Haemodynamic Effects of Eating: The Role of Meal Composition

1996 ◽  
Vol 90 (4) ◽  
pp. 269-276 ◽  
Author(s):  
U. Høst ◽  
H. Kelbaek ◽  
H. Rasmusen ◽  
M. Court-Payen ◽  
N. Juel Christensen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Portal Vein ◽  
Forearm Blood Flow ◽  
Plasma Catecholamines ◽  
Left Ventricular ◽  
Gastric Distension ◽  
Left Ventricular Volumes ◽  
Portal Vein Flow

1. The purpose of this study was to investigate the effect of fractional meal stimulation on postprandial haemodynamic changes, the possible correlation between these changes and the potential mediating role of circulating catecholamines and insulin. 2. Healthy young subjects were studied before and after ingestion of isocaloric, isovolumetric high-protein, carbohydrate or fat meals (80–85% of total energy), 60 kJ per kg of body weight. Multigated radionuclide cardiography with autologous 99mTc-labelled erythrocytes was performed for assessment of cardiac output, venous occlusion plethysmography to obtain forearm blood flow and Doppler-ultrasonography for portal vein flow. Plasma levels of catecholamines and insulin were determined by radioimmunoassay. 3. Cardiac output increased considerably after each meal, including the control meal (water) with only minor differences in extent and timing. Left ventricular volumes increased after food intake, most pronounced after carbohydrate and protein. Forearm blood flow increased only after carbohydrate and protein. Portal vein flow increased after all meals, especially after fat, but also after the control meal. There was a significant correlation between the increment in cardiac output and changes in forearm and portal vein flow, but no correlation between either haemodynamic response and plasma catecholamines or insulin. 4. Postprandial cardiovascular changes are not substantially different after various isocaloric and isovolumic meal compositions. Gastric distension seems to play a role in the increase in cardiac output, accomplished by ventricular dilatation. These changes seem to some extent to be linked to changes in muscle and splanchnic flow.

Myocardial, skeletal muscle, and renal blood flow during exercise in conscious dogs with heart failure

1997 ◽  
Vol 273 (5) ◽  
pp. H2452-H2457 ◽  
Author(s):  
Till Neumann ◽  
Gerd Heusch
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Renal Blood Flow ◽  
Plasma Catecholamines ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Ventricular Pacing ◽  
Control State

The present study characterizes the hemodynamic and neurohumoral responses to moderate treadmill exercise in conscious dogs with pacing-induced heart failure. Seven dogs were instrumented with a left ventricular micromanometer, ultrasonic crystals for the measurement of systolic wall thickening, left atrial and aortic catheters for the injection of colored microspheres and reference withdrawal, respectively, and ventricular pacing leads with a subcutaneous pacemaker. Dogs were run on a treadmill at a speed of 5 km/h. After control studies, heart failure was induced by rapid left ventricular pacing at 250 beats/min for (mean ± SD) 23 ± 6 days. In the control state, cardiac output was increased from 4.5 ± 1.5 to 7.9 ± 1.4 l/min ( P < 0.05 vs. rest). With heart failure, cardiac output was decreased to 2.5 ± 0.5 l/min at rest ( P < 0.05 vs. control state) and was only 3.0 ± 0.3 l/min during exercise ( P < 0.05 vs. control state; not significant vs. rest). Myocardial and, more so, skeletal muscle blood flows at rest were reduced in heart failure; their increases with exercise were attenuated. An increase in renal blood flow during exercise in the control state was no longer seen in heart failure. Increases in plasma catecholamines and lactate during exercise were more pronounced in heart failure. In conclusion, in heart failure, the increase in cardiac output during exercise was largely attenuated. Increased catecholamine levels may have contributed to splanchnic vasoconstriction and preferential distribution of cardiac output into the working skeletal muscle.

