Effect of acute lymphatic obstruction on fluid accumulation in the chest in dogs

Abstract

The effect of acute obstruction to lymphatic drainage on fluid accumulation in the lungs, pleura, and pericardium was assessed in the intact dog. Catheters were positioned in the venae cavase, right atrium (RA), left atrium (LA), age on fluid accumulation in the lungs, pleura, and pericardium was assessed in the intact dog. Catheters were positioned in the venae cavae, right atrium (RA), left atrium (LA), and aorta (Ao) of nine anesthetized, spontaneouly breathing dogs, and hydrostic and colloid osmotic pressures were continuously monitored. Lymphatic obstruction was achieved by raising systemic venous pressure to either 10 mmHg or 25 mmHg by a combination of fluid infusion and inflation of balloon catheters in the venae cavae for 2 h. The same constant net intravascular filtration pressure was maintained in both groups by appropriate use of saline or colloid-containing fluids. Pleural and pericardial fluids were measured postmortem and lung water content was determined by weighing before and after drying. Failure to detect greater fluid accumulation at the higher obstructing pressure (25 mmHg) than at the lower obstructing pressure (10 mmHg) suggests that over the range of obstructing pressures used there is no acute change in the magnitude of lymphatic drainage in the chest.

Systemic Disease during Streptococcus pneumoniae Acute Lung Infection Requires 12-Lipoxygenase–Dependent Inflammation

“…This finding suggests that PMN transmigration across respiratory epithelium may promote retrograde movement of pneumococci into the circulation, although it is also possible that acute pulmonary inflammation promotes systemic disease in additional ways, such as inflammatory damage to mucosal surface or seeding of the bloodstream by bacteria in (the enhanced) lymphatic drainage (7, 48, 49). Remarkably, the dramatic decrease in bacteremia corresponded to an equally dramatic effect on survival, and the virtual lack of demonstrable disease in mice unable to generate a 12-lipoxygenase-mediated acute inflammatory response provides stark evidence that a robust innate immune response contributes to, and indeed is essential for, lethality during experimental pneumococcal infection.…”

Contribution of systemic venous hypertension to the development of pulmonary edema in dogs.

“…14 Either would have been exceeded by the level of systemic venous hypertension in our experiments and often observed in patients. Pang et al 15 were unable to demonstrate differences in lung fluid accumulation between systemic venous pressures of 10 and 25 mm Hg. It is possible that pressures of 10 mm Hg used by Pang et al and the pressure of greater than 8 mm Hg used by Mellins et al partially or completely impaired control lymphatic flow.…”