Simulation study of the effects of interstitial fluid pressure and blood flow velocity on transvascular transport of nanoparticles in tumor microenvironment

2020 ◽  
Vol 193 ◽  
pp. 105493 ◽  
Author(s):  
Yan Gao ◽  
Yanbin Shi ◽  
Mengguang Fu ◽  
Yihua Feng ◽  
Guimei Lin ◽  
...  
Keyword(s):  
Blood Flow ◽  
Tumor Microenvironment ◽  
Flow Velocity ◽  
Simulation Study ◽  
Blood Flow Velocity ◽  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Interstitial Fluid Pressure

Statistical Mechanics Transport Model of Magnetic Drug Targeting in Permeable Microvessel

2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Xiaohui Lin ◽  
Chibin Zhang ◽  
Kai Li
Keyword(s):  
Blood Flow ◽  
Statistical Mechanics ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Interstitial Fluid ◽  
Transport Model ◽  
Coupling Effect ◽  
Drug Carrier ◽  
Fluid Pressure ◽  
Magnetic Drug Targeting

A transport model of magnetic drug carrier particles (MDCPs) in permeable microvessel based on statistical mechanics has been developed to investigate capture efficiency (CE) of MDCPs at the tumor position. Casson-Newton two-fluid model is used to describe the flow of blood in permeable microvessel and the Darcy model is used to characterize the permeable nature of the microvessel. Coupling effect between the interstitial fluid flow and blood flow is considered by using the Starling assumptions in the model. The Boltzmann equation is used to depict the transport of MDCPs in microvessel. The elastic collision effect between MDCPs and red blood cell is incorporated. The distribution of blood flow velocity, blood pressure, interstitial fluid pressure, and MDCPs has been obtained through the coupling solutions of the model. Based on these, the CE of the MDCPs is obtained. Present results show that the CE of the MDCPs will increase with the enhancement of the size of the MDCPs and the external magnetic field intensity. In addition, when the permeability of the inner wall is better and the inlet blood flow velocity is slow, the CE of the MDCPs will increase as well. Close agreements between the predictions and experimental results demonstrate the capability of the model in modeling transport of MDCPs in permeable microvessel.

Cerebral blood flow velocity and cerebrospinal fluid pressure after single bolus of propofol

1989 ◽  
Vol 11 (3) ◽  
pp. 150-151 ◽  
Author(s):  
A. Parma ◽  
R. Massei ◽  
A. Pesenti ◽  
C. Ferrari da Passano ◽  
G. Gran ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Fluid Pressure ◽  
Cerebrospinal Fluid Pressure ◽  
Single Bolus

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.

Hemodynamics and interstitial fluid pressure in the rat tail

1984 ◽  
Vol 247 (1) ◽  
pp. H80-H87 ◽  
Author(s):  
K. Aukland ◽  
H. Wiig
Keyword(s):  
Blood Flow ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Interstitial Fluid ◽  
Cuff Pressure ◽  
Subcutaneous Tissue ◽  
Fluid Pressure ◽  
Interstitial Fluid Pressure ◽  
Venous Stasis ◽  
Plasma Volume Expansion

Blood flow in the rat was measured during pentobarbital anesthesia by plethysmographic and thermometric techniques. Tail arterial and venous pressures (Pa and Pv) were measured by glass micropipettes and interstitial fluid pressure (PIF) by wick-in-needle technique. Large pressure gradients were measured along the tail, Pa decreasing and Pv increasing toward the tip. In the vasoconstricted tail, distal arterial and venous pressures (Pad and Pvd, respectively, 10 cm from the tail root) were 55 and 11% of aortic pressure (PA), while PIF was 0-2 mmHg. Plasma volume expansion increased blood flow by a factor of 10 to 35. Pad rose to 74% and Pvd to 20% of PA. PIF increased to 15 mmHg, in parallel with Pv. Venous stasis (cuff pressure 14.7 mmHg) increased PIF and Pv by 3.5 and 9 mmHg, respectively, while tail volume increased by 0.4 to 1.2%. In conclusion, the large flow increase induced by plasma volume expansion depends strongly on dilation of the tail artery, with two- to threefold increase in internal radius. Simultaneously the tail veins relax and expand. Subcutaneous tissue is compressed between the expanding vessels and the tight skin, and PIF increases almost sufficiently to prevent a rise in net capillary filtration pressure. This immediate edema-preventing mechanism is less efficient during venous stasis, which presumably does not induce "active" dilation of the tail vessels. Similar mechanisms probably exist in other "encapsulated" tissues.

Intestinal microvascular exchange during lipid absorption

1988 ◽  
Vol 255 (5) ◽  
pp. G690-G695 ◽  
Author(s):  
D. N. Granger ◽  
R. J. Korthuis ◽  
P. R. Kvietys ◽  
P. Tso
Keyword(s):  
Blood Flow ◽  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Glucose Absorption ◽  
Lymph Flow ◽  
Interstitial Fluid Pressure ◽  
Lipid Absorption ◽  
Oncotic Pressure ◽  
Lymphatic Fluid ◽  
Flow Capillary

The forces and membrane coefficients governing transcapillary and lymphatic fluid fluxes were measured in the cat jejunum before and during perfusion of the gut lumen with oleic acid (5 mM) solubilized with taurocholic acid (10 mM). Net transmucosal fluid flux, lymph flow, capillary pressure (Pc), blood flow, capillary filtration coefficient (Kf,c), and lymph and plasma oncotic pressures were measured under absorptive and nonabsorptive conditions. Interstitial fluid pressure was calculated for the two conditions from measured parameters. Stimulation of lipid absorption resulted in a fivefold increase in lymph flow, a threefold increase in Kf,c, a doubling of blood flow, a 2.5 mmHg increase in Pc, and a 1.0 mmHg reduction in interstitial (lymph) oncotic pressure. Lipid absorption was associated with a 3.6 mmHg increase in interstitial fluid pressure. During lipid absorption, approximately 35% of the absorbed fluid is removed from the mucosal interstitium by lymphatics while capillaries remove the remaining 65%. The results of this study indicate that the effects of lipid absorption on microvascular and lymphatic fluid dynamics are quantitatively different than those produced by glucose absorption. These differences can be largely explained by lipid absorption-induced increases in blood flow and microvascular permeability.

Sign in / Sign up

Export Citation Format

Share Document