Download Allergens and Airway Hyperreactivity by Mieczyslaw Pokorski PDF

By Mieczyslaw Pokorski

Respiratory hypersensitivity is continually encountered and is sharply at the upward push, fairly within the such a lot susceptible age-groups: little ones and seniors. hypersensitivity leads to airway hyperactivity and elevated airway resistance, with all inflammatory sequelae being ensued. The chapters convey how respiration hypersensitive reaction examine is interconnected with different disciplines through discussing neurotransmitter, membrane receptor, and ionic channel mechanisms of hypersensitive reaction and via giving diagnostic and pharmacological cues on desensitization and therapy.

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001 vs. 4 Effect of Long-Term Therapy on eNO OVA-induced allergic inflammation evoked a marked increase in eNO. Long-term treatment with both NS1619 and a control drug, budesonide, resulted in significant decreases in eNO. On the other hand, pinacidil failed to affect the level of eNO (Fig. 4). 5 Assessment of Cytokine Levels OVA-sensitization strongly enhanced the level of proinflammatory cytokines in both serum and BALF. Long-term treatment with NS1619 and pinacidil caused significant decreases in the cytokines IL-4, IL-5, IL-13, and TNF-α in both serum and BALF, which regarding the serum Potassium Ion Channels and Allergic Asthma tended to be stronger than those observed after a control drug, budesonide.

001 vs. 05 vs. OVA 40 M. Kocmalova et al. Table 1 Effects of acute and long-term treatment with K+ channels openers on tracheal and pulmonary tissue contractility Fig. 3 Ciliary beating frequency in control nonsensitized, ovalbumine (OVA)-sensitized, and in NS1619- and pinacidil-treated sensitized animals. 05 vs. 05 vs. OVA administration of the openers. However, there was a slight reduction in the contractility of tracheal tissue observed in response to acetylcholine after the long-term treatment with these K+ channels openers (Table 1).

4 Specific Airway Resistance In Vivo Reactivity of airway smooth muscles in vivo was expressed as specific airway resistance calculated according to Pennock et al. (1979). The value of specific airway resistance is proportional to the phase difference between nasal and thoracic respiratory airflows recorded in the head and thoracic chambers of the plethysmograph, respectively. The bigger phase difference the higher is the value of specific airway resistance and also a greater degree of bronchoconstriction.

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