scholarly journals Effect of Electrical Stimulation on Blood Flow in Calf Muscles in Different Body Positions

2018 ◽  
Vol 1 (96) ◽  
Author(s):  
Julius Dovydaitis ◽  
Albinas Grūnovas
Keyword(s):  
Blood Flow ◽  
Body Position ◽  
Venous Blood ◽  
The Body ◽  
Arterial Blood Flow ◽  
Reserve Capacity ◽  
Horizontal Position ◽  
Blood Flows ◽  
Arterial Blood ◽  
Electrical Muscle

Background.  In  most  studies  on  cardiovascular  system,  testing  of  subjects  was  performed  in  a  horizontal position. With the change of the body position, certain functional changes occur in the cardiovascular system. The aim of this study was to analyze the effect of electrical muscle stimulation (EMS) on arterial and venous blood flows.Methods. Eighteen athletes aged 19–23 performed two sessions of tests in horizontal and sitting positions. Changes in arterial and venous blood flows were recorded before and after EMS. In each session two occlusions were performed. In the horizontal position, the initial occlusion pressure of 20 mmHg was applied and as the balance in arterial and venous blood flow rates was reached, the additional pressure of 20 mmHg (40  mmHg in total). In the sitting position, the occlusion pressure of 40 and 20 mmHg was applied respectively (60 mmHg in total). In both sessions EMS was performed using the electrical stimulator Mioritm 021.Results. In both horizontal and vertical positions, the effect of EMS on arterial blood flow, venous reserve capacity and venous elasticity was insignificant. Arterial and venous blood flows was affected significantly by the change of the body position. In the sitting position, arterial blood flow was significantly (p < .05) lower compared to the horizontal position. Similar results were recorded in venous reserve capacity.Conclusion.  The  study  suggests  that  blood  flow  in  the  calf  muscles  is  affected  by  the  body  position  and hydrostatic pressure; arterial blood flow increases in the horizontal body position.Keywords:  electrical muscle stimulation (EMS), arterial blood flow, venous reserve capacity, venous elasticity

Glucagon increases hepatic oxygen supply-demand ratio in pigs

1987 ◽  
Vol 252 (5) ◽  
pp. G648-G653
Author(s):  
S. Gelman ◽  
E. Dillard ◽  
D. A. Parks
Keyword(s):  
Blood Flow ◽  
Oxygen Supply ◽  
Venous Blood ◽  
Portal Blood Flow ◽  
Arterial Blood Flow ◽  
Blood Flows ◽  
Arterial Blood ◽  
Young Pigs ◽  
Hepatic Venous Blood ◽  
Pentobarbital Sodium Anesthesia

The present study was performed on eight young pigs to test the hypothesis that glucagon increases hepatic oxygen supply to a greater extent than hepatic oxygen uptake, providing a better hepatic oxygen supply-demand relationship. The experiments were performed under pentobarbital sodium anesthesia and controlled ventilation. Splanchnic blood flow was studied using radioactive microspheres. Glucagon was administered in doses of 1 and 5 micrograms X kg-1 X min-1. During glucagon infusion, hepatic arterial blood flow substantially increased, splenic and pancreatic blood flows increased moderately, while stomach and intestinal blood flows, as well as portal blood flow did not change significantly. Shunting of both 9- and 15-micron spheres through preportal tissues did not change significantly. Oxygen content in arterial or portal venous blood did not change significantly, while it increased in hepatic venous blood by 30%. There were no differences in the effects between the doses of glucagon administered. There was no correlation found between changes in hepatic oxygen supply and cardiac output or blood pressure. The changes observed during glucagon administration resulted in an increase in oxygen delivery to the liver and hepatic oxygen supply-uptake ratio.

Relationship between portal venous and hepatic arterial blood flows: spectrum of response

1990 ◽  
Vol 259 (6) ◽  
pp. G1010-G1018 ◽  
Author(s):  
T. Kawasaki ◽  
F. J. Carmichael ◽  
V. Saldivia ◽  
L. Roldan ◽  
H. Orrego
Keyword(s):  
Blood Flow ◽  
Arterial Blood Flow ◽  
Portal Vein Ligation ◽  
Artery Ligation ◽  
Blood Flows ◽  
Arterial Blood ◽  
Group A ◽  
Group B ◽  
The Relationship ◽  
Group D

