Capillary pressures in rat intestinal muscle and mucosal villi during venous pressure elevation

1985 ◽  
Vol 249 (1) ◽  
pp. H174-H187 ◽  
Author(s):  
M. J. Davis ◽  
R. W. Gore
Keyword(s):  
Blood Flow ◽  
Capillary Pressure ◽  
Venous Pressure ◽  
Myogenic Response ◽  
Fluid Exchange ◽  
Pressure Elevation ◽  
Direct Measurements ◽  
Capillary Pressures ◽  
The Relationship ◽  
Blood Flow Redistribution

Whole-organ experiments designed to estimate the capillary filtration coefficient require information about the numerical relationship between capillary pressure and venous pressure. Indirect estimates using isogravimetric and isovolumetric methods indicate that 62-85% of a step change in venous pressure reaches the intestinal capillaries, taken as a whole. We have made direct measurements of capillary pressure with a servo-null micropressure system in the microcirculation of both the intestinal muscle and the mucosal villi of rats during local elevation of venous pressure. Consistent regional differences in the relationship between capillary pressure and venous pressure were observed. During increased venous pressure, submucosal arterioles constricted, while muscularis arterioles dilated. The diameter changes of the small arterioles were consistent with blood flow redistribution from mucosa to muscle during venous pressure elevation, but inconsistent with a pure myogenic response. These data raise questions about the exact role for the expression of the myogenic response during venous pressure elevation in the intestine and about previous interpretations of whole-organ experiments concerned with intestinal blood flow and fluid exchange.

Effect of luminal distension on intestinal transcapillary fluid exchange

1980 ◽  
Vol 239 (6) ◽  
pp. G516-G523
Author(s):  
D. N. Granger ◽  
P. R. Kvietys ◽  
N. A. Mortillaro ◽  
A. E. Taylor
Keyword(s):  
Blood Flow ◽  
Protein Concentration ◽  
Venous Pressure ◽  
Lymph Flow ◽  
Direct Effects ◽  
Fluid Exchange ◽  
Venous Outflow ◽  
Plasma Protein Concentration ◽  
Pressure Elevation ◽  
The Relationship

The direct effects of luminal distension pressure on intestinal transcapillary fluid exchange were studied in isolated autoperfused cat ileum preparations. Intestinal lymph flow, lymphatic pressure, lymph-to-plasma protein concentration ratio (L/P), blood flow, and perfusion pressures were allowed to reach a steady state at different luminal distension pressures (0–40 mmHg). Luminal distension was induced using a nonabsorbable silicone solution, thereby eliminating an influence of net water absorption. At a venous outflow pressure of 0 mmHg, lymph flow and lymphatic pressure increased, whereas blood flow and L/P decreased as luminal pressure was increased. The relationship between lymph flow, blood flow, and venous pressure was acquired at luminal pressures of 0 and 20 mmHg. When luminal pressure was 0, lymph flow increased and blood flow decreased progressively with venous pressure elevation; however, when luminal pressure was 20 mmHg, lymph flow and blood flow were unaffected until pressure exceeded 20 mmHg. The results of this study indicate that luminal pressure elevation enhances transcapillary fluid exchange and imposes a “waterfall” effect on the intestinal vasculature.

Microvascular control of capillary pressure during increases in local arterial and venous pressure

1988 ◽  
Vol 254 (4) ◽  
pp. H772-H784 ◽  
Author(s):  
M. J. Davis
Keyword(s):  
Hydrostatic Pressure ◽  
Capillary Pressure ◽  
Venous Pressure ◽  
The Body ◽  
Cell Velocity ◽  
Arterial Inflow ◽  
Tissue Act ◽  
Pallid Bats ◽  
Red Cell Velocity ◽  
Capillary Pressures

The extent to which capillary hydrostatic pressure might be protected from increases in local arterial and venous pressure was examined in the wing microcirculation of unanesthetized pallid bats (Antrozous pallidus). Arterial inflow and venous outflow pressures to the wing were elevated using a box technique to increase pressure around the body of the animal in steps of 12 mmHg between 0 and +60 mmHg for 3-min periods. During this time, hydrostatic pressure, diameter, and red cell velocity in single microvessels were continuously recorded. All branching orders of arterioles constricted significantly during increases in box pressure (Pb), while capillaries and venules dilated. First-order arteriole and venule pressures increased 1:1 with Pb. Capillary pressures increased by only a fraction of Pb up to +36 mmHg, but at higher Pb, the change in capillary pressure was equivalent to the change in Pb. Calculations of vascular resistance indicate that changes in both pre- and postcapillary resistance in this tissue act to prevent increases in capillary pressure during moderate, but not during large, increases in arterial and venous pressure.

