Pulmonary allergic reactions impair systemic vascular relaxation in ragweed sensitive mice

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• 作者：Surovi Hazarika ; Michael R. Van Scott ; Robert M. Lust ; Christopher J. Wingard
• 关键词：flammation ; Vascular function ; Endothelial response
• 刊名：Vascular Pharmacology
• 出版年：2010
• 出版时间：November-December 2010
• 年：2010
• 卷：53
• 期：5-6
• 页码：258-263
• 全文大小：531 K

文摘

Asthma is often associated with cardiovascular complications, and recent observations in animal models indicate that induction of pulmonary allergic inflammation increases susceptibility of the myocardium to ischemia and reperfusion injury. In this study, we used a murine model of allergen sensitization in which aspiration of allergen induces pulmonary and systemic inflammation, to test the hypothesis that pulmonary exposure to allergen alters vascular relaxation responses. BALB/C mice were sensitized by intraperitoneal injection of ragweed and challenged by intratracheal instillation of allergen. Airway hyperreactivity and pulmonary inflammation were confirmed, and endothelium-dependent and -independent reactivity of thoracic aorta rings were evaluated. Ragweed sensitization and challenge induced airway hyperreactivity to methacholine and pulmonary inflammation, but did not affect constrictor responses of the aortic rings to phenylephrine and K⁺ depolarization. In contrast, maximal relaxation of aortic rings to acetylcholine and sodium nitroprusside decreased from 87.6 ± 3.9 % and 97.7 ± 1.2 % to 32 ± 4 % and 51 ± 6 % , respectively (p < 0.05). The sensitivity to acetylcholine was likewise reduced (EC₅₀ = 0.26 ± 0.05 μM vs. 1.09 ± 0.16 μM, p < 0.001). The results demonstrate that induction of allergic pulmonary inflammation in mice depresses endothelium-dependent and -independent vascular relaxation, which can contribute to cardiovascular complications associated with allergic inflammation.