The relationship between portal tributary blood flow (PBF) and hepatic arterial blood flow (HAF) was studied in awake, unrestrained rats with the radiolabeled microsphere technique. Six distinct patterns of response emerged. In group A (PBF+, HAF 0), ethanol, acetate, glucagon, prostacyclin, and a mixed diet increased PBF without a change in HAF; in group B (PBF+, HAF+), adenosine and histamine increased both PBF and HAF; in group C (PBF 0, HAF+), isoflurane and triiodothyronine did not change PBF but increased HAF; and in group D (PBF-, HAF+), halothane and vasopressin decreased PBF and increased HAF. Acute partial portal vein ligation decreased PBF (56%) and increased HAF (436%). Hypoxia (7.5% O2) decreased PBF (28%) and increased HAF (110%). In group E (PBF+, HAF-), acute hepatic artery ligation increased PBF (35%) and reduced HAF (74%), while in group F (PBF-, HAF-), thyroidectomy reduced PBF and HAF (36 and 47%, respectively). All blood flow responses were accompanied by the expected changes in both portal tributary and hepatic arterial vascular resistances. The data suggest that the portal and hepatic arterial vascular territories have regulatory mechanisms that allow for independent changes.

Role of glucagon in splanchnic hyperemia of chronic portal hypertension

1986 ◽  
Vol 251 (5) ◽  
pp. G674-G677 ◽  
Author(s):  
J. N. Benoit ◽  
B. Zimmerman ◽  
A. J. Premen ◽  
V. L. Go ◽  
D. N. Granger
Keyword(s):  
Blood Flow ◽  
Portal Hypertension ◽  
Venous Blood ◽  
Reference Sample ◽  
Venous Hypertension ◽  
Arterial Blood Flow ◽  
Venous Blood Flow ◽  
Portal Vein Stenosis ◽  
Arterial Blood

The role of glucagon as a blood-borne mediator of the hyperdynamic circulation associated with chronic portal venous hypertension was assessed in the rat portal vein stenosis model. Selective removal of pancreatic glucagon from the circulation was achieved by intravenous infusion of a highly specific glucagon antiserum. Blood flow to splanchnic organs, kidneys, and testicles was measured with radioactive microspheres, and the reference-sample method. Glucagon antiserum had no effect on blood flow in the gastrointestinal tract of sham-operated (control) rats. However, the antiserum produced a significant reduction in hepatic arterial blood flow in the control rats, suggesting that glucagon contributes significantly to the basal tone of hepatic arterioles. In portal hypertensive rats glucagon antiserum significantly reduced blood flow to the stomach (22%), duodenum (25%), jejunum (24%), ileum (26%), cecum (27%), and colon (26%). Portal venous blood flow was reduced by approximately 30%. The results of this study support the hypothesis that glucagon mediates a portion of the splanchnic hyperemia associated with chronic portal hypertension.

Systemic and hepatic hemodynamic changes in acute liver injury

1997 ◽  
Vol 272 (3) ◽  
pp. G617-G625 ◽  
Author(s):  
A. J. Makin ◽  
R. D. Hughes ◽  
R. Williams
Keyword(s):  
Blood Flow ◽  
Liver Injury ◽  
Hepatic Injury ◽  
Acute Liver Injury ◽  
Venous Blood ◽  
Marked Change ◽  
Arterial Blood Flow ◽  
Venous Flow ◽  
Subsequent Increase ◽  
Arterial Blood

Systemic and hepatic circulatory changes were studied in rats over the course of acute liver injury. Hepatic injury was induced by intraperitoneal injection of D-galactosamine (1.1 g/kg), and systemic and hepatic hemodynamics were measured over a 72-h period using a radioactive microsphere technique with direct measurement of arterial, portal venous, and hepatic venous blood oxygen content. Cardiac output increased to a maximum at 48 h, producing a marked increase (450%) in hepatic arterial blood flow so that it became the dominant supply of oxygen at the time of maximal hepatic injury. A subsequent increase in portal venous flow resulted in an overall increase in total hepatic blood flow of 500%. At this point the oxygen delivery by the hepatic arterial and portal venous systems was equal. These circulatory changes returned to control values by 72 h with recovery of liver function. These results demonstrate the development of a hyperdynamic circulation and a marked change in the normal relationship between portal venous and hepatic arterial blood flows that occur during hepatic injury.

