New Method for Evaluating Bronchomotor and Bronchosecretory Activities: Effects of Prostaglandins and Antigen

Yamatake, Yoshikazu; Yanaura, Saiζo

doi:10.1254/jjp.28.391

Cited by 23 publications

(13 citation statements)

References 16 publications

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“…o-Adrenoceptor agonists constrict the bronchial (Bruner & Schmidt, 1947;Lung et al, 1976) and tracheal vasculature (this paper), and also decrease tracheal mucosal thickness (Laitinen et al, 1987b). Isoprenaline dilates the bronchial vessels (Lung et al, 1976;Yamatake & Yanaura, 1978) and salbutamol decreases tracheal vascular resistance (this paper). Salbutamol also decreases the permeability of bronchial venules (Persson et al, 1982).…”

Section: Discussionmentioning

confidence: 75%

“…Histamine, methacholine and isoprenaline increase bronchial blood flow in sheep when administered directly into the bronchial artery; adrenaline injected similarly reduces bronchial blood flow, and nicotine has a variable effect (Parsons et al, 1985). Histamine (Bruner & Schmidt, 1947;Yamatake & Yanaura, 1978), methacholine (Lakshminarayanan et al, 1985), isoprenaline (Yamatake & Yanaura, 1978) and prostaglandins E2 (Yamatake & Yanaura, 1978) 'Author for correspondence. 2Present address: Research Institute for Military Medicine,Central Military Hospital Tilkka,Mannerheimintie 164,00280 Helsinki 28,Finland. and F2, (Lakshminarayanan et al, 1985) increase bronchial blood flow in dogs, although one report (Yamatake & Yanaura, 1978) describes a vasoconstriction with prostaglandin F2.. Aerosolised histamine increases both bronchial blood flow and airflow resistance, and it is suggested that the action of histamine on bronchial arterioles is mediated by H2-receptors .…”

Section: Introductionmentioning

confidence: 99%

“…Histamine (Bruner & Schmidt, 1947;Yamatake & Yanaura, 1978), methacholine (Lakshminarayanan et al, 1985), isoprenaline (Yamatake & Yanaura, 1978) and prostaglandins E2 (Yamatake & Yanaura, 1978) 'Author for correspondence. 2Present address: Research Institute for Military Medicine,Central Military Hospital Tilkka,Mannerheimintie 164,00280 Helsinki 28,Finland. and F2, (Lakshminarayanan et al, 1985) increase bronchial blood flow in dogs, although one report (Yamatake & Yanaura, 1978) describes a vasoconstriction with prostaglandin F2.. Aerosolised histamine increases both bronchial blood flow and airflow resistance, and it is suggested that the action of histamine on bronchial arterioles is mediated by H2-receptors . None of these studies has included dose-response curves, and even qualitatively their interpretation is complicated because the majority of the bronchial circulation drains via bronchopulmonary anastomoses into the pulmonary circulation.…”

Section: Introductionmentioning

confidence: 99%

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Dose‐related effects of pharmacological mediators on tracheal vascular resistance in dogs

Laitinen

Widdicombe

1987

British J Pharmacology

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IVarious doses of mediators were tested on tracheal vascular resistance in dogs anaesthetized with pentobarbitone. Tracheal vascular resistance was determined by perfusing the cranial tracheal arteries at constant flows and measuring inflow pressures. 2 All drugs produced dose-related changes in vascular resistance. 3 The peptides bradykinin, substance P and vasoactive intestinal peptide (VIP) each had similar vasodilator potencies and were much more powerful than histamine, methacholine and salbutamol.4 Platelet activating factor (Paf) was a weaker dilator than the peptides. Prostaglandins D2, E, and F2,, had wide dilator potency ranges, PGE, being very effective even at low concentrations.5 Phenylephrine, an a-adrenoceptor agonist, was the only drug tested that always increased vascular resistance. 6 All the drugs studied also had effects on the contralateral tracheal vascular resistance.