Ethanol-induced increase in portal blood flow: role of adenosine

1988 ◽  
Vol 254 (4) ◽  
pp. G495-G501 ◽  
Author(s):  
H. Orrego ◽  
F. J. Carmichael ◽  
V. Saldivia ◽  
H. G. Giles ◽  
S. Sandrin ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Portal Vein ◽  
Portal Blood Flow ◽  
Portal Blood ◽  
Maximal Effect ◽  
Dependent Manner ◽  
Dose Dependent Increase ◽  
Dose Dependent

The mechanism by which ethanol induces an increase in portal vein blood flow was studied in rats using radiolabeled microspheres. Ethanol (2 g/kg) by gavage resulted in an increase of 50-70% in portal vein blood flow. The ethanol-induced increase in portal blood flow was suppressed by the adenosine receptor blocker 8-phenyltheophylline [ethanol, 61.8 +/- 4.1 ml.kg-1.min-1; ethanol + 8-phenyltheophylline (0.2 mg.kg-1.min-1), 44.2 +/- 2.0 ml.kg-1.min-1; P less than 0.05]. By itself, 8-phenyltheophylline (0.2 mg.kg-1.min-1) was without effect on cardiac output or portal blood flow. Adenosine infusion resulted in a dose-dependent increase in portal blood flow with a maximal effect at a dose of 0.17 mg.kg-1.min-1 (control, 41.3 +/- 2.3; adenosine, 81.7 +/- 8.0 ml.kg-1.min-1; P less than 0.05). This adenosine-induced increase in portal blood flow was inhibited by 8-phenyltheophylline in a dose-dependent manner [adenosine, 81.7 +/- 8.0 ml.kg-1.min-1; adenosine + 8-phenyltheophylline (0.2 mg.kg-1.min-1), 49.8 +/- 6.6 ml.kg-1.min; P less than 0.05]. Both alcohol and adenosine significantly reduced preportal vascular resistance by 40% (P less than 0.02) and 60% (P less than 0.01), respectively. These effects were fully suppressed by 8-phenyltheophylline. It is concluded that adenosine is a likely candidate to mediate the ethanol-induced increase in portal vein blood flow. It is suggested that an increase in circulating acetate and liver hypoxia may mediate the effects of alcohol by increasing tissue and interstitial adenosine levels.

Alterations in Systemic Vascular Volume of the Dog in Response to Hexamethonium and Norepinephrine

1957 ◽  
Vol 191 (2) ◽  
pp. 283-286 ◽  
Author(s):  
John C. Rose ◽  
Edward D. Freis
Keyword(s):  
Cardiac Output ◽  
Venous Return ◽  
Cardiac Activity ◽  
Left Ventricular ◽  
Vascular Volume ◽  
Vasomotor Activity ◽  
Constant Output ◽  
Arteriolar Tone ◽  
Integrated Responses

A diaphragm pump of controlled constant output was substituted for the left ventricle in dogs. Left auricular blood was conducted to a reservoir, from which it was pumped into the thoracic aorta. Left ventricular by-pass was complete. Alterations in total vascular volume were continually monitored by observation of the pump reservoir level. Sympathetic blockade (hexamethonium) increased total vascular volume (mean 15%). This resulted in decreased venous return and decreased right ventricular output. Norepinephrine constricted the total vasculature and decreased vascular volume (mean 12%). This resulted in increased venous return and cardiac output. These experiments demonstrated the complex integrated responses of the total circulation to sympathetic vasomotor activity. The role of the sympathetic nervous system not only in the regulation of arteriolar tone and cardiac activity but also in adjusting total vascular volume and venous return was emphasized. Venous return, and hence cardiac output alterations accompanying systemic vasomotor activity can only be detected by continuous methods of flow measurement.

scholarly journals Leaning during chest compressions impairs cardiac output and left ventricular myocardial blood flow in piglet cardiac arrest

2010 ◽  
Vol 38 (4) ◽  
pp. 1141-1146 ◽  
Author(s):  
Mathias Zuercher ◽  
Ronald W. Hilwig ◽  
James Ranger-Moore ◽  
Jon Nysaether ◽  
Vinay M. Nadkarni ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Arrest ◽  
Cardiac Output ◽  
Myocardial Blood Flow ◽  
Left Ventricular ◽  
Chest Compressions

Time course of hemodynamic changes in rats with healed severe myocardial infarction

1989 ◽  
Vol 257 (1) ◽  
pp. H289-H296 ◽  
Author(s):  
A. DeFelice ◽  
R. Frering ◽  
P. Horan
Keyword(s):  
Myocardial Infarction ◽  
Blood Flow ◽  
Cardiac Output ◽  
Diastolic Pressure ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Male Rats ◽  
Coronary Artery Ligation ◽  
Sham Operation ◽  
Functional Changes

