The overall objective is to study the function of dog heart, liver, small intestine and skeletal muscle lymph vessels in edema. Lymph vessels normally function to remove excess fluid from the tissues and edema can develop only when the lymph vessels are unable to remove fluid as fast as it filters into the tissues. In edema lymph flow may increase either because there is an increased pressure driving lymph from the tissues or because lymph vessel resistance is decreased. The relative contributions of these two mechanisms determines the lymphatic response to edema in a given tissue. For instance if the pressure driving lymph from a tissue is low, then the lymph vessel may not be able to transport lymph against an elevated venous pressure. Venous pressure is frequently elevated in critically ill patients. The first specific aim is to evaluate the contributions of driving pressure and lymph vessel resistance to the lymph flow response to edema in each tissue. The driving pressure and resistance will be calculated from the relationship between lymph flow and lymph vessel outflow pressure. The second specific aim is to evaluate the role of elevated venous pressure in opposing lymph flow and promoting edema. This will involve elevating the superior vena caval pressure (the pressure into which lymph vessels must flow) and estimating the amount of edema in the tissues. The third specific aim will involve estimating the effects of motion of the tissues around lymph vessels on the pressure of the lymphatic pump. This will be accomplished by measuring the lymph driving pressure in the skeletal muscle lymph vessels as skeletal muscle contraction rate is varied. These studies should increase our knowledge of the role of the lymphatic system in preventing edema in various tissues of critically ill patients.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
1R01HL036115-01
Application #
3350769
Study Section
Cardiovascular and Pulmonary Research B Study Section (CVB)
Project Start
1986-04-01
Project End
1989-03-31
Budget Start
1986-04-01
Budget End
1987-03-31
Support Year
1
Fiscal Year
1986
Total Cost
Indirect Cost
Name
University of Texas Health Science Center Houston
Department
Type
Schools of Medicine
DUNS #
City
Houston
State
TX
Country
United States
Zip Code
77225
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Shah, Shinil K; Jimenez, Fernando; Walker, Peter A et al. (2010) A novel mechanism for neutrophil priming in trauma: potential role of peritoneal fluid. Surgery 148:263-70
Radhakrishnan, Ravi S; Shah, Shinil K; Lance, Samuel H et al. (2009) Hypertonic saline alters hydraulic conductivity and up-regulates mucosal/submucosal aquaporin 4 in resuscitation-induced intestinal edema. Crit Care Med 37:2946-52
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Cox Jr, Charles S; Radhakrishnan, Ravi; Villarrubia, Lindsey et al. (2008) Hypertonic saline modulation of intestinal tissue stress and fluid balance. Shock 29:598-602
Stewart, Randolph H; Uray, Karen; Cox, Charles S et al. (2008) Myocardial fluid balance in dogs with naturally acquired heartworm infection. Am J Vet Res 69:356-61
Radhakrishnan, Ravi S; Radhakrishnan, Hari R; Xue, Hasen et al. (2007) Hypertonic saline reverses stiffness in a Sprague-Dawley rat model of acute intestinal edema, leading to improved intestinal function. Crit Care Med 35:538-43
Fischer, Uwe M; Cox Jr, Charles S; Stewart, Randolph H et al. (2006) Impact of acute myocardial edema on left ventricular function. J Invest Surg 19:31-8
Radhakrishnan, Ravi S; Xue, Hasen; Moore-Olufemi, Stacey D et al. (2006) Hypertonic saline resuscitation prevents hydrostatically induced intestinal edema and ileus. Crit Care Med 34:1713-8
Moore-Olufemi, Stacey D; Xue, Hasan; Allen, Steven J et al. (2005) Effects of primary and secondary intra-abdominal hypertension on mesenteric lymph flow: implications for the abdominal compartment syndrome. Shock 23:571-5

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