The objective of this research project is to test the hypothesis that capillary hydrostatic pressure (Pc) is regulated during changes in arterial and venous pressures. Previous estimates of capillary pressure and of pre- and postcapillary resistance in whole-organ preparations indicate a tendency for Pc to be regulated in some tissues, but these studies are limited by several critical assumptions that may consistently result in overestimating the extent to which Pc is controlled. The few microcirculatory studies which have examined this question have been performed primarily on the intestine, with quite variable results, presumably because normal vascular tone and blood flow regulation were severly compromised. Direct measurements of capillary pressure and other microvessel pressures will be made with a servo-null micropressure system while local arterial and venous pressures are varied. The experiments will be conducted in three stages. First, the intravascular pressure distribution in the entire microcirculation will be measured as arterial pressure (Pa) is lowered, and as Pa and venous pressure are raised. Possible disruption of normal control mechanisms by micropressure pipettes will be evaluated. Second, blood flow to portions of the microvascular network will be measured simultaneously with downstream capillary pressures while lowering Pa in order to determine the extent to which Pc regulation is coupled to regulation of blood flow. Third, the vascular site(s) of possible Pc control will be identified by quantitating changes in microvessel diameters, red-cell velocities, and calculated volume flows for each vascular branching order. Absolute and relative microvascular resistances will be determined during arterial and venous pressure changes using three different methods. These experiments will be conducted in cheek pouch, mesentery, and skeletal muscle micrecirculations of anesthetized hamsters, and in the cutaneous circulation of unanesthetized bats in order to determine possible variations in capillary pressure regulation among different tissues. If Pc is not regulated under these conditions, the results will have important implications about control of interstitial volume during increased gravitational loads and during arterial hypo- and hypertension.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
First Independent Research Support & Transition (FIRST) Awards (R29)
Project #
1R29HL038104-01
Application #
3470894
Study Section
Cardiovascular and Pulmonary Research B Study Section (CVB)
Project Start
1987-04-01
Project End
1992-03-31
Budget Start
1987-04-01
Budget End
1988-03-31
Support Year
1
Fiscal Year
1987
Total Cost
Indirect Cost
Name
Texas A&M University
Department
Type
Schools of Medicine
DUNS #
City
College Station
State
TX
Country
United States
Zip Code
77845
Davis, M J (1993) Spontaneous contractions of isolated bat wing venules are inhibited by luminal flow. Am J Physiol 264:H1174-86
Davis, M J; Donovitz, J A; Hood, J D (1992) Stretch-activated single-channel and whole cell currents in vascular smooth muscle cells. Am J Physiol 262:C1083-8
Kuo, L; Davis, M J; Cannon, M S et al. (1992) Pathophysiological consequences of atherosclerosis extend into the coronary microcirculation. Restoration of endothelium-dependent responses by L-arginine. Circ Res 70:465-76
Davis, M J; Shi, X; Sikes, P J (1992) Modulation of bat wing venule contraction by transmural pressure changes. Am J Physiol 262:H625-34
Kuo, L; Chilian, W M; Davis, M J (1991) Interaction of pressure- and flow-induced responses in porcine coronary resistance vessels. Am J Physiol 261:H1706-15
Falcone, J C; Davis, M J; Meininger, G A (1991) Endothelial independence of myogenic response in isolated skeletal muscle arterioles. Am J Physiol 260:H130-5
Kuo, L; Davis, M J; Chilian, W M (1990) Endothelium-dependent, flow-induced dilation of isolated coronary arterioles. Am J Physiol 259:H1063-70
Davis, M J; Sikes, P J (1990) Myogenic responses of isolated arterioles: test for a rate-sensitive mechanism. Am J Physiol 259:H1890-900
Kuo, L; Chilian, W M; Davis, M J (1990) Coronary arteriolar myogenic response is independent of endothelium. Circ Res 66:860-6
Hill, M A; Davis, M J; Meininger, G A (1990) Cyclooxygenase inhibition potentiates myogenic activity in skeletal muscle arterioles. Am J Physiol 258:H127-33

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