Abstract

Cyclically contracting venules, in close proximity to microlymphatic vessels, may affect lymphatic function by extrinsic and intrinsic mechanisms. Venomotion which can propel lymph by direct compression of lymphatic vessels, may also stretch them, triggering intrinsic contraction. We therefore hypothesized that mechanical stimuli coordinate the cyclical contraction of venules and lymphatic vessels. To test the hypothesis, we have developed a new methodology using the Pallid bat wing model, which allows in vivo, noninvasive, characterization of vascular function without the confounding effects of anesthesia. The time delay between the onset of venomotion and the initiation of lymphatic contraction was recorded to determine the degree of coordination. To characterize the effect of the amplitude of venomotion, the relative number of lymphatic contractions per venular contraction categorized by amplitude was recorded. Results indicate that >90% of lymphatic contractions occurred within 1.5s of the onset of venomotion and the incidence contraction increases with increase in the amplitude of venomotion. To determine if the coupling between venomotion and lymphatic contraction is mechanically stimulated, a lymphatic vessel (not in proximity to venule) was compressed using two micropipettes by pushing the adjacent tissue in opposing directions. Each applied mechanical stimulus invoked spontaneous contraction of the microlymphatic vessel. Thus, results from this novel methodology suggest that venomotion mechanically triggers the contraction of lymphatic vessels.

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