLUSIONS: These results suggest that the platelet lipoxygenase pathway is activated in aspirin-intolerant patients and that the production of oxygen-free radicals may differentiate aspirin-tolerant from aspirin-intolerant asthmatic subjects. Our study, however, does not support the hypothesis that an increase in lipoxygenase products may be responsible for oxygen-free radical production. Moreover, a lowered platelet GSH-Px activity does not seem to be involved in this phenomenon.

Adult↗
PubMed1995

Diffuse alveolar hemorrhage in allogeneic bone marrow transplantation. A postmortem study.

To define better the syndrome of diffuse alveolar hemorrhage (DAH), we conducted a postmortem study in 77 patients who died of pulmonary complications, distributed into three groups. Group A included 47 patients with hematologic diseases treated with allogeneic bone marrow transplant (BMT); Group B, 20 patients with hematologic diseases treated with conventional chemotherapy; and Group C, 10 patients without hematologic diseases. The diagnosis of DAH was established when there was blood in at least 30% of the lung tissue evaluated without evidence of infection or any other pathologic change that could account for its presence. The presence of an associated pulmonary complication was considered only when there was normal lung parenchyma between both blood and the specific lesions. Diffuse alveolar hemorrhage was shown in 11 patients in Group A (23%) compared with 1 patient in Group B (5%) (p < 0.05). Of the 11 patients with DAH in Group A, 10 had some associated pulmonary complication: 7 presented with diffuse alveolar damage (DAD), 2 with associated bacterial pneumonia and 1 with invasive aspergillosis, 2 others had an associated cytomegalovirus (CMV) pneumonitis, and the remaining patients had an associated herpes pneumonia. There were no clinical differences between patients with and without DAH. Of 8 patients with confirmed DAH in Group A, who had been submitted to a bronchoscopic examination within 1 wk of death, 4 had normal BAL fluid; by contrast, 7 of 13 patients without DAH had hemorrhagic BAL fluid.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Role of bronchoalveolar lavage in the diagnosis of fat embolism syndrome.

Fat embolism syndrome (FES) is a serious clinical disorder occurring in trauma patients. The diagnosis of fat embolism syndrome may be difficult to establish clinically. We therefore wanted to investigate the usefulness of bronchoalveolar lavage (BAL) in the diagnostic evaluation of fat embolism syndrome. We analysed the presence of fat droplets in BAL cells in 32 trauma patients (7 with full diagnostic criteria of fat embolism syndrome, 17 with incomplete diagnostic criteria, and 8 with no diagnostic criteria at the time of bronchoscopy), 9 nontrauma patients with acute respiratory failure and radiographic pulmonary infiltrates, and a control group composed of 10 individuals. An increased percentage of oil red O positive alveolar macrophages (cut-off point > 3%) in BAL was found in 6 out of 7 patients with definite clinical criteria of fat embolism syndrome, and in 6 out of 20 trauma patients without the clinical diagnosis of fat embolism syndrome. In two patients with fat embolism syndrome, sequential BAL showed that the percentage of positive macrophages decreased when the clinical manifestations disappeared. An increased number of BAL macrophages with fat droplets was also observed in two trauma patients without evidence of fat embolism syndrome after long-bone surgical intervention. By contrast, all non-trauma patients had a percentage of positive cells lower than 3%. Our findings suggest that BAL oil red O positive macrophages are frequently observed in trauma patients irrespective of the presence of fat embolism syndrome. Conceivably, a high number of oil red O positive macrophages could reflect clinically silent fat embolization.

Adult↗
PubMed1994

[Acute myopathy related to the administration of glucocorticoids and neuromuscular blockers].

Two cases of acute myopathy following the administration of high doses of glucocorticoids in patients requiring mechanical ventilation and who were also administered neuromuscular blockers are presented. The patients were two women of 57 and 73 years of age. The doses of methylprednisolone administered were of 810 and 1,180 mg during the first 7 and 17 days, respectively. With regard to the total doses of neuromuscular blockers the first patient received 76 mg of pancuronium over 4 days while the second received 1,180 mg of atracurium over 17 days. This myopathy is characterized by a clinical and histological picture which differs from that associated to the chronic use of glucocorticoids being attributed to a toxic action of these drugs somewhat favored by immobilization due to the use of neuromuscular blockers. Given the lack of references in the literature on this entity in Spain a review was undertaken with the need for correct early diagnosis allowing differentiation from other causes of weakness such as ischemia of the cerebral trunk, polyradiculoneuritis and polyneuritis of critical patients being of note. Muscular biopsy is therefore very useful since very suggestive signs of this myopathy may be found. The disease is reversible with no effective treatment. An early rehabilitation program is the only method of shortening the convalescence period.