Male rats were monitored for 8 mo after severe myocardial infarction (MI) to chronicle hemodynamic and left ventricular (LV) functional changes. Blood pressure (BP), heart rate (HR), cardiac output index (CO), regional blood flow, and systemic vascular resistance (SVR) were measured with catheters and radiolabeled microspheres at 4, 7, 10, 20, and 35 wk after coronary artery ligation (n = 10–16/group) or sham operation (control; n = 9–14/group). At 4 wk, 43 +/- 1% of the LV circumference was scarred, peak LV BP, LV dP/dtmax, mean BP, SVR, and HR were 11–38% less than control (P less than 0.05), and LV end-diastolic pressure (LVEDP) was increased by 313% (P less than 0.05). Mean BP, LVEDP, LVBP, and LV dP/dtmax did not further deviate after 4 wk. However, CO and SVR changed progressively and were 67 and 33%, respectively, of control by 35 wk (P less than 0.05) when blood flow to stomach, small intestine, and kidney was 55, 38, and 27% of control. Lung and heart weights were significantly increased by 148 and 22% at 4 wk, and remained elevated, and lung dry weight-to-wet weight ratio was reduced at 7 and 10 wk. Thus the trajectory of rats with healed severe MI reflects progressive cardiac decompensation, cardiac output redistribution, and terminal heart failure.

Effect of nerve block on response of forearm blood flow to local temperature

1986 ◽  
Vol 61 (1) ◽  
pp. 227-232 ◽  
Author(s):  
C. B. Wenger ◽  
L. A. Stephenson ◽  
M. A. Durkin
Keyword(s):  
Blood Flow ◽  
Nerve Block ◽  
Forearm Blood Flow ◽  
Brachial Plexus Block ◽  
Thermal Sensation ◽  
Strain Gauges ◽  
Forearm Skin ◽  
Plastic Bag ◽  
Plexus Block

To determine the role of neurotransmitter in the response of forearm blood flow (ABF) to local (forearm) skin temperature (Tsk) we measured ABF of six subjects at Tsk from 25 to 40 degrees C before (control) and after brachial plexus block (BPB). Control experiments were conducted in an ambient temperature of 27–29 degrees C, adjusted to minimize the subject's overall thermal sensation. Tsk was regulated by blowing a controlled-temperature airstream through a plastic bag enclosing the arm. We first lowered Tsk to 25 degrees C and after 20 min began to measure ABF with Whitney strain gauges. We then raised Tsk by 2.5 degrees C steps to 40 degrees C and measured ABF every 30 s for at least 10 min at each level of Tsk. Mean ABF rose from 1.1 ml X 100 ml-1 X min-1 at Tsk of 25 degrees C to 2.1 ml X 100 ml-1 X min-1 at 32.5 degrees C to 13.7 ml X 100 ml-1 X min-1 at 40 degrees C in control experiments and from 2.8 to 4.4 to 14.8 ml X 100 ml-1 X min-1 after BPB. The effect of Tsk on ABF was highly significant (P less than 0.0001) but the effect of BPB was not (P approximately equal to 0.2). At thermoneutrality, the effect of Tsk on ABF is largely independent of neural activity, since this effect is unaffected by nerve block.

scholarly journals Effects of Endothelin-1 on Hepatic Blood Flow

HPB Surgery ◽  
1996 ◽  
Vol 9 (3) ◽  
pp. 153-159 ◽  
Author(s):  
Kjetil Unneberg ◽  
Marianne Mjaaland ◽  
Elin Helseth ◽  
Arthur Revhaug
Keyword(s):  
Liver Transplantation ◽  
Blood Flow ◽  
Portal Vein ◽  
Plasma Concentrations ◽  
Hepatic Clearance ◽  
Elevated Plasma ◽  
Central Venous ◽  
Portal Vein Pressure ◽  
Portal Vein Flow ◽  
Endothelin 1

Endothelin-1 belongs to a family of potent vasoconstrictors, recently isolated from endothelial cells. Endothelin-1 has a variety of hepatic effects and hepatic clearance from the circulation is important. Elevated plasma concentrations of Endothelin-1 are found after orthotopic liver transplantation and in cirrhosis with ascites.This study in piglets on hepatic bloodflow was designed to compare differences in effects between central venous and intraportal injection of endothelin-1, and to evaluate effects of repeated injections. Central venous injection of endothelin-1 caused a larger reduction in portal vein flow, while intraportal injection caused a larger increase in portal vein pressure. Repeated injections resulted in a reduction in portal vein flow and an increase in portal vein vascular resistance.

