R H Stewart1, G A Laine. 1. Michael E. DeBakey Institute, Texas A&M University, College Station, TX 77843-4466, USA. rstewart@cvm.tamu.edu
Abstract
OBJECTIVE: Lymph from both the liver and intestine flows into the cisterna chyli. We hypothesized that increasing liver lymph flow would increase cisterna chyli pressure and, thereby, decrease intestinal lymph flow, potentiating intestinal edema formation. METHODS: Anesthetized dogs were instrumented to measure and manipulate portal vein pressure and cisterna chyli pressure. The effects of directly increasing portal pressure with and without directly increasing cisterna chyli pressure on intestinal wet-to-dry ratio and intestinal ascites formation rate were determined. Target values for portal and cisterna chyli pressures were determined following elevation of inferior vena caval pressure to levels seen in patients with obstructive caval disease. RESULTS: Direct elevation of portal pressure (P(port)) alone to 17.5 mm Hg caused a significant increase in intestinal wet-to-dry ratio (3.98 +/- 0.24 vs. 3.40 +/- 0.43) and the rate of ascites formation (0.36 +/- 0.12 vs. 0.05 +/- 0.03 mL/g dry wt/h). Simultaneous direct elevation of cisterna chyli pressure to 6.0 mm Hg and P(port) to 17.5 mm Hg caused further increases in intestinal wet-to-dry ratio (5.52 +/- 1.20) and ascites formation (0.57 +/- 0.11 mL/g dry wt./h). CONCLUSIONS: Inferior vena caval hypertension increases liver lymph flow that elevates cisterna chyli pressure, which inhibits intestinal lymph flow and augments intestinal edema formation.
OBJECTIVE: Lymph from both the liver and intestine flows into the cisterna chyli. We hypothesized that increasing liver lymph flow would increase cisterna chyli pressure and, thereby, decrease intestinal lymph flow, potentiating intestinal edema formation. METHODS: Anesthetized dogs were instrumented to measure and manipulate portal vein pressure and cisterna chyli pressure. The effects of directly increasing portal pressure with and without directly increasing cisterna chyli pressure on intestinal wet-to-dry ratio and intestinal ascites formation rate were determined. Target values for portal and cisterna chyli pressures were determined following elevation of inferior vena caval pressure to levels seen in patients with obstructive caval disease. RESULTS: Direct elevation of portal pressure (P(port)) alone to 17.5 mm Hg caused a significant increase in intestinal wet-to-dry ratio (3.98 +/- 0.24 vs. 3.40 +/- 0.43) and the rate of ascites formation (0.36 +/- 0.12 vs. 0.05 +/- 0.03 mL/g dry wt/h). Simultaneous direct elevation of cisterna chyli pressure to 6.0 mm Hg and P(port) to 17.5 mm Hg caused further increases in intestinal wet-to-dry ratio (5.52 +/- 1.20) and ascites formation (0.57 +/- 0.11 mL/g dry wt./h). CONCLUSIONS: Inferior vena caval hypertension increases liver lymph flow that elevates cisterna chyli pressure, which inhibits intestinal lymph flow and augments intestinal edema formation.
Authors: Christopher M Quick; Bruce L Ngo; Arun M Venugopal; Randolph H Stewart Journal: Am J Physiol Heart Circ Physiol Date: 2009-01-02 Impact factor: 4.733
Authors: R M Dongaonkar; T L Nguyen; C M Quick; J Hardy; G A Laine; E Wilson; R H Stewart Journal: Am J Physiol Heart Circ Physiol Date: 2013-05-10 Impact factor: 4.733
Authors: Christopher M Quick; John C Criscione; Akhilesh Kotiya; Ranjeet M Dongaonkar; Joanne Hardy; Emily Wilson; Anatoliy A Gashev; Glen A Laine; Randolph H Stewart Journal: Am J Physiol Regul Integr Comp Physiol Date: 2014-03-26 Impact factor: 3.619
Authors: Shinil K Shah; Fernando Jimenez; Phillip A Letourneau; Peter A Walker; Stacey D Moore-Olufemi; Randolph H Stewart; Glen A Laine; Charles S Cox Journal: Scand J Trauma Resusc Emerg Med Date: 2012-04-03 Impact factor: 2.953