Pulmonary blood flow, pressure and resistance following tetraethylammonium and aminophylline

1961 ◽  
Vol 200 (2) ◽  
pp. 287-291 ◽  
Author(s):  
M. Harasawa ◽  
S. Rodbard
Keyword(s):  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Systemic Blood Pressure ◽  
Arterial Blood Flow ◽  
Tetraethylammonium Chloride ◽  
Blood Flows ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
Flow Pressure

The effects of tetraethylammonium chloride (TEAC) and aminophylline on the pulmonary vascular resistance were studied in thoracotomized dogs. Pulmonary arterial blood flow and pressure, and systemic blood pressure were measured simultaneously. Both drugs showed marked hypotensive effects on the systemic vessels. In every instance pulmonary arterial pressures and blood flows were reduced by TEAC given via the pulmonary artery and increased by aminophylline. However, the calculated pulmonary vascular resistance remained essentially unchanged in all experiments. These data challenge the concept that the pulmonary vessels respond to these drugs by active vasodilatation

Response to cold of Eskimos of the eastern Canadian Arctic

1963 ◽  
Vol 18 (5) ◽  
pp. 970-974 ◽  
Author(s):  
G. Malcolm Brown ◽  
Robert E. Semple ◽  
C. S. Lennox ◽  
G. S. Bird ◽  
C. W. Baugh
Keyword(s):  
Blood Flow ◽  
Venous Blood ◽  
Canadian Arctic ◽  
The Body ◽  
Arterial Blood ◽  
Acute Cold Exposure ◽  
Body Core ◽  
Average Skin ◽  
Skin Temperatures ◽  
Eastern Canadian Arctic

Skin, muscle, and rectal temperatures, and O2 consumption of Eskimos and Caucasians have been compared during an acute cold exposure involving immersion of one hand and forearm in a 5 C water bath. The Eskimos consumed less O2, maintained their rectal temperatures at a higher level, and gave up less heat from the muscles of the limbs. Though the Eskimos had significantly more adipose tissue, average skin temperatures were the same in the two groups. The pattern of temperatures noted now and the previously observed higher blood flow in the hand and forearm of Eskimos point to increased cooling of arterial blood by returning venous blood in the extremities with resultant preservation of heat in the body core. Submitted on August 6, 1962

Effects of systemic arterial hypoperfusion on splanchnic hemodynamics and hepatic arterial buffer response in pigs

2001 ◽  
Vol 280 (5) ◽  
pp. G819-G827 ◽  
Author(s):  
S. M. Jakob ◽  
J. J. Tenhunen ◽  
S. Laitinen ◽  
A. Heino ◽  
E. Alhava ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Tamponade ◽  
Venous Blood ◽  
Liver Blood Flow ◽  
Hepatic Function ◽  
Arterial Blood Flow ◽  
Cellular Damage ◽  
Aortic Blood Flow ◽  
Venous Blood Flow ◽  
Arterial Blood

The hepatic arterial buffer response (HABR) tends to maintain liver blood flow under conditions of low mesenteric perfusion. We hypothesized that systemic hypoperfusion impairs the HABR. In 12 pigs, aortic blood flow was reduced by cardiac tamponade to 50 ml · kg−1 · min−1 for 1 h (short-term tamponade) and further to 30 ml · kg−1 · min−1 for another hour (prolonged tamponade). Twelve pigs without tamponade served as controls. Portal venous blood flow decreased from 17 ± 3 (baseline) to 6 ± 4 ml · kg−1 · min−1 (prolonged tamponade; P = 0.012) and did not change in controls, whereas hepatic arterial blood flow decreased from 2 ± 1 (baseline) to 1 ± 1 ml · kg−1 · min−1 (prolonged tamponade; P = 0.050) and increased from 2 ± 1 to 4 ± 2 ml · kg−1 · min−1in controls ( P = 0.002). The change in hepatic arterial conductance (Δ C ha) during acute portal vein occlusion decreased from 0.1 ± 0.05 (baseline) to 0 ± 0.01 ml · kg−1 · min−1 · mmHg−1(prolonged tamponade; P = 0.043). In controls, Δ C ha did not change. Hepatic lactate extraction decreased, but hepatic release of glutathione S-transferase A did not change during cardiac tamponade. In conclusion, during low systemic perfusion, the HABR is exhausted and hepatic function is impaired without signs of cellular damage.