Acute Disease↗
PubMed1994

Comparison of the role of nasal polyp and normal nasal mucosal epithelial cells on in vitro eosinophil survival. Mediation by GM-CSF and inhibition by dexamethasone.

Eosinophilic infiltration of the respiratory mucosa is considered an inflammatory hallmark of allergic rhinitis, bronchial asthma and nasal polyposis. However, the mechanisms involved in this infiltration have not yet been totally elucidated. The objective of this study was to investigate and compare the influence of epithelial cell secretions from both nasal polyps (NP) and normal nasal mucosa (NM) on in vitro eosinophil survival. Epithelial cells were identified by microscopy and immunohistochemistry, cultured to confluence, and human epithelial cell conditioned media (HECM) was generated from cultures. Eosinophils were isolated at high viability and purity (> 90%) from peripheral blood and incubated with HECM. HECM from both NM and NP increased eosinophil survival in a dose-dependent manner, this effect being maximal at a concentration of 25% for NM (73.4% +/- 5.5%, n = 26, P < 0.001) and of 10% for NP (74.5% +/- 8.4%, n = 18, P < 0.001). Incubation of monoclonal antibody to human GM-CSF with HECM, neutralized the induction of eosinophil survival by HECM from both NM and NP. HECM from NP contained higher concentrations of GM-CSF (111 +/- 25.4 pg/ml, n = 17) than HECM from NM (97.1 +/- 15.2 pg/ml, n = 8), without reaching statistical significance. Pre-incubation of dexamethasone with eosinophils also blocked HECM-induced eosinophil survival from both NM (10(-8)-10(-5) M; IC50 = 9.5 nM) and NP (10(-7)-10(-5) M; IC50 = 83 nM). These results suggest that: firstly eosinophil infiltration into the respiratory mucosa during allergic reaction and nasal polyposis may be modulated at least in part by GM-CSF from epithelial cells; and secondly epithelial cells from NP might have a more potent effect on inducing eosinophil infiltration of the respiratory mucosa than epithelial cells from NM. Finally, we may consider this as a reliable in vitro model to compare the role of epithelial cells from inflammatory (NP) and non-inflammatory (NM) tissue in respiratory inflammation.

Cell Survival↗
PubMed1994

Prevention of further bone mass loss by nasal calcitonin in patients on long term glucocorticoid therapy for asthma: a two year follow up study.

BACKGROUND: Injectable calcitonin is effective in reducing spinal bone loss in steroid-dependent asthma but side effects are frequent. In contrast, a nasal spray presentation has been shown to be effective and well tolerated in involutional osteoporosis. To test the efficacy of nasal calcitonin a two year prospective trial was conducted in 44 steroid-dependent asthmatic patients. METHODS: All patients received a calcium supplement of 1000 mg and were allocated randomly into two groups treated with either salmon calcitonin nasal spray (200 IU every other day, n = 22) or calcium alone (n = 22) for two years. All patients completed the first year of the study. Five patients in each group dropped out during the second year. In the calcitonin group one patient developed generalised pruritus and four lost steroid dependence, and in the calcium alone group five were no longer dependent on steroids. The efficacy of treatment was evaluated as follows: bone turnover assessed by biochemical markers, bone loss assessed by serial measurement of lumbar spine density, and rates of bone fractures. RESULTS: The bone mass in the calcitonin group increased by 2.7% in the first year while in the group receiving calcium alone it decreased by 2.8%; this difference was significant. Calcitonin prevented more bone loss during the second year while the calcium alone group continued losing bone mass (-7.8%). The difference between means was 0.1077 (95% CI 0.0381 to 0.1773). Three new fractures occurred in both groups. No changes in biochemical parameters were detected in either group. CONCLUSIONS: Calcitonin given intranasally increased spinal bone mass during the first year of treatment and maintained bone mass in a steady state during the second year. These results suggest that calcitonin may be a useful agent to prevent steroid-induced osteoporosis. However, the lack of effect of calcitonin on the rate of vertebral fractures does not permit its recommendation for routine use in preventing steroid-induced osteoporosis.

Administration, Intranasal↗
PubMed1994

Response of the nose to exercise in healthy subjects and in patients with rhinitis and asthma.

