MXPA03001840A - Apparatus for treatment of chronic obstructive pulmonary disease and associated method. - Google Patents

Abstract

An apparatus and method for treatment of a patient having a pulmonary disease involving chronic obstruction of the airways includes a container having therein a chamber containing a composition of L-tartrate in a pharmaceutically acceptable carrier; an opening connected to the chamber so as to provide an outlet thereof, the opening sized for producing droplets of a predetermined size range responsive to the composition being motivated from the chamber through the opening; and a source of motivating force connected with the chamber so as to motivate the compositions through the opening to thereby cause nebulization of the composition. A treatment kit comprises the container described and a mouthpiece connectable to the container so as to be in fluid connection with the opening and downstream therefrom to thereby convey the nebulized composition into a patient s mouth to thereby facilitate oral inhalation of the nebulized composition by the patient.

Description

APPARATUS FOR THE TREATMENT OF CHRONIC OBSTRUCTIVE PULMONARY PAD AND ASSOCIATED METHOD RELATED APPLICATION This application claims priority of the provisional application for E. U. Serial No. 60 / 229,066 filed on August 30, 2000, and which is incorporated herein by reference in its entirety.

FIELD OF THE INVENTION The present invention relates to the medical field, and more particularly to a treatment of a pulmonary condition that includes chronic obstruction of the respiratory tract, to a nebulizer apparatus for delivering the medicament, and to a treatment equipment for the same. REFERENCES CITED 1. Addington WR, Stephens RE, Gilliland K, Rodriguez M. Assesing the laryngeal cough reflex and the risk of developing pneumonia after stroke. Arch Phys ed Rehabil. 1999; 80: 150-4. 2. Addington WR, Stephens RE, Gilliland K, Rodríguez M. Assesing the laryngeal cough reflex and the risk of developing pneumonia after stroke: an interhospital comparison. Stroke. 1999; 30: 1203-7. 3. Tomori Z, Stransky A. Electroneurographic and pneumotachographic analysis of the expiration reflex. Physiol. Bohemoslov. 1973; 22: 589-601. 4. Fujimura M, Sakamoto S, Kamio Y, uda T. Cough receiver sensitivity and bronchial responsiveness in normal and asthc subjects. Eur Respir J. 1992; 5; 291 -5. 5. Fujimura M, Sakamoto S, Kamio Y, Saito M, Miyake Y, Yasui M, uda T. Cough threshold to inhaled tartaric acid and bronchial responsiveness to metacholine in patients with asthma and sino-bronchial syndrome. I ntern Med. 1992; 31: 17-21. 6. Addington WR, Stephens RE, Ockey RR, Kann D, Rodriguez M. A new aspiration screening test to assess the need for modified barium swallow study [abstract]. Arch Phys Med Rehabil. nineteen ninety five; 76: 1040. 7. Widdicombe JG. Reflexes from the upper respiratory tract. Bethesda, MD: The American Physiological Society; 1986. 8. Addington WR, Stephems RE, Gilliland K, Milar SP. Tartaric acid-induced cough and the superior laryngeal nerve evoked potential. Am J Phys Med Rehabil. 1998; 77: 523-6. 9. Sakamoto S, Fujirama M, Kamio Y, Saito M, Yasui M, Myayake Y, uda T, [Relationship between cough threshold to inhaled tartaric acid and sex, smoking and atopy in humans]. Nihon Kyobu Shikkam Gakkal Zasshi. 1990; 28: 1478-81. 10. Fujimura M, Sakamoto S, Kamio Y. uda T. Sex difference in the inhaled tartaric acid cough threshold in non-atopic healthy subjects. Thorax 1990; 45: 633-4. eleven . Tomori Z, Widdicombe JG. Muscular, bronchomotor and cardiovascular reflexes elicited by mechanical stimulation of the respiratory tract. J Physiol (Lond). 1969; 200: 25-49. 12. Sant'Ambrogio G, Widdicombe J. Reflexes from airway rapidly adapting raceptors. Respir Physiol.2001; 125: 33-45. 13. Addington WR, Stephens RE, Goulding RE. Anesthesia for the superior laryngeal nerves and tartaric acid-induced cough. Arch Phys Med Rehabil. 199; 80: 1584-6. 14. Coleridge JC, Coleridge HM. Afferent vagal C fiber nnervation of the lungs and airways and its functional significance. Rev Physiol Biochem Pharmacol. 1984; 99: 1-110. 15. Widdicombe JG. Afferent receptors in the airways and cough. Respir Physiol. 1998 Oct; 114: 5-15. 16. Widdicombe J. Airway receptors. Respir Physiol. 2001; 125: 3-15. 17. Widdicombe JG. Chemoreceptor control of airways. Respir Physiol. 1T92 Mar; 87: 373-8. 18. Youtsey JW. Egan's Fundamentals of Respiratory Care.

