Participation of adrenoceptors in liver blood flow regulation in anesthetized dogs

We evaluated involvement of adrenergic receptors in the responses of the hepatic vasculature to reduction either of portal venous flow or hepatic arterial inflow. Portal vein occlusion caused an increase in hepatic arterial blood flow (HAF) and decreases in hepatic arterial pressure (HAP) and hepatic arterial vascular resistance (HAR) in the intact group. After pretreatment with either yohimbine or prazosin, but not propranolol, occlusion of the portal vein produced a greater decrease in HAP as compared with that in the intact group. No significant changes in HAF, HAR, or hepatic tissue blood flow (HTF) occurred after the treatment. These results indicate that the compensatory response of the hepatic arterial vasculature to altered portal blood flow (PVF) is regulated independently of the intrahepatic adrenergic receptors. Hepatic arterial occlusion caused a significant decrease in portal venous pressure, PVF, and HTF. Portal venous vascular resistance (PVR) was reduced slightly, but not significantly. After pretreatment with either yohimbine or prazosin, but not propranolol, occlusion of the hepatic artery produced an opposite effect: to increase PVF and significantly decrease PVR. These results indicate that intrahepatic alpha-adrenoceptors participate in the regulation of portal vascular tone to maintain portal vein pressure at a steady level, when inflow from the hepatic artery is reduced.

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H2S contributes to the hepatic arterial buffer response and mediates vasorelaxation of the hepatic artery via activation of KATP channels

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.90484.2008 ◽

2008 ◽

Vol 295 (6) ◽

pp. G1266-G1273 ◽

Cited By ~ 44

Author(s):

Nikolai Siebert ◽

Daniel Cantré ◽

Christian Eipel ◽

Brigitte Vollmar

Keyword(s):

Blood Flow ◽

Portal Vein ◽

Hepatic Artery ◽

Buffer Capacity ◽

Venous Blood ◽

Control Level ◽

Vena Cava ◽

Arterial Blood Flow ◽

Venous Blood Flow ◽

Arterial Blood

Hepatic blood supply is uniquely regulated by the hepatic arterial buffer response (HABR), counteracting alterations of portal venous blood flow by flow changes of the hepatic artery. Hydrogen sulfide (H2S) has been recognized as a novel signaling molecule with vasoactive properties. However, the contribution of H2S in mediating the HABR is not yet studied. In pentobarbital-anesthetized and laparotomized rats, flow probes around the portal vein and hepatic artery allowed for assessment of the portal venous (PVBF) and hepatic arterial blood flow (HABF) under baseline conditions and stepwise reduction of PVBF for induction of HABR. Animals received either the H2S donor Na2S, DL-propargylglycine as inhibitor of the H2S synthesizing enzyme cystathionine-γ-lyase (CSE), or saline alone. Additionally, animals were treated with Na2S and the ATP-sensitive potassium channel (KATP) inhibitor glibenclamide or with glibenclamide alone. Na2S markedly increased the buffer capacity to 27.4 ± 3.0% ( P < 0.05 vs. controls: 15.5 ± 1.7%), whereas blockade of H2S formation by DL-propargylglycine significantly reduced the buffer capacity (8.5 ± 1.4%). Glibenclamide completely reversed the H2S-induced increase of buffer capacity to the control level. By means of RT-PCR, Western blot analysis, and immunohistochemistry, we observed the expression of both H2S synthesizing enzymes (CSE and cystathionine-β-synthase) in aorta, vena cava, hepatic artery, and portal vein, as well as in hepatic parenchymal tissue. Terminal branches of the hepatic afferent vessels expressed only CSE. We show for the first time that CSE-derived H2S contributes to HABR and partly mediates vasorelaxation of the hepatic artery via activation of KATP channels.