Continuous Airway Pressure Breathing With the Head-Box in the Newborn Lamb: Effects on Regional Blood Flows

PEDIATRICS ◽  
1977 ◽  
Vol 59 (6) ◽  
pp. 858-864
Author(s):  
G. Gabriele ◽  
C. R. Rosenfeld ◽  
D. E. Fixler ◽  
J. M. Wheeler
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Airway Pressure ◽  
Left Ventricular Pressure ◽  
Blood Gases ◽  
Ocular Blood Flow ◽  
Left Ventricular ◽  
Positive Pressure ◽  
Blood Flows ◽  
Arterial Blood

Continuous airway pressure delivered by a head-box is an accepted means of treating clinical hyaline membrane disease. To investigate hemodynamic alterations resulting from its use, eight newborn lambs, 1 to 6 days of age, were studied at 6 and 11 mm Hg of positive pressure, while spontaneously breathing room air. Organ blood flows and cardiac output were measured with 25 µ-diameter radioactive microspheres. Heart rate, left ventricular pressure, and arterial blood gases did not change during the study. Jugular venous pressures increased from 6.4 mm Hg to 18.6 and 24.2 mm Hg at 6 and 11 mm Hg, respectively (P &lt; .005). Cardiac output decreased approximately 20% at either intrachamber pressure setting. Renal blood flow fell 21% at 11 mm Hg. No significant changes in blood flow were found in the brain, gastrointestinal tract, spleen, heart, or liver when compared to control flows. Of particular interest was the finding of a 28% reduction in ocular blood flow at 6 mm Hg and 52% at 11 mm Hg. From these results, we conclude that substantial cardiovascular alterations may occur during the application of head-box continuous airway pressure breathing, including a significant reduction in ocular blood flow.

Abstract 67: Vasopressin impairs Brain, Heart and Kidney Perfusion in Acute Heart Failure

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Stig Müller ◽  
Ole-Jakob How ◽  
Stig E Hermansen ◽  
Truls Myrmel
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Heart Function ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Arterial Blood Flow ◽  
Organ Blood Flow ◽  
Arterial Blood ◽  
Time Flow ◽  
The Brain

Arginin Vasopressin (AVP) is increasingly used to restore mean arterial pressure (MAP) in various circulatory shock states including cardiogenic shock. This is potentially deleterious since AVP is also known to reduce cardiac output by increasing vascular resistance. Aim: We hypothesized that restoring MAP by AVP improves vital organ blood flow in experimental acute cardiac failure. Methods: Cardiac output (CO) and arterial blood flow to the brain, heart, kidney and liver were measured in nine pigs by transit-time flow probes. Heart function and contractility were measured using left ventricular Pressure-Volume catheters. Catheters in central arteries and veins were used for pressure recordings and blood sampling. Left ventricular dysfunction was induced by intermittent coronary occlusions, inducing an 18 % reduction in cardiac output and a drop in MAP from 87 ± 3 to 67 ± 4 mmHg. Results: A low-dose therapeutic infusion of AVP (0.005 u/kg/min) restored MAP but further impaired systemic perfusion (CO and blood flow to the brain, heart and kidney reduced by 29, 18, 23 and 34 %, respectively). The reduced blood flow was due to a 2.0, 2.2, 1.9 and 2.1 fold increase in systemic, brain, heart and kidney specific vascular resistances, respectively. Contractility remained unaffected by AVP. The hypoperfusion induced by AVP was most likely responsible for observed elevated plasma lactate levels and an increased systemic oxygen extraction. Oxygen saturation in blood drawn from the great cardiac vein fell from 31 ± 1 to 22 ± 3 % dropping as low as 10 % in one pig. Finally, these effects were reversed forty minutes after weaning the pigs form the drug. Conclusion: The pronounced reduction in coronary blood flow point to a potentially deleterious effect in postoperative cardiac surgical patients and in patients with coronary heart disease. Also, this is the first study to report a reduced cerebral perfusion by AVP.

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