In: Egan DF, Scanlan CL, Spearman CB, Sheldon RL, eds. 5th / ed. St. Louis: Mosby; 1990; p.387.

BACKGROUND OF THE INVENTION The laryngeal cough reflex (LCR) and its precursor, the laryngeal cough expiratory reflex (LCER), are primordial brain-mediated reflexes that in humans have been shown to protect the upper respiratory tract from the aspiration of potentially harmful rial in the lungs. [1,2] LCER, when stimulated through the inhalation of a nebulized composition of tartaric acid, activates a cascade of neurological events that ultily result in contraction of the muscles, intercostal and abdominal, to produce an initial expiration in an attempt to clear the abnormal aspirant. This is followed by a series of more forced coughs with inspiratory and expiratory components (LCRs). [3]. Limited research has been conducted on the use of inhaled tartaric acid to induce cough in asthmatic subjects. A study by Fujimura and co-collaborators showed that the threshold of cough to tartaric acid does not differ between normal and asthmatic subjects and found that there is no correlation between the cough threshold and the bronchial response, which supports the hypothesis that cough and Bronchoconstriction are reflexes of the airways separated. [4,5], No previous study has fully described the effects of inhaled tartaric acid on pulmonary function parameters in asthmatics. During the last seven years we have tested LCER / LCR with nebulized compositions of tartaric acid (the cough reflex test, or RCT) to assess the integrity of the protective mechanism of the respiratory tract of the subjects and thus decide the feeding strategy appropriate to avoid aspiration pneumonia in patients with deterioration or neurological damage. RCT has also been performed in normal subjects and in patients with multiple co-morbidities, including asthma and COPD. [1, 2,6]. There have been no obvious adverse events related to the inhalation of this chemo-irritant, and therefore, we expect that the lung function parameters do not change significantly in either the normal group or an asthmatic group after inhalation of the nebulized tartaric acid composition. . However, laryngeal irritation by other chemo-irritants can cause reflex bronchoconstriction, mucosal vasodilation, and excess mucus secretion. [7] According to the above, one would expect the mechanical effects of the first two but not the last to drop quickly. In addition, the forced respiratory movements of the cough could disturb the function of the respiratory tract. Thus, there was the potential for adverse changes as the result of inhalation of tartaric acid, and it is theorized that these can be detected through pulmonary function tests (PFT). The original intent of this research, therefore, was to use PFTs to examine the effects of tartaric acid-induced cough on lung function in healthy, normal asthmatic individuals. The resulting measurements included specific pulmonary functions, and the occurrence of airway obstruction or bronchospasm.

