Effect Of Changes In Blood Flow Research Articles

Remodeling of the arterial wall: Response to restoration of normal blood flow after flow reduction

Although many studies have shown that arteries change diameter in response to chronic change in blood flow (BF), keeping wall shear stress (WSS) at physiologically normal levels, relatively little is known about the effects of flow restoration after flow reduction and also the role of vascular smooth muscle (VSM) during such a remodeling process. To elucidate the biomechanical responses of the arterial wall to the restoration of normal BF after flow reduction and compare the results with our previous results observed in response to decreased BF alone. Carotid artery BF in the Wistar rat was decreased by ligation and then restored to normal levels by release of the ligation. The effects of BF changes on the biomechanical properties of the carotid arterial wall were determined from measurements of diameters and pressures of excised artery segments. During BF reduction and restoration, WSS was maintained at physiological levels by changes in the internal diameter. No significant changes in the incremental elastic modulus were found in response to changes in BF. VSM tone was significantly enhanced during the changes in BF. Arteries change diameters in response to BF reduction and also flow restoration to normal after flow reduction, keeping WSS at physiologically normal levels. The lack of changes in vascular elasticity suggests that there were no significant changes in major wall constituents, such as elastin and collagen. VSM may play the dominant role in observed arterial remodeling and adaptation.

The relative influence of hematocrit and red blood cell velocity on oxygen transport from capillaries to tissue.

Oxygen transport to parenchymal cells occurs mainly at the microvascular level and depends on convective RBC flux, which is proportional in an individual capillary to the product of capillary hematocrit and RBC velocity. This study investigates the relative influence of these two factors on tissue PO2 . A simple analytical model is used to quantify the respective influences of hematocrit, RBC velocity, and RBC flow on tissue oxygenation around capillaries. Predicted tissue PO2 levels are compared with a detailed computational model. Hematocrit is shown to have a larger influence on tissue PO2 than RBC velocity. The effect of RBC velocity increases with distance from the arterioles. Good agreement between analytical and numerical results is obtained, and the discrepancies are explained. Significant dependence of MTCs on RBC velocity at low hematocrit is demonstrated. For a given RBC flux in a capillary, the PO2 in the surrounding tissue increases with increasing hematocrit, as a consequence of decreasing IVR to diffusive oxygen transport from RBCs to tissue. These results contribute to understanding the effects of blood flow changes on oxygen transport, such as those that occur in functional hyperemia in the brain.

Effects of chronic hypoxia and altered hemodynamics on endothelial nitric oxide synthase expression in the adult rat lung.

Mechanisms that regulate endothelial nitric oxide synthase (eNOS) expression in normal and hypoxic pulmonary circulation are poorly understood. Lung eNOS expression is increased after chronic hypoxic pulmonary hypertension in rats, but whether this increase is due to altered hemodynamics or to hypoxia is unknown. Therefore, to determine the effect of blood flow changes on eNOS expression in the normal pulmonary circulation, and to determine whether the increase in eNOS expression after chronic hypoxia is caused by hemodynamic changes or low oxygen tension, we compared eNOS expression in the left and right lungs of normoxic and chronically hypoxic rats with surgical stenosis of the left pulmonary artery (LPA). LPA stenosis in normoxic rats reduced blood flow to the left lung from 9.8+/-0.9 to 0.8+/-0.4 ml/100 mg/min (sham surgery controls vs. LPA stenosis, P < 0.05), but there was not a significant increase in right lung blood flow. When compared with the right lung, eNOS protein and mRNA content in the left lung was decreased by 32+/-7 and 54+/-13%, respectively (P < 0.05), and right lung eNOS protein content was unchanged. After 3 wk of hypoxia, LPA stenosis reduced blood flow to the left lung from 5.8+/-0.6 to 1.5+/-0.4 ml/100 mg/min, and increased blood flow to the right lung from 5.8+/-0.5 to 10.0+/-1.4 ml/ 100 mg/min (sham surgery controls vs. LPA stenosis, P < 0.05). Despite reduced flow and pressure to the left lung and increased flow and pressure to the right lung, left and right lung eNOS protein and mRNA contents were not different. There were also no differences in lung eNOS protein levels when compared with chronically hypoxic sham surgery controls (P > 0.05). We conclude that reduction of pulmonary blood flow decreases eNOS mRNA and protein expression in normoxic adult rat lungs, and that hypoxia increases eNOS expression independently of changes in hemodynamics. These findings demonstrate that hemodynamic forces maintain eNOS content in the normoxic pulmonary circulation of the adult rat, and suggest that chronic hypoxia increases eNOS expression independently of changes in hemodynamics.

Obesity, hyperinsulinemia, and portal blood flow. A theoretic study of the effects of increased portal blood flow upon fasting peripheral insulin concentrations.

A mathematical model of steady state insulin metabolism was developed to predict the effects of blood flow changes upon fasting arterial insulin concentration. In addition to blood flows to major organs and tissues, the model includes representations for insulin feedback regulation of hepatic insulin clearance and pancreatic insulin secretion. Within the range of insulin sensitivities assumed for hepatic and pancreatic feedback regulation and the range of initial insulin secretion rates employed, the model predicts that the fasting arterial insulin concentration rises by up to 20 muU. per milliliter as portal blood flow increases. The necessary elevations in portal blood flow lie well inside the range of increased total hepatic blood flow observed in obese subjects. The results of this study suggest that a significant portion of the elevation in fasting insulin concentrations seen in obesity may be the result of increased portal blood flow and that other clinical observations and metabolic changes that accompany obesity may also be related to altered portal flow.