BACKGROUND: Although the nose and the bronchi are both involved in the process of regulating respiratory heat exchange, thermal changes may precipitate airway obstruction during exercise but rarely cause nasal obstruction in patients with rhinitis. The cause of the different response of the nose and bronchial tree has hardly been investigated. This study was performed to assess the response of the nose during exercise in the presence of rhinitis, asthma, and in normal controls. METHODS: Ten healthy subjects (group 1), 15 patients with asthma and rhinitis (group 2), 10 with rhinitis only (group 3), and 11 with asthma only (group 4) were included in the study. Exercise was performed on a bicycle ergometer for six minutes, reaching a heart rate of 80% of predicted. Bronchial and nasal responses were measured by forced expiratory volume in one second (FEV1) and posterior rhinomanometry, respectively. A drop in the FEV1 of 20% or more was considered a positive exercise induced asthma challenge test. RESULTS: Heart rate and ventilation increased by a similar proportion in the four groups. The FEV1 significantly decreased in asthmatic patients (groups 2 and 4) but it did not change in healthy subjects (group 1) or in those with rhinitis (group 3). Thirteen asthmatic patients developed exercise induced asthma. Nasal patency increased with exercise by a similar proportion in all groups, and no differences were detected between those with rhinitis (groups 2 and 3) and those without (groups 1 and 4). Nasal patency had returned to basal values at 25 minutes after completion of exercise in the four groups. The nose of patients with exercise induced asthma, however, remained significantly more patent than in patients without exercise induced asthma between 10 and 30 minutes after exercise. CONCLUSIONS: These results suggest that the nose responds differently from the bronchi during exercise induced airway obstruction: whereas the bronchial tree responds by becoming narrowed, the nose becomes more patent. These findings suggest that the mechanisms regulating the response of the nose to exercise are different from those involved in the response of the bronchial tree.

Adult↗
PubMed1993

Patients with chronic glucocorticoid treatment develop changes in muscle glycogen metabolism.

High dose glucocorticoid may induce a significant myopathy with loss of thick myofilament from muscle, particularly if administered in conjunction with depolarizing drugs. Remarkably, the effect of chronic low dose glucocorticoid in muscle is vastly different, although it may induce changes in muscle glycogen metabolism as evidenced in animal experimental trials. However, there is no clear confirmation that these changes could develop similarly in patients. We evaluate clinical, functional, histological and metabolic muscle changes during chronic low-dose glucocorticoid treatment in 11 asthmatic patients. Remarkably, these patients did not develop clinical symptoms of myopathy nor significant muscle weakness or morphological changes in muscle histology. However, glycogen concentration and the activity of the main regulatory enzymes of glycogen metabolism, aldolase and creatine kinase were modified in comparison with controls. An increase in the synthesis and muscle cell deposition of glycogen and a decrease in the muscle glycogen degradation process have been suggested. These changes were not related with malnutrition. There was not correlation between histological and biochemical changes. We conclude that chronic treatment with glucocorticoid causes clear changes in glycogen metabolism in the skeletal muscle, resulting in glycogen muscle storage. The significance of these biochemical changes is unknown, but it can be well an associated phenomenon with glucocorticoid treatment.

Adult↗
PubMed1993

Release of chemical mediators and inflammatory cell influx during early allergic reaction in the nose: effect of furosemide.

BACKGROUND: We evaluated the effect of furosemide on allergen-induced rhinitis in a double-blind, crossover, placebo-controlled experiment. METHODS: Fourteen patients with rhinitis who were allergic to house dust were nebulized with an intranasal dose of 20 mg of furosemide or placebo before allergen challenge with an extract of Dermatophagoides pteronyssinus (100 BU). Clinical evaluation and nasal lavages with normal saline solution were performed at baseline; after placebo-furosemide nebulization, and at 10, 30, and 60 minutes after allergen challenge. Number of sneezes and a composite symptom score were recorded to evaluate clinical response. Prostaglandin E2 (PGE2), PGD2 peptide leukotrienes and 15-hydroxy, 5,8,11,13-eicosatetraenoic acid (15-HETE) were measured by radioimmunoassay in nasal lavages. Cells were counted and classified as epithelial cells, neutrophils, eosinophils, and others. RESULTS: No differences in either clinical symptoms or cell influx after allergen challenge were found between furosemide and placebo groups. PGE2 levels did not change after provocation, and furosemide had no effect on its production. Ten minutes after antigen challenge there was a marked increase of PGD2 (p < 0.01), peptide leukotrienes (p < 0.01), and 15-HETE (not significant) on both study days. However, no significant differences in the release of eicosanoids were found between furosemide and placebo groups. CONCLUSIONS: Our observations in the nasal mucosa suggest that furosemide has no effect on the release of proinflammatory and bronchoconstrictor metabolites (PGD2, peptide leukotrienes, and 15-HETE). In contrast to bronchial asthma, allergen-induced rhinitis was not effectively prevented by furosemide.

