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2 Fig. 1 Schema of experiment. Single injections of arachidonic acid or blocker were given via the jugular vein. Airway pressure (Paw) and systemic blood pressure (S.B.P.) were observed.
3 Flg.2 Dose-related changes in increase of airway pressure ( Paw) following single injection of arachidonic acid in guinea pigs. Table 1 Clinical Data of Aspirin-Sensitive Asthmatic Patients *: Acetylcholin **: Diagnosed by oshima's classification. 10)
4 Table 2 Results of Provocation Tests *o Saturated solution is estimated for 3 mg/ml. Fig. 3 Time course of bronchial inhalation chalet lenge with sulpyrine (1)-(7): case number. ( ):concentration of sulpyrine. (mg/ml)
5 Fig. 4 Time course of bronchial inhalation challenge with aspirin. (1)-(7) : case number ( ) : concentration of aspirin. (mg/ml) Fig. 5 Time course of intravenous injection challenge with sulpyrine. (1) -(7): case number. ( ): dose of sulpyrine. (mg) Fig. 6 Blocking effects of aspirin and sulpyrine on arachidonic acid-induced bronchoconstriction in guinea pigs. The bars represent SE of the means. ( ): number of guinea pigs experimented.
6 Fig. 7 Dynamic blocking effects of aspirin-like drugs on arachidonic acid-induced bronchoconstrlctlon in guinea pigs. Fig. 8 Dynamic change of midimum effective doses of aspirin-like drugs required to block arachidonic acid-induced bronchoconstriction in guinea pigs completely.
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9 1) Yurchak, A.M., Wicher, K. & Arbesman, C.E.: Immunologic studies on aspirin. J. Allergy, 46: 245, 1970.
10 2) Samter, M. & Beers, R.F.: Intolerance to aspirin. Clinical studies and consideration its pathogenesis. Ann. Intern. Med., 68: 975, ) Vane, JR.: Inhibition of prostaglandin synthesis as a mechanism of of action for aspirinlike drugs. Nature (New Biol.), 231: 232, ) Szczeklik, A., Gryglewski, R.J. & Czerniawska- Mysik, G.: Relationship of inhibition of prostaglandin biosynthesis by analgesics to asthma attacks in aspirin-sensitive patients. Br. Med. J., 1: 67, ) Piper, P. & Vane, J.: The release of prostaglandins from lung and other tissues. Ann. N.Y. Acad. Sci., 180: 363, ) Frey, H.H. & Deng jel, C.: Antagonism of arachidonic acid-induced bronchoconstriction in cats by aspirin-like analgesics. Eur. J. Pharmacol., 40: 345, ) Settipane, GA. & Pudupakkam, R.K. : Aspirin intolerance. Subtypes, familial occurrence, and cross-reactivity with tartrazine. J. Allergy Clin. Immunol., 56: 215, ) Chafee, F.H. & Settipane, GA.: Aspirin intolerance. I. Frequency in an allergic population. J. Allergy Clin. Immunol., 53: 193, ) Szczeklik, A., Gryglewski, R.J., Czerniawska- Mysik, G. & Zmuda, A.: Aspirin-induced asthma. J. Allergy Clin, Immunol., 58: 10, ) Szczeklik, A., Gryglewski, R.J. & Czerniawska- Mysik, G.: Clinical patterns of hypersensitivity to nonsteroidal anti-inflammatory drugs and their pathogenesis. J. Allergy Clin. Immunol., 60: 276, ) Stone, K.J., Mather, S.J. & Gibson, R.P. : Selective inhibition of prostaglandin biosynthesis by gold salts and phenylbutazone. Prostaglandins, 10: 241, ) Orehek, J., Douglas, J.S. & Bouhuys, A.: Contractile responses of the guinea-pig trachea in vitro. Modification by prostaglandin synthesis-inhibiting drugs. J. Pharmacol, Exp. Ther., 194: 554, ) Stevenson, D.D., Arroyave, CM., Bhat, K.N. & Tan, E.M.: Oral aspirin challenges in asthmatic patients. A study of plasma histamin. Clin. Allergy, 6: 493, ) Basomba, A., Romar, A., Pelaez, A., Villalmanzo, I.G. & Campos, A.: The effect of sodium cromoglycate in preventing aspirin induced bronchospasm. Clin. Allergy, 6: 269, ) Svensson,,J., Strandberg, K., Tuvemo, T. & Hamberg, M.: Thromboxane A. Effects on airway and vascular smooth muscle. Prostaglandins, 14: 425, ) Flower, R.J. & Vane, JR.: Inhibition of prostaglandin biosynthesis. Biochemical Pharmacol., 23: 1439, 1974.
11 Abstract Aspirin-induced Asthma Detection by Inhalation Challenge with Sulpyrine- Tsutomu Saga The Third Department of Internal Medicine, School of Medicine, Kanazawa University Seven patients with aspirin-induced asthma werechallenged with intravenous injection of sulpyrine, inhalation of sulpyrine and of aspirin. FEV1.0 and clinical symptoms were recorded serially. In all of seven patients, inhalation of sulpyrine solution with concentrations from 3 to 50 mg /ml induced bronchoconstriction, but this reaction was weaker and milder than did aspirin. A close correlation was found among the minimumeffective doses of the drugs used in these three challenge tests studied. We also studied the in vimo inhibitory action of aspirin, sulpyrine and some other aspirin-like drugs on arachidonic acid-induced bronchoconstriction in the guinea pig and found that sulpyrine is weaker and milder in activity than is aspirin and one of the most reversible of the tested drugs which is consistent with the above clinical findings. Our results are compatible with the hypothesis that aspirin hypersensitivity is related to theinhibition of prostaglandin synthetase in the lung.
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