Anti-Allergic Effects of Milrinone and Sulmazole in Isolated Rat Lungs in Comparison with Theophylline

Post, Mark J.; Biesebeek, J.D. te; Rooij, H.H. van; Wemer, J.; Porsius, A. J.

doi:10.1159/000234914

Cited by 8 publications

(6 citation statements)

References 15 publications

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“…Moreover, in the isolated perfused Brown Norway rat lung, PAP increased only by 1.7-2.2 mmHg. 22 These findings contrast with those of other experimental in vivo models of anaphylactic shock in dogs, 7,8 monkeys, 6 rabbits, 9 and sheep, 5 where PAP increased by 11-16 mmHg after antigen administration. This indicates that the anaphylactic pulmonary vasoconstriction is much weaker in rats than in other mammals.…”

Section: Discussionmentioning

confidence: 76%

“…This finding is in disagreement with that reported in isolated perfused lungs of ovalbumin-sensitized Brown Norway rats, in which PAP increased significantly at a constant flow perfusion in response to the antigen. 22 One of the reasons for this discrepancy may be the rat strain difference: the Brown Norway rat is well known to be very sensitive to anaphylaxis. 23 Another reason is the presence of the sympathetic nervous system in the current anesthetized rats, but not in the isolated perfused lungs 22 : our in vivo rats were substantially influenced by the adrenal gland-derived epinephrine, which can exert a vasodilator effect via ␤ 2 -adrenoceptor.…”

Section: Discussionmentioning

confidence: 99%

“…22 One of the reasons for this discrepancy may be the rat strain difference: the Brown Norway rat is well known to be very sensitive to anaphylaxis. 23 Another reason is the presence of the sympathetic nervous system in the current anesthetized rats, but not in the isolated perfused lungs 22 : our in vivo rats were substantially influenced by the adrenal gland-derived epinephrine, which can exert a vasodilator effect via ␤ 2 -adrenoceptor. Actually, the plasma epinephrine concentration increased after antigen, and the adrenalectomy clearly caused the antigen-induced pulmonary vasoconstriction in the current study.…”

Section: Discussionmentioning

confidence: 99%

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Pulmonary Vasoconstrictive and Bronchoconstrictive Responses to Anaphylaxis Are Weakened via β2-adrenoceptor Activation by Endogenous Epinephrine in Anesthetized Rats

Zhang

Shibamoto

Kuda³

et al. 2011

Anesthesiology

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Background: Patients treated with propranolol, a nonselective ␤-adrenoceptor antagonist, have increased incidence and severity of anaphylaxis. We determined whether ␤ 1 -or ␤ 2 -adrenoceptor antagonist modulated pulmonary vasoconstriction and bronchoconstriction in rat anaphylactic hypotension. Methods: Anesthetized ovalbumin-sensitized male SpragueDawley rats were randomly allocated to the following pretreatment groups (n ϭ 7/group): (1) sensitized control (nonpretreatment), (2) propranolol, (3) the selective ␤ 2 -adrenoceptor antagonist ICI 118,551, (4) the selective ␤ 1 -adrenoceptor antagonist atenolol, and (5) adrenalectomy. Shock was induced by an intravenous injection of the antigen. Mean arterial pressure, pulmonary arterial pressure, left atrial pressure, central venous pressure, portal venous pressure, airway pressure, and aortic blood flow were continuously measured. Results: In either sensitized control or atenolol-pretreated rats, mean arterial pressure and aortic blood flow decreased substantially, whereas pulmonary arterial pressure and airway pressure did not increase soon after antigen injection. In contrast, in rats pretreated with either propranolol, ICI 118,551, or adrenalectomy, airway pressure significantly increased by 14 cm H 2 O, and pulmonary arterial pressure by

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Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Pulmonary Vasoconstrictive and Bronchoconstrictive Responses to Anaphylaxis Are Weakened via β2-adrenoceptor Activation by Endogenous Epinephrine in Anesthetized Rats

Zhang

Shibamoto

Kuda³

et al. 2011

Anesthesiology

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“…We already demonstrated distinct anti-allcrgic effects of milrinone and sulmazole in the isolated rat lung. Antigen-induced bronchoconstriction and pul monary vasoconstriction were inhibited by these drugs, concomitant with inhibition of anaphylactic production of leukotrienes [4],…”

Section: Introductionmentioning

confidence: 94%

Comparison of the Anti-Anaphylactic Effects of Milrinone, Sulmazole and Theophylline in the Rat