BRIEF DESCRIPTION OF THE INVENTION With the foregoing in mind, the present invention advantageously provides a nebulizer apparatus for the treatment of a patient having a lung disease that includes chronic obstruction of the respiratory tract. The apparatus is adapted for self-treatment by the patient, and comprises a container sized to be carried by the patient and having therein a chamber containing a composition comprising a pharmaceutically acceptable carrier mixed with tartaric acid L. A nebulization valve which has a - ß - aperture connected to the camera is positioned to provide an output thereof, and a source of motivational force connected with the camera to motivate the composition through the opening in the nebulizer valve to thereby cause nebulization the composition . In the apparatus, the nebulization comprises droplets having a diameter in the air of less than about 10 μP? , and tartaric acid L is mixed in the composition in an amount effective to cause an increase in maximum respiratory flow when inhaled by the patient. The invention also includes a method for the treatment of a patient who has a lung disease that includes chronic obstruction of the respiratory tract. The method comprises inhaling by the patient a nebulized composition comprising a pharmaceutically acceptable carrier mixed with tartaric acid L in an amount effective to cause an increase in maximum respiratory flow. The pharmaceutically acceptable carrier preferably comprises a solution having at least about 0.1 M sodium chloride, and at least about 20% L tartrate. A treatment kit is adapted for self-treatment by a patient having a pulmonary disease that includes chronic obstruction of the respiratory tract. The equipment comprises a container sized to be carried by the patient, and containing a pharmaceutically acceptable carrier mixed with tartaric acid L in an amount effective to cause an increase in maximum respiratory flow when inhaled by the patient, a nebulizer valve connected to the patient. the chamber, and a source of pneumatic pressure to motivate the composition through the valve to thereby generate a nebulized composition comprising droplets having a diameter in the air of less than about 10 μ? t ?. The kit also includes a generally tubular mouthpiece connectable to the container to be in fluid connection with the nebulization valve for transmitting the nebulized composition in a patient's mouth for oral inhalation by the patient. Optionally, the equipment may also comprise a removable cap that fits over the mouthpiece, nose clips to assist the patient in oral inhalation of the composition, and a respiratory flow meter to determine the increase in maximum respiratory flow.

BRIEF DESCRIPTION OF THE DRAWINGS Some of the features, advantages and benefits of the present invention that have been established will be apparent as the invention proceeds when taken in conjunction with the accompanying drawings in which: Figure 1 is a flow chart illustrating a method of treatment according to an embodiment of the present invention; Figure 2 shows the nebulizer apparatus of the present invention in use; and Figure 3 is a top plan view of an equipment comprising the invention described for self-treatment by a patient.

