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.

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 < .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.

Cardiac output distribution and regional blood flow during hypocarbia in monkeys

1985 ◽  
Vol 58 (4) ◽  
pp. 1225-1230 ◽  
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.

Cardiac output and redistribution of organ blood flow in hypermetabolic sepsis

1984 ◽  
Vol 246 (3) ◽  
pp. R331-R337 ◽  
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)

Effect of Two Models of Portal Hypertension on Splanchnic Organ Blood Flow in the Rat

1985 ◽  
Vol 68 (1) ◽  
pp. 23-28 ◽  
Author(s):  
D. Lebrec ◽  
L. Blanchet
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Portal Hypertension ◽  
Portal Vein ◽  
Arterial Blood Flow ◽  
Organ Blood Flow ◽  
Portal Vein Stenosis ◽  
Arterial Blood ◽  
Duct Ligation ◽  
Vein Stenosis

1. Splanchnic organ blood flow and cardiac output were measured by the microsphere method in fasted rats with prehepatic portal hypertension due to portal vein stenosis, in rats with intrahepatic portal hypertension due to bile duct ligation, and in unoperated normal rats. 2. Portal venous pressure was higher in both groups of portal hypertensive rats than in normal rats. Cardiac output was significantly higher in portal hypertensive rats than in normal rats. 3. In rats with portal vein stenosis, splanchnic blood flow was higher than in controls. This increase was caused by increased perfusion of all organs drained by the portal vein, and by increased hepatic arterial blood flow. In rats with bile duct ligation, splanchnic blood flow was not significantly higher than in normal rats: haemoperfusion of all organs contributing to the portal circulation decreased, whereas hepatic arterial blood flow increased. As cardiac output rose similarly, the differences observed between the two types of portal hypertension depend mainly on the difference in distribution of flow within the splanchnic bed.

L-propionylcarnitine increases postischemic blood flow but does not affect recovery of energy charge

1991 ◽  
Vol 261 (1) ◽  
pp. H172-H180 ◽  
Author(s):  
L. M. Sassen ◽  
K. Bezstarosti ◽  
W. J. Van der Giessen ◽  
J. M. Lamers ◽  
P. D. Verdouw
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Contractile Function ◽  
Energy Charge ◽  
Left Ventricular ◽  
Arterial Blood

Effects of pretreatment with L-propionylcarnitine (50 mg/kg, n = 9) or saline (n = 10) were studied in open-chest anesthetized pigs, in which ischemia was induced by decreasing left anterior descending coronary artery blood flow to 20% of baseline. After 60 min of ischemia, myocardium was reperfused for 2 h. In both groups, flow reduction abolished contractile function of the affected myocardium and caused similar decreases in ATP (by 55%) and energy charge [(ATP + 0.5ADP)/(ATP + ADP + AMP); decrease from 0.91 to 0.60], mean arterial blood pressure (by 10-24%), the maximum rate of rise in left ventricular pressure (by 26-32%), and cardiac output (by 20-30%). During reperfusion, “no-reflow” was attenuated by L-propionylcarnitine, because myocardial blood flow returned to 61 and 82% of baseline in the saline- and L-propionylcarnitine-treated animals, respectively. Cardiac output of the saline-treated animals further decreased (to 52% of baseline), and systemic vascular resistance increased from 46 +/- 3 to 61 +/- 9 mmHg.min.l-1, thereby maintaining arterial blood pressure. In L-propionylcarnitine-treated pigs, cardiac output remained at 75% of baseline, and systemic vascular resistance decreased from 42 +/- 3 to 38 +/- 4 mmHg.min.l-1. In both groups, energy charge but not the ATP level of the ischemic-reperfused myocardium tended to recover, whereas the creatine phosphate level showed significantly more recovery in saline-treated animals. We conclude that L-propionylcarnitine partially preserved vascular patency in ischemic-reperfused porcine myocardium but had no immediate effect on “myocardial stunning.” Potential markers for long-term recovery were not affected by L-propionylcarnitine.

Circulatory and Ventilatory Responses of Rainbow Trout (Salmo gairdneri) to Artificial Manipulation of Gill Surface Area

1971 ◽  
Vol 28 (10) ◽  
pp. 1609-1614 ◽  
Author(s):  
John C. Davis
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Rainbow Trout ◽  
Surface Area ◽  
Salmo Gairdneri ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Gill Area ◽  
Gill Surface Area ◽  
The Brain

Reductions in surface area of the gill were artificially produced by ligating various gill arches and occluding their blood supply. Rainbow trout (Salmo gairdneri) responded to a 40–57% reduction in gill area, by increasing cardiac output and ventilation volume, and probably by redistributing blood within the remaining functional gill area. Fish with blood flow to gill arches one and three only, could maintain arterial PO2 at 90–100 mm Hg, whereas, in those with blood flow to arches three and four only, arterial PO2 fell to around 40 mm Hg. The presence of a chemoreceptor site for the regulation of arterial PO2 associated with the efferent blood vessels of arch number one is discussed. Such a receptor may be located in the pseudobranch or in the portion of the brain supplied with arterial blood from the first gill arch.

