Local and systemic autonomic nervous effects on cell migration to the spleen

2003 ◽  
Vol 94 (2) ◽  
pp. 469-475 ◽  
Author(s):  
Heiner Rogausch ◽  
Detlev Zwingmann ◽  
Mirjam Trudewind ◽  
Adriana del Rey ◽  
Karl-Heinz Voigt ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Perfusion ◽  
Sympathetic Nerves ◽  
Lymphoid Cells ◽  
Cell Uptake ◽  
Organ Blood Flow ◽  
Splenic Blood Flow ◽  
Circulating Cells ◽  
Arterial Blood ◽  
Microsphere Method

This work is based on the hypothesis that sympathetic nerves regulate the uptake of circulating cells by the spleen by affecting splenic blood flow and that the quantity of cells sequestered depends on whether changes in noradrenergic transmission occur at local or systemic levels. Fluorescently labeled lymphoid cells were injected into rats, and organ blood flow was measured by the microsphere method. Increased retention of cells in the spleen paralleled by increased blood flow was detected after local denervation of this organ or administration of bacterial endotoxin. A comparable enhanced splenic blood flow was observed after general sympathectomy. However, the redistribution of blood perfusion during general vasodilatation resulted in deviation of leukocyte flow from the spleen, thus resulting in reduced uptake of cells by this organ. These results indicate that, although the uptake of cells by the spleen depends on arterial blood supply, enhanced perfusion does not always result in increased cell sequestration because general vasodilatation reduces cell uptake by this organ and even overrides stimulatory effects of endotoxin.

l-Arginine restores splenocyte functions after trauma and hemorrhage potentially by improving splenic blood flow

1999 ◽  
Vol 276 (1) ◽  
pp. C145-C151 ◽  
Author(s):  
Martin K. Angele ◽  
Nadia Smail ◽  
Markus W. Knöferl ◽  
Alfred Ayala ◽  
William G. Cioffi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Immune Responses ◽  
Male Rats ◽  
Sham Operation ◽  
Organ Blood Flow ◽  
Shed Blood ◽  
Splenic Blood Flow ◽  
Arterial Blood ◽  
Constitutive Nitric Oxide Synthase ◽  
Oxide Synthase

Several studies indicate that immune responses are markedly depressed early after onset of hemorrhage. Decreased organ blood flow has been implicated in the pathophysiology of altered immune responses after trauma-hemorrhage. In this regard, administration ofl-arginine has been shown to restore depressed intestinal and hepatic blood flow after trauma-hemorrhage, probably due to provision of substrate for constitutive nitric oxide synthase (cNOS). It remains unknown, however, whether administration ofl-arginine also ameliorates depressed splenic blood flow and whether this agent has any salutary effects on depressed splenocyte functions after trauma-hemorrhage. Male rats underwent sham operation or laparotomy and were bled to and maintained at a mean arterial blood pressure of 40 mmHg until 40% of maximum shed blood volume (MBV) was returned as Ringer lactate (RL). Hemorrhaged rats were then resuscitated with RL (4 times MBV over 1 h). During resuscitation, rats received 300 mg/kgl-arginine or saline (vehicle) intravenously; 4 h later, splenic blood flow, splenocyte proliferation, and splenocyte interleukin (IL)-2 and IL-3 were determined. Administration of l-arginine improved depressed splenic blood flow and restored depressed splenocyte functions after trauma-hemorrhage. Therefore, provision ofl-arginine during resuscitation after trauma-hemorrhage should be considered a novel and safe approach for improving splenic organ blood flow and depressed splenocyte functions under such conditions.

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.

Glucagon inhibition of hepatic arterial responses to hepatic nerve stimulation

1977 ◽  
Vol 233 (6) ◽  
pp. H647-H654 ◽  
Author(s):  
P. D. Richardson ◽  
P. G. Withrington
Keyword(s):  
Blood Flow ◽  
Nerve Stimulation ◽  
Perfusion Pressure ◽  
Sympathetic Nerves ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Vascular Bed ◽  
Arterial Responses ◽  
Sympathetic Discharge ◽  
Glucagon Concentration