DETAILED DESCRIPTION OF THE PREFERRED MODALITY The present invention will now be described more fully below with reference to the accompanying drawings, in which preferred embodiments of the invention are shown. This invention can, however, be included in many different forms and should not be construed as limiting the illustrated embodiments set forth herein. Preferably, these illustrated embodiments are provided so that this description will be direct and complete, and will fully convey the scope of the invention to those skilled in the art. Study Subjects After health history interviews and informed consent, 20 healthy volunteers and 20 asymptomatic medicated asthmatics are included in a two-part evaluation of PFT. The forty subjects were non-smokers. The study is done in the doctor's office. A certified respiratory therapist administered RCT and performed all PFTs. Study Design RCT stimulates cough receptors in the vestibule of the larynx and initiates LCER / LCR. [4,5,8-10] RCT (Pneumoflex Systems, Inc., Orlando, FL) is performed by administering to the subjects a composition comprising a 20% solution of pharmaceutical grade L tartaric acid, dissolved in 0.15M of sterile NaCl solution, and inhale from a Bennett Twin nebulizer. During inhalation, the nose of the subject is squeezed. The nebulizer outlet was approximately 0.2 ml / min. [1, 2,4-6,8, 10] Subjects are tested in a stopped position for all RCT and PFT tests. The subjects were tested for two effective inhalations. The subject was asked to exhale, then insert the mouthpiece, and take a deep, sharp inhalation. The spill around the mouthpiece and "snorting" by the nebulizer are not considered effective inhalations. The respiratory therapist used a Spiromate AS-600 for all PFTs (SN6546, Riko Medical and Scientific Corporation Instruments). In the first part of the baseline PFT assessment is performed, followed by two separate inhalations of a nebulized solution of 20% tartaric acid. In the second part, PFT is repeated 5 min after the second inhalation. After RCT, each subject answers questions regarding the effects and sensations experienced during inhalation. The subjects are monitored and asked about the residual effects for 15 minutes after the procedure. An ongoing 24-hour interview is conducted considering the experience of the procedure. Five specific lung variables are examined, both before and after the administration of RCT, including: FEV1 (Pr * -RCT) Forced Expiratory Volume in 1 s before RCT FEV1 (p0 «t-5 RCT) Forced Expiratory Volume in 1 s 5 min after RCT FVC (Pre-RCT) Vital capacity forced before RCT FVC (or «t-5 RCT) Vital capacity forced 5 min after RCT FEV1 / FVC (Pr-RCT) FEV1 / FVC observed before RCT FEV1 / FVC (Po.ts RCT) FEV1 / FVC observed 5 min after RCT Maximum inspiratory force before RCT Ipspiratory force Maximum 5 min after RCT Expiratory force Maximum before RCT Maximum Expiratory Force 5 min after RCT Analysis The data collection is conducted in each subject and includes informed consent, health history questionnaire and an impression of pulmonary function data. Twenty normal subjects and twenty asthmatics are selected to determine the statistical differences between pre- and post-PFT variables. Both test groups had 1 0 males and 1 0 females. The average age is calculated for each group. Two non-parametric techniques are used according to the amount of twisting, which is determined by comparing g = k / s with the critical value in < x = 0.05, where At a = 0.05 the critical value of two sides is .942 for n = 20. If g > .942 then the twisting is significant. A positive value for g > 0 means that there is positive twisting (Average <Average). Differences that are significantly distorted are examined when using the signal test. However, the differences that are not significantly skewed are examined by using a more powerful technique, the Wilcoxon Signed Rank Test. Results The average age of the normal and asthmatic subjects was 36.85 + 8.62 (S.D.) and 66.20 + 13.13, respectively. All subjects had a normal reflex response to RCT, consisting of LCER efforts followed by CSF with no adverse effects. A. Statistical Comparison for Normal Subjects The statistics of twisting are displayed in Table 1. Five pairwise comparisons are investigated. The appropriate statistical tests and the corresponding P values are shown in Table 1; PIF (Pre-RCT) is significantly smaller than PIF (Pott-S R CT), by approximately 21%. B. Statistical Comparison for Subjects with Asthma The statistics of twisting are shown in Table 2. Five pairwise comparisons are investigated. The appropriate statistical tests and the corresponding P values are shown; PEF (p ".N CT) is significantly smaller than PEF (p0.ts RCTJ.) By approximately 7% C. Comparison between Asthma data and Normal data Table 3 shows that for each of the ten variables investigated, the Normal group always had higher average values than the group with asthma.

