Abstract
The role played by the mechanical tissue stress in supporting lymph formation and propulsion in thoracic tissues was studied in deeply anesthetized rats ( n = 13) during spontaneous breathing or mechanical ventilation. After arterial and venous catheterization and insertion of an intratracheal cannula, fluorescent dextrans were injected intrapleurally to serve as lymphatic markers. After 2 h, the fluorescent intercostal lymphatics were identified, and the hydraulic pressure in lymphatic vessels (Plymph) and adjacent interstitial space (Pint) was measured using micropuncture. During spontaneous breathing, end-expiratory Plymph and corresponding Pint were −2.5 ± 1.1 (SE) and 3.1 ± 0.7 mmHg ( P < 0.01), which dropped to −21.1 ± 1.3 and −12.2 ± 1.3 mmHg, respectively, at end inspiration. During mechanical ventilation with air at zero end-expiratory alveolar pressure, Plymph and Pint were essentially unchanged at end expiration, but, at variance with spontaneous breathing, they increased at end inspiration to 28.1 ± 7.9 and 28.2 ± 6.3 mmHg, respectively. The hydraulic transmural pressure gradient (ΔPtm = Plymph − Pint) was in favor of lymph formation throughout the whole respiratory cycle (ΔPtm = −6.8 ± 1.2 mmHg) during spontaneous breathing but not during mechanical ventilation (ΔPtm = −1.1 ± 1.8 mmHg). Therefore, data suggest that local tissue stress associated with the active contraction of respiratory muscles is required to support an efficient lymphatic drainage from the thoracic tissues.

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