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Increased vascular resistance in paralyzed legs after spinal cord injury is reversible by training

Journal of Applied Physiology ◽

10.1152/japplphysiol.00897.2001 ◽

2002 ◽

Vol 93 (6) ◽

pp. 1966-1972 ◽

Cited By ~ 64

Author(s):

Maria T. E. Hopman ◽

Jan T. Groothuis ◽

Marcel Flendrie ◽

Karin H. L. Gerrits ◽

Sibrand Houtman

Keyword(s):

Blood Pressure ◽

Spinal Cord ◽

Spinal Cord Injury ◽

Blood Flow ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Vascular Resistance ◽

Arterial Blood Flow ◽

Arterial Blood ◽

Cord Injury

The purpose of the present study was to determine the effect of a spinal cord injury (SCI) on resting vascular resistance in paralyzed legs in humans. To accomplish this goal, we measured blood pressure and resting flow above and below the lesion (by using venous occlusion plethysmography) in 11 patients with SCI and in 10 healthy controls (C). Relative vascular resistance was calculated as mean arterial pressure in millimeters of mercury divided by the arterial blood flow in milliliters per minute per 100 milliliters of tissue. Arterial blood flow in the sympathetically deprived and paralyzed legs of SCI was significantly lower than leg blood flow in C. Because mean arterial pressure showed no differences between both groups, leg vascular resistance in SCI was significantly higher than in C. Within the SCI group, arterial blood flow was significantly higher and vascular resistance significantly lower in the arms than in the legs. To distinguish between the effect of loss of central neural control vs. deconditioning, a group of nine SCI patients was trained for 6 wk and showed a 30% increase in leg blood flow with unchanged blood pressure levels, indicating a marked reduction in vascular resistance. In conclusion, vascular resistance is increased in the paralyzed legs of individuals with SCI and is reversible by training.

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Effects of Intraabdominanlly Insufflated Carbon Dioxide and Elevated Intraabdominal Pressure on Splanchnic Circulation

Anesthesiology ◽

10.1097/00000542-199808000-00025 ◽

1998 ◽

Vol 89 (2) ◽

pp. 475-482 ◽

Cited By ~ 78

Author(s):

Manfred Blobner ◽

Ralph Bogdanski ◽

Eberhard Kochs ◽

Julia Henke ◽

Alexander Findeis ◽

...

Keyword(s):

Carbon Dioxide ◽

Blood Flow ◽

Vascular Resistance ◽

Mesenteric Artery ◽

Splanchnic Circulation ◽

Arterial Blood Flow ◽

Intraabdominal Pressure ◽

Arterial Blood ◽

Baseline Values ◽

Air Insufflation

Background Intraabdominally insufflated carbon dioxide (CO2) during laparoscopy may have a specific effect on splanchnic circulation that may be unrelated to the effects of increased intraabdominal pressure alone. Therefore, the influences of insufflation with CO2 versus air on splanchnic circulation were compared. Methods Pigs were chronically instrumented for continuous recording of mesenteric artery, portal venous, inferior vena cava, and pulmonary arterial blood flow and portal venous pressure. After induction of anesthesia, CO2 or air was insufflated in 14 and 10 pigs, respectively. With the pigs in the supine position, intraabdominal pressure was increased in steps of 4 mmHg up to 24 mmHg by graded gas insufflation. Results During air insufflation, mesenteric artery vascular resistance was unchanged, whereas mesenteric arterial blood flow decreased with increasing intraabdominal pressure. Shortly after CO2 insufflation to an intraabdominal pressure of 4 mmHg, mean arterial pressure, mesenteric arterial blood flow, and mesenteric arterial vascular resistance were increased by 21%, 12% and 9%, respectively. Subsequently, with the onset of CO2 resorption in the third minute, mean arterial pressure declined to baseline values and mesenteric arterial vascular resistance declined to 85% of baseline values, whereas mesenteric arterial blood flow continued to increase to a maximum of 24% higher than baseline values. At steady-state conditions during CO2 insufflation, mesenteric arterial blood flow was increased up to an intraabdominal pressure 16 mmHg but decreased at higher intraabdominal pressures. Conclusions In contrast to air insufflation, intraabdominal insufflation of CO2 resulted in a moderate splanchnic hyperemia at an intraabdominal pressure < or = 12 mmHg. At higher intraabdominal pressure values, pressure-induced changes became more important than the type of gas used.

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Pulmonary blood flow, pressure and resistance following tetraethylammonium and aminophylline

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1961.200.2.287 ◽

1961 ◽

Vol 200 (2) ◽

pp. 287-291 ◽

Cited By ~ 10

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

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

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.2001.280.5.g819 ◽

2001 ◽

Vol 280 (5) ◽

pp. G819-G827 ◽

Cited By ~ 30

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.

