Bronchial asthmatic response

Karol et aJL (23), are among the research" workers who have investigated the mechanism of bronchial asthmatic response. Only in cases that have developed an extreme sensitivity as demonstrated by bronchial asthmatic response to a few minutes exposure to concentrations of isocyanate on the order of 25 ug/m3 has there been a demonstration of a circulating antibody that will react with a human serum albumin-toluene monoisocyanate antigen. Research is continuing to define the mechanism or mechanisms of the bronchial asthmatic response that some persons develop from exposures to isocyanates. 

Single dose or short-term treatment with aerosolized steroids inhibits both the late asthmatic response and allergen-induced bronchial hyperresponsiveness (45,92). However it does not affect the early asthmatic response nor does it induce bronchodilation (45,92). Long-term treatment with steroids protects against both the early and late asthmatic responses and also reduces bronchial hyperresponsiveness (44,71,86,93). Over time, the airways relax (dilate) and measures of airway function, such as forced expiratory volume in one second (FEV ), gradually return to almost normal levels. 

Nasal vasculature may offer some insight into this question, though research to date has been equivocal. Nasal turbinate vessels can be classified as either capacitance vessels or resistive vessels. Capacitance vessels appear to vasodilate in response to infection while resistance vessels appear to respond to cold stimuli by vasoconstriction. Buccal vascular structures also respond to thermal stimuli but appear to respond principally to cutaneous stimuli. How pharyngeal and tracheobronchial submucosal vessels react to thermal stimuli is not known, though cold-induced asthma is believed to result from broncho-spasms caused by susceptible bronchial smooth muscle responding to exposure to cold dry air.- This asthmatic response suggests an inadequate vascular response to surface cooling. 

Chronic exposure to fumes of heated glacial acetic acid in a canning factory has been associated with a late airway response resulting in chronic inflammation and severe bronchial asthma. Inhalation challenge induced a late asthmatic response, confirming sensitization. ... 

Lai CK, Twentyman OP, Holgate ST. The effect of an increase in inhaled allergen dose after rimiterol hydrobromide on the occurrence and magnitude of the late asthmatic response and the associated change in nonspecific bronchial responsiveness Am Rev Respir Dis 1989 140(4) 917-23. 

Cartier, A., Thomson, N.C., Frith, P.A., Roberts, R and Har-greave, F.E. (1982). Allergen-induced increase in bronchial responsiveness to H relationship to the late asthmatic response and change in airway calibre. J. Allergy Clin. Immunol. 70, 170-177. 

There are numerous reports on changes in SOD and catalase activities in various diseases [30,41, 97,150], e.g., reduced SOD activity in lung cells (by about 50% in bronchial epithehal cells) was found in asthma and suggested to be a marker of the inflammation characterizing asthma [194]. Loss of SOD occurs within minutes of an acute asthmatic response [195]. 

Inflammatory disease associated with bronchial hyperactivity (BHR), bronchospasm, T mucus secretion, edema, and cellular infiltration. Early asthmatic responses (EAR) lasting from 30 to 60 min are associated with bronchospasm from the actions of released histamine and leukotrienes late asthmatic responses (LAR) involve infiltration of eosinophils and lymphocytes into airways - > bronchoconstriction and inflammation with mucus plugging. 

The fact that these concentrations have been measured does not mean that occupational exposures occur persons may use respiratory protection equipped to prevent exposure. All persons who have excessive occupational exposure to isocyanates may experience primary irritant effects in the respiratory tract depending on the extent of excessive exposure. Brief accidental exposures to concentrations of isocyanates tenfold or more above the TLV may cause short term respiratory irritation with recovery 24-48 hours following cessation of exposure. Continuing repeated workday exposures several-fold higher than the TLV can cause chronic respiratory irritation. All individuals will not suffer the same degree of respiratory irritation from excessive exposures due to individual biochemical and physiological differences. Studies have shown that on the order of five percent of persons who have had an occupational exposure to TDI develop a bronchial asthmatic type of response to subsequent exposures that are below concentrations causing any detectable primary irritation. 

Fluticasone is a respiratory inhalant combination. Fluticasone inhibits multiple cell types (e.g., mast cells) and mediator production or secretion (e.g., histamine) involved in the asthmatic response. Salmeterol produces bronchodi-lation by relaxing bronchial smooth muscle through beta-2-receptor stimulation. Indications they are indicated in... 

Mast cells release histamines, leukotrienes and other mediators of the inflammatory process. Mast cell stabilizer drugs inhibit the early asthmatic response and the late asthmatic response. They have no bronchodilator effect nor do they have any effect on any inflammatory mediators already released in the body. They are indicated for the prevention of bronchospasms and bronchial asthma attacks. They are administered by aerosol inhalation. The exact action of the drugs have not been determined. However, they are believed to have a modest effect in lowering the required dose of corticosteroids. The most common mast stabilizer dmgs are cromolyn (Intal) and nedocromil (Tilade). 

Long-term exposure studies at levels below the established TLV values of Table 14.1 have established for TDI, MDI and NDI that loss of pulmonary function does not occur compared with control groups. However, there is an important qualification to this generalization in that when respiratory sensitization to isocyanates has occurred, it is no longer safe to be exposed to even the TLV value and further contact with isocyanate must be avoided as a short instantaneous exposure will usually bring about an instantaneous asthmatic response. Individuals who suffer from constitutional respiratory problems or acquire hyperactivity of the bronchial system are always at greater risk from isocyanate exposure and should avoid its use. 

Cartier A, Thomson NC, Erith PA, Roberts R, Hargreave FE. Allergen-induced inaease in bronchial responsiveness to histamine relationship to the late asthmatic response and change in airway caliber. J Allergy Clin Immunol 1982 70 170-177. 

Cockcroft DW, Murdock KY. Comparative effects of inhaled salbutamol, sodium cromoglycate and beclomethasone dipropionate on aUergen-induced early asthmatic responses, late asthmatic responses and increased bronchial responsiveness to histamine. J Allergy Chn Immunol 1987 79 734-740. 

Asthma is an extremely complex condition characterized by variable and reversible airways obstmction combiaed with nonspecific bronchial hypersensitivity (1 3). The cause of asthma, which is not always readily diagnosed (4), remains unknown. Days, if not weeks, ate needed to document the spontaneous reversal of the airways obstmction ia some patients. Asthmatics experience both an immediate hypersensitivity response and a delayed late-phase reaction, each mediated by a different pathway. Chronic asthma has come to be viewed as an inflammatory disease (5). The late-phase reaction plays a key role ia iaduciag and maintaining the inflammatory state which ia turn is thought to iaduce the bronchial hyperresponsiveness (6). The airways obstmction results from both contraction of airways smooth muscle and excessive bronchial edema. Edema, a characteristic of inflammatory states, is accompanied, ia this case, by the formation of a viscous mucus which can completely block the small airways. 

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