Adult↗
PubMed1993

Immunocytologic analysis of nasal cells obtained by nasal lavage: a comparative study with a standard method of cell identification.

For evaluation of two methods of nasal cell identification, cell morphology and immunocytologic analysis, nasal lavage was performed in 16 healthy subjects and 29 patients suffering from rhinitis. Nasal lavage smears were stained with May-Grünwald-Giemsa (MGG), and cells were identified according to their structure as epithelial cells, neutrophils, lymphocytes, eosinophils, and metachromatic cells (basophils and mast cells). Immunocytologic analysis was performed with monoclonal antibodies by the immunoalkaline phosphatase method. The following monoclonal antibodies were used: CK1, EG2, and CD3, which identify epithelial cells, activated eosinophils, and T lymphocytes, respectively; CD15, which recognizes mature granulocytic cells; and CD14, which reacts with monocytes and macrophages. A significant difference was observed between the two methods in the number of identified epithelial cells, in both controls (64.6 +/- 7.8% with MGG, 14.2 +/- 3.5% with CK1 analysis) and patients with rhinitis (56.9 +/- 7.6% with MGG, 18.2 +/- 3.7% with CK1 analysis). In contrast, no significant differences were found in eosinophil and neutrophil counts when the two methods were compared. After nasal allergic provocation, a significant increase in the number of eosinophils was observed with both methods in seven patients with rhinitis. The results of this study indicate that: 1) MGG staining is a useful method to identify the cells obtained by nasal lavage, and 2) immunocytologic analysis with monoclonal antibodies accurately identifies granulocytic cells, while only a low proportion of epithelial cells are detected, probably because anticytokeratin monoclonal antibody reacts only with viable cells.

Adult↗
PubMed1993

Aerosolised ribavirin in patients with advanced cryptogenic fibrosing alveolitis: a pilot study.

BACKGROUND: A report has recently been published concerning a patient with a cryptogenic fibrosing alveolitis who showed a striking improvement after being treated with the antiviral drug ribavirin (tribavirin, Virazid). The objective of this study was to further evaluate, in an open trial, the efficacy of rivabirin in cryptogenic fibrosing alveolitis. METHODS: Ten patients (eight women) with advanced cryptogenic fibrosing alveolitis received aerosolised ribavirin (6 g/day for 15 days). Chest radiographs, lung function, and severity of dyspnoea were evaluated before and after two weeks of rivabirin treatment and also at three and 12 months. RESULTS: No differences in radiographs, lung function impairment, or severity of dyspnoea were found after treatment. No side effects were detected. CONCLUSIONS: Administration of high doses of aerosolised ribavirin has no beneficial effects in patients with advanced cryptogenic fibrosing alveolitis.

Aerosols↗
PubMed1993

Failure of frusemide to increase production of prostaglandin E2 in human nasal mucosa in vivo.

BACKGROUND: It has been suggested that inhaled frusemide protects subjects with asthma against bronchoconstriction by enhancing the synthesis of prostaglandin E2 (PGE2). To evaluate this hypothesis the effect of frusemide on PGE2 production from nasal mucosa was studied. METHODS: Two main arachidonic acid metabolites produced by epithelial cells, PGE2 and 15-hydroxy 5,8,11,13-eicosatetraenoic acid (15-HETE), were measured by radioimmunoassay in nasal secretions obtained by nasal lavages with saline. Eleven healthy volunteers were randomly assigned to two study days, one week apart, in a double blind crossover study. Nasal instillation with three increasing doses of frusemide (5, 10, and 20 mg) or placebo was carried out at intervals of 15 minutes. Nasal lavages were performed immediately before nasal instillations and 15, 30, and 60 minutes after the last instillation. RESULTS: Baseline concentrations of 15-HETE were at least six times higher than PGE2. No differences between frusemide and placebo were detected either on PGE2 or 15-HETE release. CONCLUSIONS: The findings do not support the hypothesis that the antiasthmatic effect of frusemide may be due to increased synthesis of PGE2 or release in the respiratory mucosa.