Table 1. Turning Statistics and Comparisons Parametric for Normal Subjects Statistical Differences Twisted or Test P-value of symmetric twisting statistics FEV1 (Pr FEV1 (Poit-s +2,510 Twisted Test of .359 FVC signal (Pre) -FVC (Po.t-5 +1.973 Twisted Test of .648 FEV1 / FVC signal) -FEV1 / FVC + 3.808 Twisted Test of .503 (Po.t-S signal PIF [Pre) -PIF (pomi.B - 204 Symmetric Wllcoxon .004 EF (Pre F (0, t-5 +1,046 Twisted Test of .824 signal Table 2. Turning Statistics and Comparisons No Parametric for Subjects with Asthma Difference * Statistics Twisted or Test P value of statistical symmetric distortion FEV1 (Pr FEV1 (Po.t-3 + .143 Symmetric Wllcoxon .198 FVCfPre -FVCíPo.t-í + .T76 Twisted Test of .503 to FEV1 / FVC (Pre.RCT) -FEV1 / FVC -3.232 Twisted Test of .503 (Po »t-5 signal PIF (Pr) -PIF (Pott-5 -1.202 Twisted Test of .210 EF signal (pr« RCT) - PEF (p0 «t-5 -.023 symmetric Wilcoxon .014 Table 3. Descriptive Comparison between Normal Subjects and with Asthma Variables Mean Average Deviation Standard (standard) deviation (Asthma) standard (normal) (Asthma) FEV1 (pf # -RCT) 3.99 .74 1 .98 .820 FEV1 (Po "ts 3.88 .77 2.07 .653 RCT) FVC (Pr # -RCT) 4.93 .94 2.92 1 .06 FVC (Po« t-5 RCT ) 4.87 1 .01 2.97 1 .04 FEV1 / FVC 81.18 5.77 67.39 19.70 (Pr «-RCT) FEV1 / FVC 75.60 19.00 74.00 17.70 IPo.t-6 RCT1 PIF (Prn-RCT) 5.26 1 .79 2.79 1 .09 PIF (Po, t.6 RCT1 6.38 2.05 3.24 1 .62 PEF (pre-ncT) 7.83 2.20 3.67 1 .98 PEF (p0 «t-5 RCT) 7.65 1 .95 4.03 2.24 Discussion There is no significant reduction in either asthmatic or normal lung function parameters after inhalation of tartaric acid. This supported our expectation that CR has no adverse effects, despite potential increases in bronchodus- tonus, mucosal vasodilation or lower mucus secretion from the airways. Since these last three changes are almost invariably induced by induced irritations of the laryngeal mucosa [7], it is unlikely that a direct reflex of the laryngeal region can explain the increases in maximum expiratory and inspiratory flows. Mechanical irritation of the nasopharyngeal mucosa! bronchodilation [1 1], but the receptors for this reflex are not very chemosensitive and the associated respiratory changes are not expiration or coughs are inspiratory efforts (the aspiration reflex). Based on this, it would seem that it is unlikely that nasopharyngeal reflexes are to mediate any branching after TCR. The laryngeal receptors for LCER and CSF are receptors that adapt almost certainly almost ("irritant") (RARs), both in experimental animals [12] and in man [8], and that are stimulated by acid solutions. C-fiber receptors in the trachea, bronchi and alveolar walls are also stimulated by acidic solution, and although the response of laryngeal C-fiber receptors to acid does not seem to have been studied, there is no reason to believe that they behave differently from those anywhere in the respiratory tract. In humans, however, bilateral anesthesia of the internal branch of the superior laryngeal nerve eliminates the cough induced by tartaric acid and allows tidal respiration of the nebulized vapor without cough, supporting the proposition that RARs are responsible for the laryngeal cough. [13] In contrast, stimulation of C-fiber receptors in the lower respiratory tract causes rapid low breathing or apnea, bronchoconstriction, mucus secretion, and mucosal vasodilation by central nervous reflexes [14, 15] and, for changes in Respiratory tract by local release of sensory neuropeptides such as substance P [16]. These responses are not consistent with the increases in maximum respiratory flows described herein. In this way, it is difficult to attribute unexpected increases in maximum flow to known neurological mechanisms. One possibility is that strong mechanical events triggered by laryngeal cough could be responsible for increases in peak flow. Long inflations of the lung do not extend the airways and can open any collapsed airway. In asthmatics, if any mucus is present in the respiratory tract, the cough can remove it and thus increase the caliber of the respiratory tract. Hyperventilation of cough can cause bronchodilation, since hypercapnia and hypoxia are stimulants to bronchoconstriction. [17] An additional possibility is that the pronounced cardiovascular changes associated with cough may include a release of catecholamines from the adrenal glands, which could have a long-lasting bronchodilator effect. We can not explain the unexpected result where healthy subjects demonstrated an RCT that shows maximum inspiratory flow, whereas in asthmatics it was the maximum expiratory flow that increased. Possibly, the considerable differences in the average age and lung function parameters between the two groups (Table 3) may be a factor. Although maximum flow measurements can be influenced by subject cooperation and effort, no lack of cooperation was apparent in this subjects. [18] Accordingly, we conclude that RCT does not cause adverse changes in lung function parameters, but preferably unexpectedly brings about an improvement in maximum respiratory flow in both normal and asthmatic subjects by an unknown mechanism.