Intestinal capillary filtration in acute and chronic portal hypertension

1988 ◽  
Vol 254 (3) ◽  
pp. G339-G345 ◽  
Author(s):  
R. J. Korthuis ◽  
D. A. Kinden ◽  
G. E. Brimer ◽  
K. A. Slattery ◽  
P. Stogsdill ◽  
...  
Keyword(s):  
Blood Flow ◽  
Portal Hypertension ◽  
Capillary Pressure ◽  
Vascular Resistance ◽  
Interstitial Fluid ◽  
Venous Pressure ◽  
Fluid Pressure ◽  
Lymph Flow ◽  
Interstitial Fluid Pressure ◽  
Capillary Filtration

The impact of acute and chronic portal hypertension on the dynamics of intestinal microvascular fluid exchange was examined in anesthetized, fasted, sham-operated control rats with normal portal pressures (CON), during acute elevations in portal pressure (APH) in control rats, and in rats in which chronic portal hypertension (CPH) was produced by calibrated stenosis of the portal vein 10 days prior to the experiments. Although intestinal blood flow and vascular resistance were not altered by APH in control rats, CPH was associated with an increased intestinal blood flow and reduced intestinal vascular resistance when compared with CON and APH. Intestinal capillary pressure and lymph flow were elevated in APH and CPH relative to control values. However, the increase in both variables was greater in CPH. The capillary filtration coefficient was elevated only in CPH. The transcapillary oncotic pressure gradient was not altered by APH or CPH. Interstitial fluid pressure was increased from -1.1 mmHg in CON to 3.9 mmHg during APH and to 5.0 mmHg in CPH. The results of this study indicate that chronic elevations in portal venous pressure produce larger increments in intestinal capillary pressure and filtration rate than do acute elevations in portal venous pressure of the same magnitude. However, the potential edemagenic effects of elevated capillary pressure in both acute and chronic portal hypertension are opposed by increases in lymph flow and interstitial fluid pressure.

scholarly journals Intrarenal distribution of blood flow and renin release during renal venous pressure elevation

1973 ◽  
Vol 4 (4) ◽  
pp. 259-266 ◽  
Author(s):  
Taketoshi Kishimoto ◽  
Masanobu Maekawa ◽  
Youichi Abe ◽  
Kenjiro Yamamoto
Keyword(s):  
Blood Flow ◽  
Venous Pressure ◽  
Renin Release ◽  
Pressure Elevation ◽  
Intrarenal Distribution

A new method for estimating skeletal muscle capillary pressure

1984 ◽  
Vol 246 (6) ◽  
pp. H880-H885
Author(s):  
R. J. Korthuis ◽  
D. N. Granger ◽  
A. E. Taylor
Keyword(s):  
Skeletal Muscle ◽  
Capillary Pressure ◽  
Venous Pressure ◽  
Arterial Occlusion ◽  
Venous Occlusion ◽  
Fluid Filtration ◽  
Arterial Inflow ◽  
Capillary Pressures ◽  
Highly Correlated ◽  
Artificial Plasma