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Section: Discussionmentioning

confidence: 75%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Dose‐related effects of pharmacological mediators on tracheal vascular resistance in dogs

Laitinen

Widdicombe

1987

British J Pharmacology

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“…In the present study, at first, we confirmed that the peripheral antitussive effects of local anesthetics can be evaluated by using this preparation, and secondly, investigated peripheral effects of morphine and codeine on the cough reflex. Effects of morphine and codeine on the bronchoconstriction induced by vagal stimulation were also investigated using the method for evaluating airway responses (10).…”

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confidence: 99%

Peripheral effects of Morphine and Codeine on the cough reflex.

et al. 1981

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Abstract-Peripheral effects of morphine and codeine on the cough reflex were investigated using our in situ upper trachea perfusion preparation which allows for a direct drug administration to the local site around the tracheal mucosa, this site being electrically stimulated to induce coughing. An i.a. administration of procaine or lidocaine into the tracheal vascular bed inhibited both cough response and tracheal constriction accompanied by coughings. On the other hand, benzonatate inhibited the tracheal constriction without influencing the cough response. These results indicate that the in situ upper trachea perfusion preparation is useful for evaluating effects of drugs on the cough receptor level. Morphine, 0.1 mg, and codeine, 1.0 mg, injected intraarterially into the tracheal artery, produced no tracheal constriction. Such administrations had no influence on the cough response elicited by mucosal stimulation, whereas the tracheal constriction accompanied by cough reflex was inhibited by both drugs. On the other hand, both drugs inhibited the bronchoconstriction induced by electrical stimulation of the vagus nerve. These findings suggest that both morphine and codeine inhibit the tracheal constriction accompanied by cough reflex without producing a tracheal constriction, in addition to their central antitussive action.

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“…We developed the stopper method in which airway secretory activity can be evaluated by measuring the output of RTF accumulating in the trachea, under conditions of normal ventilation (4,5). This method, however, cannot detect slight changes in the output or allow for an accurate determination of the time course of secretory conditions.…”

Section: Abstract-wementioning

confidence: 99%

Continuous determination of tracheobronchial secretory activity in dogs.

Misawa

Yanaura

1980

Jpn.J.Pharmacol

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Abstract-Wehave designed a new method for continuous recording of the output of respiratory tract fluid, the approach representing a modification and combination of the intratracheal electrode and stopper methods which we had employed originally. Electrical resistance change indicated alteration in the output of respiratory tract fluid, without alteration in composition and temperature of fluid, tracheal muscular tone or respiratory movement, at least, within a physiological range. Among the expectorant drugs thus tested, pilocarpine, 100 and 200 pg/kg given intravenously, significantly and in a dose dependent manner augmented the output of the fluid about 5 minutes after the administration.Given orally in a dose of 2 mg/kg, the output of fluid in creased in about 20 minutes. Senega syrup, 0.3 ml/ kg had no effect when given intra venously, yet, 2 ml/kg given orally increased the output of fluid within 5 minutes, thereby suggesting that the related secretagogic activity is due to a reflex action following stimulation of the gastric mucosa. Emetine, 2 mg/kg given orally increased the output about 20 minutes after administration while glyceryl guaiacolate, 50 mg/kg had no effect. We propose that our method be used to evaluate expectorants for clinical use as the continuous monitoring of the output of respiratory tract fluid apparently provides a more accurate assessment.In pulmonary disorders such as bronchial asthma and chronic bronchitis, a considerable amount of airway mucus is synthesized and excreted from glandular and goblet cells of the trachea and bronchi. Basic research on respiratory tract secretion and the evaluation and application of expectorants have not progressed as there was no adequate laboratory model for determining mucus production.To evaluate airway secretory activity, Henderson and Taylor in 1910 (1) attempted to measure the increase in weight of a calcium chloride tube attached to a tracheal cannula.In 1940, Sakuno (2) indirectly estimated the activity by measuring the amount of dye leaked from the lungs following systemic dye injection. A quantitative method for collecting respiratory tract fluid (RTF) was first described by Perry and Boyd in 1941 (3) and with this method, the volume output of RTF draining from a tracheal cannula during a 2 to 4 hr period can be measured with a graduated test tube connected to the cannula. These methods are however, inadequate.We developed the stopper method in which airway secretory activity can be evaluated by measuring the output of RTF accumulating in the trachea, under conditions of normal ventilation (4, 5). This method, however, cannot detect slight changes in the output or allow for an accurate determination of the time course of secretory conditions. In con tinuing studies, we found that airway secretory activity could be estimated by determining

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New Method for Evaluating Bronchomotor and Bronchosecretory Activities: Effects of Prostaglandins and Antigen

Abstract: Abstract-We devised a new

Cited by 23 publications

References 16 publications

Dose‐related effects of pharmacological mediators on tracheal vascular resistance in dogs

Dose‐related effects of pharmacological mediators on tracheal vascular resistance in dogs

Peripheral effects of Morphine and Codeine on the cough reflex.

Continuous determination of tracheobronchial secretory activity in dogs.

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