Relationship between systemic blood pressure, airway blood flow and plasma exudation in guinea‐pig

Abstract

Plasma exudation in the airways is mainly dependent on microvascular permeability of the tracheobronchial circulation and may be affected by local blood flow. Aortic blood pressure provides the major inflow pressure to tracheobronchial circulation. Therefore, systemically administered vasoconstrictors, in doses enough to increase systemic blood pressure, may theoretically increase the blood flow in the tracheobronchial circulation by enhancing inflow pressure. Consequently, this may influence plasma exudation induced by inflammatory mediators in the airways. To test this hypothesis, we used guinea-pigs to study: (1) the effects of i.v. vasoconstrictors (methoxamine and angiotensin II) on blood flow in the tracheal mucosa and in the leg skeletal muscle (Laser-Doppler flowmetry); (2) the effects of i.v. vasoconstrictors on plasma exudation induced by tracheal administration of the inflammatory mediator bradykinin (150 nmol). We found that i.v. methoxamine and angiotensin II significantly increase tracheal mucosa blood flow and systemic blood pressure. The increase in tracheal mucosa blood flow was, in the case of angiotensin II, found to be significantly related to the increase in systemic blood pressure. In separate experiments, pre-treatment with i.v. methoxamine and angiotensin II significantly potentiates Evan's Blue dye exudation induced by bradykinin in the trachea and main bronchi. We conclude that i.v. methoxamine and angiotensin II potentiate bradykinin-induced plasma exudation in the guinea-pig airways, possibly by increasing the local blood flow. The increase in the local blood flow is most likely induced by enhanced systemic blood pressure (inflow pressure), owing to a redistribution of the total body blood flow.