Dose-Dependent Effects of Meclofenamate on Peripheral Vasculature of Conscious Rabbits

1983 ◽  
Vol 64 (5) ◽  
pp. 471-474 ◽  
Author(s):  
R. A. Banks ◽  
L. J. Beilin ◽  
J. Soltys
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Organ Blood Flow ◽  
Hepatic Circulation ◽  
Peripheral Vasculature ◽  
Conscious Rabbits ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
The Brain ◽  
Intravenous Sodium

1. Changes in systemic haemodynamics and organ blood flow were measured in conscious rabbits after various doses of intravenous sodium meclofenamate, an inhibitor of prostaglandin cyclo-oxygenase. 2. Meclofenamate had no effect on arterial pressure or cardiac output but caused a dose-dependent fall in renal blood flow. 3. Meclofenamate also reduced adrenal perfusion but, in contrast, caused a dose-dependent increase in blood flow to the brain, bronchial and hepatic circulation and to the testis. No effect was demonstrated on other organs studied. 4. The effect on the cerebral circulation was observed at the lowest dose of meclofenamate (0.75 mg/kg). Higher total doses were necessary for an effect on the renal and bronchial (3 mg/kg) and testicular and hepatic arteries (6 mg/kg). 5. The results suggest a variety of local vasomotor influences of renal and non-renal prostaglandins in conscious rabbits.

PV Loops and REBOA During Hemorrhage and Resuscitation

2021 ◽  
Author(s):  
David P Stonko ◽  
Joseph Edwards ◽  
Hossam Abdou ◽  
Noha N Elansary ◽  
Eric Lang ◽  
...  
Keyword(s):  
Blood Flow ◽  
Hemorrhagic Shock ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Balloon Occlusion ◽  
Aortic Occlusion ◽  
Loop Analysis ◽  
Time Period ◽  
Great Vessels ◽  
The Brain

Abstract Retrograde Endovascular Balloon Occlusion of the Aorta (REBOA) is frequently used in hemorrhagic shock to facilitate resuscitation. In theory, aortic occlusion increases afterload and focuses perfusion to the coronary arteries and great vessels; also to focus perfusion to the brain. It is, however, unknown exactly how and to what extent REBOA impacts cardiovascular parameters such as preload, afterload and contractility, or coronary artery blood flow. It is also not known how these parameters evolve over time during REBOA as it is shifted from fully to partially occlusive, or weaned down entirely. We aim to use left ventricular Pressure-Volume (PV) loop analysis and directly measure coronary flow in swine as they descend into hemorrhagic shock, are resuscitated with full aortic occlusion with REBOA, transitioned to partial aortic occlusion with REBOA, and then weaned completely off of the REBOA and are resuscitated. We will examine, specifically, measures of preload, afterload, contractility and coronary blood flow during each study time period (baseline, hemorrhagic shock, full aortic occlusion, partial aortic occlusion, and post-occlusion during resuscitation).

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.

Distribution of respiratory muscle and organ blood flow during endotoxic shock in dogs

1985 ◽  
Vol 59 (6) ◽  
pp. 1802-1808 ◽  
Author(s):  
S. N. Hussain ◽  
C. Roussos
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Respiratory Muscle ◽  
Muscle Blood Flow ◽  
Endotoxic Shock ◽  
Organ Blood Flow ◽  
Similar Reduction ◽  
Arterial Blood

Respiratory muscle blood flow and organ blood flow during endotoxic shock were studied in spontaneously breathing dogs (SB, n = 6) and mechanically ventilated dogs (MV, n = 5) with radiolabeled microspheres. Shock was produced by a 5-min intravenous injection of Escherichia coli endotoxin (0.55:B5, Difco, 10 mg/kg) suspended in saline. Mean arterial blood pressure and cardiac output in the SB group dropped to 59 and 45% of control values, respectively. There was a similar reduction in arterial blood pressure and cardiac output in the MV group. Total respiratory muscle blood flow in the SB group increased significantly from the control value of 51 +/- 4 ml/min (mean +/- SE) to 101 +/- 22 ml/min at 60 min of shock. In the MV group, respiratory muscle perfusion fell from control values of 43 +/- 12 ml/min to 25 +/- 3 ml/min at 60 min of shock. In the SB group, 8.8% of the cardiac output was received by the respiratory muscle during shock in comparison with 1.9% in the MV group. In both groups of dogs, blood flow to most organs was compromised during shock; however, blood flow to the brain, gut, and skeletal muscles was higher in the MV group than in the SB group. Thus by mechanical ventilation a fraction of the cardiac output used by the working respiratory muscles can be made available for perfusion of other organs during endotoxic shock.

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