Preferred Modalities of the Invention With the foregoing in mind, the invention includes a method for the treatment of a patient having a lung disease that includes chronic obstruction of the respiratory tract. The method comprises inhaling a nebulized composition of tartrate L in a pharmaceutically acceptable carrier in an amount effective to cause an increase in maximum respiratory flow. As shown in Figure 1, the method starts [Block 5] with the preparation of the composition [Block 7], followed by nebulization of the composition [Block 9], inhalation of the composition nebulized by the patient [Block 11] , and finally when measuring the maximum respiratory flow [Block 13]. Inhalation can be repeated if no increase is measured [Block 15]. If the increased flow is observed, the method stops [Block 17]. As noted above, the inhalation of tartrate L will cause the patient to cough, however, it is not known if the cough mechanism is instrumental in producing the increase discovered in maximum respiratory flow after treatment. The tartrate L is preferably in a form substantially soluble in an aqueous solution of isotonic sodium chloride. A concentration of tartrate L that is preferred in the present invention is about 20% tartrate L. The skilled artisan will appreciate that the nebulized composition preferably comprises droplets having an air diameter of about 10pp or less to promote penetration into the tracts. lower respiratory The composition was found to be nebulized adequately at a rate of about 0.2 ml per minute. In the present invention, the pulmonary condition comprises the group of chronic obstructive pulmonary diseases consisting of chronic simple bronchitis, asthma and asthmatic bronchitis, chronic obstructive bronchitis, efisema, bronchiectasis, cystic fibrosis and broncholitis. Another aspect of the invention includes a nebulizer apparatus 20 adapted for self-treatment by a patient having a pulmonary condition that includes chronic airway obstruction, as shown in use in Figure 2. The nebulizer includes a vessel 22 dimensioned to be carried by the patient and having therein a chamber containing a composition comprising a pharmaceutically acceptable carrier mixed with tartaric acid L in an amount effective to cause an increase in maximum respiratory flow when inhaled by the patient. As is known in the art, a nebulization valve having an opening is connected to the chamber to provide an outlet therefrom. A source of motivational force communicates with the chamber to motivate the composition through the opening in the nebulization valve to thereby cause nebulization of the composition to comprise droplets having a diameter in the air of less than about 10 μ? P . Typically, the container 22 comprises a metal cylinder, and the motivating force source comprises pneumatic pressure, and preferably a compressed gas within the container. Additionally, the nebulizer apparatus 20 comprises a mouthpiece 24 placed in fluid connection with the opening and downstream thereof to thereby transmit the nebulized composition to the mouth of the patient to facilitate oral inhalation. The pharmaceutically acceptable carrier preferably comprises a solution of at least about 0.15 M sodium chloride, and is prepared with at least about 20% tartaric acid L. Yet another aspect of the invention, as shown in Figure 3, includes a treatment equipment 30 adapted for self-treatment by a patient who has a pulmonary condition that includes chronic obstruction of the respiratory tract. The equipment 30 comprises the container 22 described above, and a mouthpiece 24 connectable to the container to be in fluid connection with the opening of the valve and downstream thereof to thereby transmit the nebulized composition in a patient's mouth to facilitate oral inhalation . The treatment equipment advantageously may further comprise a removable lid 26 that fits over the mouthpiece 24 for protection. further, the treatment equipment may include a plurality of containers providing thus replacements, and may also include nose clips 28, and a respiry flow meter 32 to measure the increased maximum respiry flow. According to the foregoing, the specification describes a typical preferred embodiment of the invention, and although specific terms are employed, the terms are used in a descriptive sense only and not for purposes of limitation. The invention has been described in considerable detail with specific reference to these illustrated embodiments. It will be apparent, however, that various modifications and changes may be made within the spirit and scope of the invention, as described in the above specification and as defined in the appended claims.