Post

Biesebeek²,

Wemer³

et al. 1989

Int Arch Allergy Immunol

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Milrinone and sulmazole, two recently developed cardiotonic drugs, inhibit specific fractions of the phosphodiesterase (PDE) isozyme system, while theophylline inhibits the PDE complex aspecifically. Since these drugs were shown to have anti-allergic effects in isolated lungs, we wanted to study milrinone and sulmazole in comparison with theophylline in an in vivo model of anaphylaxis. For this purpose, actively sensitized rats were intravenously challenged with antigen, while tracheal pressure, oesophageal pressure, blood pressure and airflow were continuously monitored. Antigen challenge induced a transient bronchoconstriction and a persistent fall in blood pressure until death occurred. Anaphylactic shock was consistently followed by metabolic acidosis. Milrinone, 3 mg/kg, and theophylline, 40 mg/kg (but not 10 mg/kg), reduced anaphylactic bronchoconstriction. Sulmazole, 40 mg/kg, almost abolished bronchoconstriction. Although milrinone, sulmazole and theophylline, 40 mg/kg, caused a fall in blood pressure prior to antigen challenge, total fall in blood pressure (drug-induced and antigen-induced) was not affected by these drugs. Surprisingly, sulmazole reduced mortality significantly. This phenomenon is probably related to the less severe metabolic acidosis in the presence of sulmazole.

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“…Theophylline inhibits antigen and agonists-induced bronchospasm in guinea pigs (3,4), and it also has an anti allergic effect in rats (5,6). Similarly, beta adrenoceptor agonists, salbutamol and iso proterenol, and the adenylate cyclase activator forskolin have anti-asthmatic and anti-allergic activity (7,8).…”

mentioning

confidence: 99%

Reversing Effect of Anti-Asthmatic Drugs on Bronchoconstriction Induced by Antigen Challenge and Histamine in Anesthetized Guinea Pigs.

et al. 1992

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We performed an in vivo evaluation of bronchodilation using a model of antigen-induced bronchoconstriction in anesthetized guinea pigs pretreated with in domethacin, pyrilamine and propranolol, and the results were compared with those for the histamine-induced response. Test drugs were administered intravenously when the antigen or histamine response reached its peak. Leukotriene (LT) D4 antagonists, FPL55712 and LY171883, gradually reduced the antigen-induced response, whereas the lipoxygenase inhibitor phenidone had no such effect. The bronchodilator theophylline rapidly reduced the antigen-induced response, and the adenylate cyclase activator forskolin had a similar effect. The following drugs also had no effect: nifedi pine (calcium-channel antagonist), cromakalim (potassium-channel opener), amlex anox and disodium cromoglycate: DSCG (anti-allergic drugs), OKY-046 (thrombox ane A2 synthetase inhibitor), and dapsone (anti-inflammatory drug). Theophylline, the beta-adrenoceptor agonist salbutamol and the histamine H1-blocker pyrilamine had only a small reversing effect on histamine-induced bronchoconstriction. These re sults suggest that antigen-, but not histamine-, induced bronchoconstriction in anesthe tized guinea pigs is a useful in vivo model for evaluating the bronchodilating effect of anti-asthmatic drugs.Bronchodilators, theophylline and beta adrenoceptor agonists are widely used in the therapy of asthma (1, 2). Theophylline inhibits antigen and agonists-induced bronchospasm in guinea pigs (3, 4), and it also has an anti allergic effect in rats (5, 6). Similarly, beta adrenoceptor agonists, salbutamol and iso proterenol, and the adenylate cyclase activator forskolin have anti-asthmatic and anti-allergic activity (7,8). Calcium-channel antagonists (9, 10) and potassium channel openers (11-13) also exhibit bronchodilating effects in the guinea pig, and anti-allergic drugs, DSCG and amlexanox (14), and the TXA2 synthetase in hibitor OKY-046 (15) inhibit antigen-induced bronchospasm in the guinea pig. However, the bronchodilating effect of these drugs on bron choconstriction in vivo have not been investi gated in detail.The purpose of the present study was to de velop an in vivo system for examining the bronchodilating effect of anti-asthmatic drugs. Therefore, we examined the reversing effects of anti-asthmatic drugs on antigen-induced bronchoconstriction in anesthetized guinea pigs, because antigen causes slowly developing and sustained bronchoconstriction in sensitized guinea pigs pretreated with indomethacin,

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Anti-Allergic Effects of Milrinone and Sulmazole in Isolated Rat Lungs in Comparison with Theophylline

Cited by 8 publications

References 15 publications

Pulmonary Vasoconstrictive and Bronchoconstrictive Responses to Anaphylaxis Are Weakened via β2-adrenoceptor Activation by Endogenous Epinephrine in Anesthetized Rats

Pulmonary Vasoconstrictive and Bronchoconstrictive Responses to Anaphylaxis Are Weakened via β2-adrenoceptor Activation by Endogenous Epinephrine in Anesthetized Rats

Comparison of the Anti-Anaphylactic Effects of Milrinone, Sulmazole and Theophylline in the Rat

Reversing Effect of Anti-Asthmatic Drugs on Bronchoconstriction Induced by Antigen Challenge and Histamine in Anesthetized Guinea Pigs.

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