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Effect of orthotopic transplantation of liver on systemic and splanchnic hemodynamics in conscious rat

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1995.269.1.g153 ◽

1995 ◽

Vol 269 (1) ◽

pp. G153-G159 ◽

Cited By ~ 1

Author(s):

L. V. Kuznetsova ◽

D. Zhao ◽

A. M. Wheatley

Keyword(s):

Blood Flow ◽

Vascular Resistance ◽

Portal Pressure ◽

Peripheral Resistance ◽

Vena Cava ◽

Cardiovascular Effects ◽

Suture Technique ◽

Arterial Blood Flow ◽

Conscious Rat ◽

Arterial Blood

The long-term cardiovascular effects of orthotopic liver transplantation (OLT) were studied in conscious Lewis rats with a radioactive microsphere technique. Three months after OLT with an all-suture technique for graft revascularization (s-OLT), all hemodynamic parameters were similar to control. OLT with "cuffs" fitted to the portal vein and infrahepatic inferior vena cava (c-OLT) led to prominent hemodynamic disturbances including 1) hyperkinetic circulation with increased cardiac index (CI; 22%; P < 0.05) and decreased mean arterial pressure (15%; P < 0.05) and total peripheral resistance (TPR; 28%; P < 0.05); 2) a slight increase in portal pressure (11.8 +/- 0.9 vs. 9.3 +/- 1.7 mmHg in control) and marked portal-systemic shunting (51 +/- 11 vs. 0.05 +/- 0.04% in control; P < 0.05); 3) increased hepatic arterial blood flow (0.49 +/- 0.06 vs. 0.27 +/- 0.04 ml.min-1.g liver wt-1; P < 0.05); 4) splanchnic vasodilation with vascular resistance significantly (P < 0.05) lower in the liver, stomach, and large intestine; and 5) increased blood flow and decreased vascular resistance in the kidneys and heart. Ganglionic blockade with chlorisondamine (5 mg/kg body wt iv) indicated that the increase in CI seen in the c-OLT rats was probably sympathetically mediated, whereas the increase in renal blood flow was a reflection of the increase in CI. After ganglionic blocker administration, TPR and regional vascular resistances decreased to approximately the same extent in the control and c-OLT groups, indicating that vascular sympathetic tone was unchanged in the c-OLT rats.(ABSTRACT TRUNCATED AT 250 WORDS)

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L-arginine augments nitric oxide production and mesenteric blood flow in ovine endotoxemia

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1996.271.4.h1296 ◽

1996 ◽

Vol 271 (4) ◽

pp. H1296-H1301

Author(s):

K. G. Allman ◽

A. P. Stoddart ◽

M. M. Kennedy ◽

J. D. Young

Keyword(s):

Nitric Oxide ◽

Blood Flow ◽

Systemic Vascular Resistance ◽

Vascular Resistance ◽

Arterial Blood Flow ◽

Nitric Oxide Production ◽

Mesenteric Blood Flow ◽

Oxide Production ◽

Arterial Blood ◽

Nitrate Concentrations

We studied the effects of administrating the nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), or the nitric oxide precursor, L-arginine, on hemodynamic variables and serum nitrate concentrations in an anesthetized ovine model of endotoxemia to assess the effects on regional visceral blood flow and to determine whether L-arginine availability limits nitric oxide production. Animals received Escherichia coli endotoxin (2 micrograms/kg) followed 2 h later by L-NAME (25 mg/kg), L-arginine (0.575 g/kg), or saline administered over 1 h followed by an infusion of the same dose over 8 h (n = 6 per group). Renal and mesenteric blood flow were measured by placement of electromagnetic flow probes, and serum nitrate concentrations were determined using vanadium III chloride or nitrate reductase reduction to nitric oxide or nitrite, respectively. The results showed L-NAME significantly increased systemic vascular resistance (P < 0.01), decreased serum nitrate concentrations (P < 0.05), and caused a transient reduction in mesenteric blood flow (P < 0.05). L-Arginine caused a reduction in systemic vascular resistance (P < 0.01), increased mesenteric blood flow (P < 0.001) and conductance (P < 0.05). There were no significant changes in renal arterial blood flow in either group. We conclude that the availability of L-arginine limits nitric oxide production in endotoxemia and, furthermore, that L-arginine administration in this model causes significant mesenteric vasodilatation. L-NAME administration had only limited effect on visceral blood flow despite a marked increase in systemic vascular resistance and a reduction in nitric oxide production.

