The overall objective of our research on skeletal muscle blood flow is identification of the mechanisms responsible for vasodilation associated with exercise. The major focus of this application is the role of endothelial cells in mediating the vasodilation of distributing arteries which are responsible for maintaining the pressure head to the microcirculation during exercise. We are also interested in the role of endothelial cells in the dilation and development of collateral vessels which supply the microcirculation when distributing arteries are occluded. We propose to elucidate the physiologic importance of endothelial cells in mediating the vasodilation of distributing arteries. Our goals are (a) to determine the physiologic role of distributing artery flow-dependent dilation in exercise hyperemia, (b) to further characterize the mechanism of flow-dependent dilation in the canine femoral artery, and (c) to determine the role of endothelial cells in the dilation and growth of collateral vessels during acute and chronic occlusion of the distributing artery. We will also examine the effect of heartworm (Dirofilaria immitis), a common filarial parasitic infection of domestic dogs, on endothelium-dependent vasodilation.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Project (R01)
Project #
5R01AI035757-15
Application #
2071660
Study Section
Tropical Medicine and Parasitology Study Section (TMP)
Project Start
1980-04-01
Project End
1996-07-31
Budget Start
1994-08-01
Budget End
1995-07-31
Support Year
15
Fiscal Year
1994
Total Cost
Indirect Cost
Name
Michigan State University
Department
Physiology
Type
Schools of Medicine
DUNS #
193247145
City
East Lansing
State
MI
Country
United States
Zip Code
48824
Kaiser, Lana; Williams, Jeffrey F (2004) Dirofilaria immitis: worm burden and pulmonary artery proliferation in dogs from Michigan (United States). Vet Parasitol 124:125-9
Kaiser, L; Geary, T G; Williams, J F (1998) Dirofilaria immitis and Brugia pahangi: filarial parasites make nitric oxide. Exp Parasitol 90:131-4
Kaiser, L; Williams, J F (1998) Dirofilaria immitis: heartworm infection converts histamine-induced constriction to endothelium-dependent relaxation in canine pulmonary artery. Exp Parasitol 88:146-53
Maksimowich, D S; Bell, T G; Williams, J F et al. (1997) Effect of arsenical drugs on in vitro vascular responses of pulmonary artery from heartworm-infected dogs. Am J Vet Res 58:389-93
Mupanomunda, M; Williams, J F; Mackenzie, C D et al. (1997) Dirofilaria immitis: heartworm infection alters pulmonary artery endothelial cell behavior. J Appl Physiol 82:389-98
Maksimowich, D S; Mupanomunda, M; Williams, J F et al. (1997) Effect of heartworm infection on in vitro contractile responses of canine pulmonary artery and vein. Am J Vet Res 58:395-7
Kaiser, L; Mupanomunda, M; Williams, J F (1996) Brugia pahangi-induced contractility of bovine mesenteric lymphatics studied in vitro: a role for filarial factors in the development of lymphedema? Am J Trop Med Hyg 54:386-90
Mupanomunda, M; Williams, J F; Kaiser, L (1996) Effect of heartworm infection on fade of norepinephrine-induced constriction in canine pulmonary vein. Am J Vet Res 57:172-7
Maksimowich, D S; Williams, J F; Kaiser, L (1996) Thiacetarsamide depresses relaxation of canine pulmonary artery in vitro. Vet Parasitol 64:251-6
Tithof, P K; Schwartz, A J; Mupanomunda, M et al. (1994) Dirofilaria immitis: depression of endothelium-dependent relaxation of canine femoral artery seen in vivo does not persist in vitro. Exp Parasitol 79:159-65

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