Venous (Pc,vo) and arterial occlusion capillary pressures were simultaneously compared with isogravimetric capillary pressure (Pci) in isolated rat hindquarters and canine gracilis muscles perfused with blood or an artificial plasma. Arterial or venous pressure transients following rapid occlusion of arterial inflow or venous outflow, respectively, were analyzed for the inflection point between rapid and slow components. This transition point was assumed to represent the beginning of discharge of blood stored in (arterial occlusion) or the addition of blood to (venous occlusion) skeletal muscle microvessels and was defined as the effective capillary pressure. In all preparations, Pc,vo was identical to Pci. Arterial occlusion pressures were the same as Pci and Pc,vo in artificial plasma-perfused preparations but were significantly greater (P less than 0.01) than Pci and Pc,vo obtained in blood-perfused preparations. This inequality between arterial occlusion pressure and Pci may be related to a critical closure of small precapillary vessels or the non-Newtonian behavior of blood. In addition, venous occlusion pressures were highly correlated (r = 0.95, P less than 0.01) to calculated capillary pressures obtained following simultaneous equivalent elevations of arterial and venous pressure. These results indicate that the primary sites of vascular compliance and fluid filtration reside at or very near one another in the skeletal muscle microcirculation and that the more easily determined venous occlusion capillary pressure is an adequate measure of the effective capillary pressure in skeletal muscle.

Postural changes in capillary pressure in the hallux of healthy volunteers

2003 ◽  
Vol 95 (6) ◽  
pp. 2223-2228 ◽  
Author(s):  
Jurgen C. de Graaff ◽  
Dirk T. Ubbink ◽  
Sjoerd M. Lagarde ◽  
Michael J. H. M. Jacobs
Keyword(s):  
Healthy Volunteers ◽  
Capillary Pressure ◽  
Capillary Flow ◽  
Venous Pressure ◽  
Capillary Perfusion ◽  
Postural Changes ◽  
Capillary Pressures ◽  
Peripheral Arterial ◽  
Capillary Circulation ◽  
Toe Pressure

Capillary circulation is delicately regulated by microvascular constriction mechanisms, thereby controlling capillary perfusion and transmural pressure. The influence of posture on capillary flow has been investigated in both diseased and healthy people. However, its influence on capillary pressure has rarely been investigated. We measured capillary pressures in the supine and sitting positions in the hallux of healthy volunteers. The capillaries in the eponychium of the hallux were punctured by using a micropipette connected to a micropressure system (900A, WPI). Also, peripheral arterial and venous pressures were measured in both positions. The rise in systolic capillary pressure from supine to sitting position (32 mmHg; from 39 to 71 mmHg, respectively) was significantly ( P < 0.001) smaller than the rise in systolic arterial toe pressure (57 mmHg, from 87 to 144 mmHg, respectively) and venous pressure (41 mmHg, from 26 mmHg to 67 mmHg, respectively). This study shows that the postural rise in precapillary arteriolar pressure is not completely transmitted to the capillaries, probably because of activation of peripheral vasoconstriction mechanisms.

Pancreatic circulation: intrinsic regulation

1982 ◽  
Vol 242 (6) ◽  
pp. G596-G602
Author(s):  
P. R. Kvietys ◽  
J. M. McLendon ◽  
G. B. Bulkley ◽  
M. A. Perry ◽  
D. N. Granger
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Filtration Coefficient ◽  
Pancreatic Blood Flow ◽  
Capillary Filtration ◽  
Pressure Elevation ◽  
Capillary Filtration Coefficient ◽  
Intrinsic Regulation

The purpose of the present study was to characterize the intrinsic mechanisms involved in the regulation of blood flow and oxygenation in the totally isolated, perfused canine pancreas. Arterial pressure, venous outflow pressure, blood flow, arteriovenous oxygen difference, and capillary filtration coefficient were measured during graded arterial pressure reductions and venous pressure elevation. Reductions in arterial pressure caused pancreatic blood flow and vascular resistance to decrease, whereas venous pressure elevation resulted in a decreased blood flow and increased vascular resistance. The reductions in blood flow produced by arterial and venous pressure alterations were associated with increases in oxygen extraction and capillary filtration coefficient. During the same pressure perturbations, oxygen uptake remained constant between blood flows of 40-100 ml.min-1.100 g-1, yet decreased progressively as blood flow was reduced below 40 ml.min-1.100 g-1. Arterial occlusion resulted in a postocclusive reactive hyperemia, the magnitude of which was related to the duration of occlusion. The findings of this study suggest that intrinsic regulation of pancreatic blood flow can be attributed to both metabolic and myogenic mechanisms. Resistance and exchange vessels both appear to play a role in the regulation of oxygen delivery to the pancreatic parenchyma.

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