Claims (1)

1. CLAIMS 1. A nebulizer apparatus containing a medicament composition adapted for self-treatment by a patient having a pulmonary condition including chronic obstruction of the respiratory tract, comprising: a container sized to be carried by the patient and having therein a chamber containing the medicament composition comprising a pharmaceutically acceptable carrier mixed with tartaric acid L; a misting valve having an opening connected to said chamber to provide an outlet therefor; and a source of motivational force connected to said chamber to motivate said composition through the opening in said nebulization valve to thereby cause the nebulization of said composition; wherein the nebulization comprises drops having a diameter in the air of less than about 10 μ? t ?, and wherein the tartaric acid L is mixed in the composition in an amount effective to cause bronchodilation resulting in an increase in flow maximum respiratory rate after the medication is inhaled by the patient. 2. The nebulizer apparatus according to claim 1, characterized in that said pharmaceutically acceptable carrier comprises a solution of sodium chloride. 3 . The nebulizer apparatus according to claim 1, characterized in that said pharmaceutically acceptable carrier comprises a solution of at least about 0.15 M sodium chloride. The nebulizer apparatus according to claim 1, characterized in that the composition is prepared with at least about 20% tartaric acid L. 5. The nebulizer apparatus according to claim 1, characterized in that it further comprises a mouthpiece placed in fluid connection with said device. opening of the valve and downstream thereof to thereby transmit the nebulized composition to facilitate oral inhalation of the nebulized composition by a patient. 6. A device adapted for the self-treatment of therapeutic bronchodilation by a patient, said equipment comprising: a tartaric acid drug composition L contained in a container sized to be carried by the patient, said container having a chamber containing the composition that it comprises a pharmaceutically acceptable carrier mixed with tartaric acid L, a nebulization valve having an opening connected to said chamber to provide an outlet therefor, and a pneumatic pressure source connected to said chamber to motivate said composition through the opening in said nebulization valve to thereby generate a nebulized composition comprising droplets having a diameter in the air of less than about 10 μ? , and wherein the tartaric acid L is mixed in the composition in an amount effective to cause bronchodilation which results in an increase in maximum respiratory flow after the composition is inhaled by the patient; and a generally tubular mouthpiece connectable to said container to be in fluid connection with said opening and downstream therefrom to thereby transmit the nebulized composition to a mouth of the patient for oral inhalation. The treatment equipment according to claim 6, further comprising a removable lid that fits over said mouthpiece. The treatment equipment according to claim 6, further comprising a plurality of containers thus providing replacements. 9. The treatment equipment according to claim 6, further comprising clamps. 10. The treatment equipment according to claim 6, further comprising a respiratory flow meter. eleven . Use of tartaric acid L for the manufacture of a therapeutic medicament comprising a composition of tartaric acid L in an amount effective to cause an increase in maximum respiratory flow after the medicament is inhaled by a patient. 12. A composition of tartaric acid L for therapeutic use as a medicament in a patient having a pulmonary condition including chronic obstruction of the respiratory tract, the composition comprising a pharmaceutically acceptable carrier mixed with an effective amount of tartaric acid L to cause a increase in maximum respiratory flow after the medication is inhaled by a patient. RESU EN An apparatus and method for the treatment of a patient having a pulmonary condition including chronic obstruction of the respiratory tract, includes a container having therein a chamber containing an L-tartrate composition in a pharmaceutly acceptable carrier; an opening connected to the chamber to provide an outlet therefrom, the aperture sized to produce droplets of a predetermined size range responsive to the motivating composition of the chamber through the aperture; and a source of motivational force connected with the camera to motivate the compositions through the opening to thereby cause the nebulization of the composition. A treatment device comprises the container described and a mouthpiece connectable to the container to be in fluid connection with the opening and downstream thereof to thereby transmit the nebulized composition to the mouth of the patient to thereby facilitate oral inhalation of the nebulized composition for the patient.