Adult↗
PubMed1993

Cell content and albumin concentration in nasal lavage from patients with rhinitis.

Influx of inflammatory cells in the nose was evaluated in 14 patients with rhinitis and 11 healthy subjects. Nasal secretions were obtained by nasal lavages. Total cell count and differential count were carried out with a Neubauer chamber and in cytospin slides, respectively. Cells were classified according to their morphology as epithelial cells without nuclei (degenerated), epithelial nucleated cells, neutrophils, eosinophils, and other. Total protein and albumin concentration were measured by the Lowry method and a nephelometric assay respectively. A statistically significant difference was found in total nucleated epithelial cells (P < .01), total neutrophils (P < .01), and total eosinophils (P < .05) between patients and healthy subjects. A significant correlation was found between albumin/total protein concentration with eosinophil numbers (r = .83, P < .001) in patients with rhinitis. These findings suggest that eosinophils participate in the inflammatory process taking place in rhinitis. Since the cellularity present in the nose of rhinitic patients is similar to that usually found in the bronchial secretions of asthmatic patients obtained by bronchoalveolar lavage, our results also suggest that nasal lavage may be used in the study of the inflammatory cells involved in airway diseases.

Adult↗
PubMed1993

[Thoracic actinomycosis. Presentation of 3 cases].

We have had the chance to follow three patients with thoracic actinomycosis in a relatively short period of time (18 months). They were three male patients, with chronic dental infections. The illness appeared as toxic syndrome and fever. In all three cases diagnosis was made through samples obtained through fibropticbronchoscopy. At the same time all of them evolved favorably to the antibiotic treatment (penicillin and/or tetracyclines) prescribed. We conclude that the diagnosis of thoracic actinomycosis should be suspected in those patients with a compatible clinical and radiological condition, and who has suffered previous weakening diseases and periodontal lesions.

Actinomycosis↗
PubMed1993

BAL lymphocyte activation antigens and diffusing capacity are related in mild to moderate pulmonary sarcoidosis.

To investigate the relationship [corrected] between immunocytological features of bronchoalveolar lavage (BAL) and clinical indices in sarcoidosis, we studied the lymphocyte subsets, as well as the expression of human leucocyte antigen-DR (HLA-DR) and interleukin 2 receptor (IL-2R) antigens in BAL lymphocytes. We studied 16 patients with untreated sarcoidosis and 12 control subjects. We found significantly higher absolute numbers of lymphocytes bearing the IL-2R antigen in sarcoidosis. A stronger difference between groups was observed in both the percentage and absolute numbers of HLA-DR+ lymphocytes. We also found a moderate but significant correlation between the number of lymphocytes expressing the activation antigens and single breath carbon monoxide diffusing capacity in patients with sarcoidosis: DLCO vs HLA-DR+ lymphocytes (r = -0.60); DLCO vs IL-2R+ lymphocytes (r = -0.62); carbon monoxide transfer coefficient (KCO vs HLA-DR+ lymphocytes (r = -0.53); and KCO vs IL-2R+ lymphocytes (r = -0.58). Our results suggest that the reduction in diffusing capacity, expressed as either DLCO or KCO, results from the severity of alveolitis in mild to moderate sarcoidosis.

Adult↗
PubMed1992

Early and late-phase asthmatic reactions: a hypothesis.

Why might a foreign particle, exercise or fog inhalation precipitate two asthmatic reactions? It is reasonable to suspect that asthmatic patients develop two reactions because healthy subjects may also develop two physiological responses to the same stimuli. This suggestion is supported by the observation that living things have developed adaptative systems to confront either sudden or persistent changes in the environment or within the internal milieu. The results of several studies suggest that the early phase response (EPR) usually involves cells which are normal residents of the respiratory epithelium (mast cells) and pre-formed substances (histamine), whereas cells participating in the late phase reaction (LPR) are recruited from the circulation (eosinophils, basophils and T cells). Up to now most of the studies of the EPR and LPR have been addressed to detecting a cell or metabolite abnormality. This simplistic approach would probably not improve the knowledge of the mechanisms involved in asthmatic responses. Since the presence of isolated or dual responses seems to depend on the intensity and duration of the stimuli it is reasonable to suspect that EPR and LPR are the result of an excessive adaptative response of the bodies of asthmatics to sudden and prolonged/strong stimuli, respectively.

Acute Disease↗