Increase in hepatic blood flow during early sepsis is due to increased portal blood flow

1991 ◽  
Vol 261 (6) ◽  
pp. R1507-R1512 ◽  
Author(s):  
P. Wang ◽  
Z. F. Ba ◽  
I. H. Chaudry
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Hepatic Blood Flow ◽  
Portal Blood Flow ◽  
Portal Blood ◽  
Arterial Blood Flow ◽  
Blood Flows ◽  
Arterial Blood ◽  
Total Hepatic Blood Flow ◽  
Early Sepsis

Although hepatic blood flow increases significantly during early sepsis [as produced by cecal ligation and puncture (CLP)], it is not known whether this is due to the increase in portal or hepatic arterial blood flows. To study this, rats were subjected to CLP, after which they and sham-operated rats received either 3 or 6 ml normal saline/100 g body wt subcutaneously (i.e., all rats received crystalloid therapy). Blood flow in various organs was determined by using a radioactive microsphere technique at 5 and 20 h after CLP or sham operation. Portal blood flow was calculated as the sum of blood flows to the spleen, pancreas, gastrointestinal tract, and mesentery. Total hepatic blood flow was the sum of portal blood flow and hepatic arterial blood flow. A significant increase in portal blood flow and in total hepatic blood flow was observed at 5 h after CLP (i.e., early sepsis), and this was not altered by doubling the volume of crystalloid resuscitation after the induction of sepsis. In contrast, hepatic arterial blood flow during early sepsis was found to be similar to control; however, it was significantly reduced in late sepsis (i.e., 20 h after CLP). Cardiac output was significantly higher than the control in early sepsis. However, even in late sepsis, cardiac output and total hepatic blood flow were not significantly different from controls. These results indicate that the increased total hepatic blood flow during early hyperdynamic sepsis is solely due to the increased portal blood flow.

Splenic baroreceptors control splenic afferent nerve activity

2006 ◽  
Vol 290 (2) ◽  
pp. R352-R356 ◽  
Author(s):  
Karli Moncrief ◽  
Susan Kaufman
Keyword(s):  
Blood Flow ◽  
Venous Pressure ◽  
Venous Blood ◽  
Splenic Vein ◽  
Afferent Nerve ◽  
Arterial Blood Flow ◽  
Venous Blood Flow ◽  
Nerve Activity ◽  
Vein Occlusion ◽  
Arterial Blood

Stenosis of either the portal or splenic vein increases splenic afferent nerve activity (SANA), which, through the splenorenal reflex, reduces renal blood flow. Because these maneuvers not only raise splenic venous pressure but also reduce splenic venous outflow, the question remained as to whether it is increased intrasplenic postcapillary pressure and/or reduced intrasplenic blood flow, which stimulates SANA. In anesthetized rats, we measured the changes in SANA in response to partial occlusion of either the splenic artery or vein. Splenic venous and arterial pressures and flows were simultaneously monitored. Splenic vein occlusion increased splenic venous pressure (9.5 ± 0.5 to 22.9 ± 0.8 mmHg, n = 6), reduced splenic arterial blood flow (1.7 ± 0.1 to 0.9 ± 0.1 ml/min, n = 6) and splenic venous blood flow (1.3 ± 0.1 to 0.6 ± 0.1 ml/min, n = 6), and increased SANA (1.7 ± 0.4 to 2.2 ± 0.5 spikes/s, n = 6). During splenic artery occlusion, we matched the reduction in either splenic arterial blood flow (1.7 ± 0.1 to 0.7 ± 0.05, n = 6) or splenic venous blood flow (1.2 ± 0.1 to 0.5 ± 0.04, n = 5) with that seen during splenic vein occlusion. In neither case was there any change in either splenic venous pressure (−0.4 ± 0.9 mmHg, n = 6 and +0.1 ± 0.3 mmHg, n = 5) or SANA (−0.11 ± 0.15 spikes/s, n = 6 and −0.05 ± 0.08 spikes/s, n = 5), respectively. Furthermore, there was a linear relationship between SANA and splenic venous pressure ( r = 0.619, P = 0.008, n = 17). There was no such relationship with splenic venous ( r = 0.371, P = 0.236, n = 12) or arterial ( r = 0.275, P = 0.413, n = 11) blood flow. We conclude that it is splenic venous pressure, not flow, which stimulates splenic afferent nerve activity and activates the splenorenal reflex in portal and splenic venous hypertension.

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