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Cardiac output distribution and regional blood flow during hypocarbia in monkeys

Journal of Applied Physiology ◽

10.1152/jappl.1985.58.4.1225 ◽

1985 ◽

Vol 58 (4) ◽

pp. 1225-1230 ◽

Cited By ~ 6

Author(s):

S. Gelman ◽

K. C. Fowler ◽

S. P. Bishop ◽

L. R. Smith

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Regional Blood Flow ◽

Arterial Blood Flow ◽

Tissue Blood Flow ◽

Base Line ◽

Output Distribution ◽

Arterial Blood ◽

Cardiac Output Distribution ◽

The Brain

Cardiac output distribution and regional blood flow were studied during hypocarbia independent of changes in ventilatory parameters. Fifteen cynomolgus monkeys were anesthetized with methohexital sodium (8 mg/kg im) and hyperventilated through an endotracheal tube. Hypocarbia at two levels, 28 +/- 1.8 and 17 +/- 0.6 Torr, was achieved by a stepwise decreasing CO2 flow into the semiclosed system. Regional blood flow was determined with labeled microspheres. At each stage of experiments two sets of microspheres (9 and 15 microns diam) were used simultaneously. The use of two microsphere sizes allowed evaluation of the relationship between total (nutritive and nonnutritive) tissue blood flow, determined with 15-microns spheres, and nutritive blood flow, determined with 9-microns spheres. There was no change in cardiac output or arterial pressure during both degrees of studied hypocarbia. Hypocarbia was accompanied by a decrease in myocardial blood flow determined with 15-microns spheres and preservation of the flow determined with 9-microns spheres. Splenic blood flow was decreased, whereas hepatic arterial blood flow was increased during both levels of hypocarbia. Blood flow through the brain, renal cortex, and gut showed a biphasic response to hypocarbia: during hypocarbia at 28 +/- 1.8 Torr, blood flow determined with 15-microns spheres was unchanged (in the gut) or decreased (in the brain and kidneys), whereas blood flow determined with 9-microns spheres was decreased. During hypocarbia at 17 +/- 0.6 Torr, blood flow determined with 9-microns spheres had a tendency to restore to base-line values.

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Cardiac output and redistribution of organ blood flow in hypermetabolic sepsis

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1984.246.3.r331 ◽

1984 ◽

Vol 246 (3) ◽

pp. R331-R337 ◽

Cited By ~ 8

Author(s):

C. H. Lang ◽

G. J. Bagby ◽

J. L. Ferguson ◽

J. J. Spitzer

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Muscle Blood Flow ◽

Intraperitoneal Administration ◽

Peripheral Resistance ◽

Arterial Blood Flow ◽

Tissue Blood Flow ◽

Organ Blood Flow ◽

Arterial Blood ◽

Over Time

Cardiac output (CO) and the distribution of blood flow were studied in chronically catheterized conscious rats during sustained (4 days) sepsis. Septicemia was induced by intraperitoneal administration of a pooled fecal inoculum, and tissue blood flow and CO were determined daily with 15-micron radioactive microspheres. Mean arterial blood pressure (MABP, 113 +/- 2 mmHg), CO (244.5 +/- 11.4 ml X min-1 X kg-1), and total peripheral resistance (TPR, 1.36 +/- 0.07 mmHg X ml-1 X min) were stable in control rats over the 4 days postinoculation. Septic animals showed a consistent tachycardia with MABP significantly reduced only on days 3 and 4 (86 +/- 4 mmHg). A hyperdynamic response to sepsis was indicated by an elevated CO (27%) and similarly reduced TPR on day 2. The calculated stroke volume averaged 0.22 +/- 0.01 ml/beat and did not vary over time or between the two groups. There was a 40-70% increase in blood flow to the heart, spleen, adrenal glands, and small intestine, and a greater than sixfold increase in hepatic arterial blood flow. The sustained elevation of coronary blood flow, observed in septic animals, was independent of myocardial work and is consistent with impaired myocardial function. Pancreas, stomach, and skeletal muscle blood flow was consistently compromised (24, 39, and 52%, respectively) during sepsis. Blood flow in other organs remained unchanged over time. Sepsis-induced changes in the fractional distribution of blood flow to various organs were similar to those described for absolute flow. (ABSTRACT TRUNCATED AT 250 WORDS)

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