The hepatic arterial vascular bed of the chloaralose-urethan-anesthetized dog was perfused with blood from a cannulated femoral artery. Hepatic arterial blood flow and perfusion pressure were measured. The hepatic periarterial postganglionic sympathetic nerves were stimulated supramaximally at 0.1, 0.5, 1, 2, 5, 10, and 20 Hz; this caused frequency-dependent rises in the calculated hepatic arterial vascular resistance at all frequencies above the threshold of 0.1 or 0.5 Hz. Glucagon was infused intra-arterially in dosese from 0.25 to 10 microgram/min; glucagon antagonized both the vasoconstrictor effects of hepatic nerve stimulation and of intra-arterial injections of norepinephrine. The degree of antagonism of these responses was significantly correlated with the calculated hepatic arterial glucagon concentration. It is possible that glucagon released physiologically in stress and hypoglycemia may protect the hepatic arterial vasculature from the effects of increased sympathetic discharge.

Effect of vasopressors on organ blood flow during endotoxin shock in pigs

1987 ◽  
Vol 252 (2) ◽  
pp. H291-H300 ◽  
Author(s):  
M. J. Breslow ◽  
C. F. Miller ◽  
S. D. Parker ◽  
A. T. Walman ◽  
R. J. Traystman
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Left Ventricle ◽  
Arterial Blood Pressure ◽  
Endotoxin Shock ◽  
Organ Blood Flow ◽  
Shock Model ◽  
Blood Pressure Elevation ◽  
Arterial Blood

A volume-resuscitated porcine endotoxin shock model was used to evaluate the effect on organ blood flow of increasing systemic arterial blood pressure with vasopressors. Administration of 0.05–0.2 mg/kg of Escherichia coli endotoxin (E) reduced mean arterial blood pressure (MAP) to 50 mmHg, decreased systemic vascular resistance to 50% of control, and did not change cardiac output or heart rate. Blood flow to brain, kidney, spleen, and skeletal muscle was reduced during endotoxin shock, but blood flow to left ventricle, small and large intestine, and stomach remained at pre-endotoxin levels throughout the study period. Four groups of animals were used to evaluate the effect of vasopressor therapy. A control group received E and no vasopressor, whereas the other three groups received either norepinephrine, dopamine, or phenylephrine. Vasopressors were administered starting 60 min after E exposure, and the dose of each was titrated to increase MAP to 75 mmHg. Despite the increase in MAP, brain blood flow did not increase in any group. Norepinephrine alone increased blood flow to the left ventricle. Kidney, splanchnic, and skeletal muscle blood flow did not change with vasopressor administration. The dose of norepinephrine required to increase MAP by 20–25 mmHg during E shock was 30 times the dose required for a similar increase in MAP in animals not receiving E. We conclude that hypotension in the fluid resuscitated porcine E shock model is primarily the result of peripheral vasodilatation, that the vascular response to vasoconstrictors in this model is markedly attenuated following E administration, that blood pressure elevation with norepinephrine, dopamine, and phenylephrine neither decreases blood flow to any organ nor increases blood flow to organs with reduced flow, and that norepinephrine, dopamine, and phenylephrine affect regional blood flow similarly in this model.

Hemodynamic Effects of CCl4 in the Intact Liver of the Cat

1974 ◽  
Vol 52 (3) ◽  
pp. 727-735 ◽  
Author(s):  
W. W. Lautt ◽  
G. L. Plaa
Keyword(s):  
Blood Flow ◽  
Hepatic Blood Flow ◽  
Sympathetic Nerves ◽  
Causative Factor ◽  
Arterial Infusion ◽  
Total Blood ◽  
Arterial Blood ◽  
Reflex Activation ◽  
Total Blood Flow ◽  
Early Phases

Blood flow in the intact liver of anesthetized cats did not change significantly over a period of 4 h following intraduodenal injection of CCl4 (1 ml/kg). Hepatocellular disruption was well underway by 2 h after the injection. Twenty-four hours following an oral dose of CCl4, the hepatic arterial resistance to blood flow was reduced and total blood flow to the liver was at least as high as in control animals. At this time, the hepatic artery appeared fully dilated and was less responsive to humoral (intra-arterial infusion of noradrenaline) and neural (reflex activation of the sympathetic nerves) constrictor influences. Thus, alterations in hepatic blood flow do not occur during the early phases of CCl4-induced hepatic injury. These data indicate that diminished blood flow is not a causative factor in the initial phases of CCl4-induced liver injury. By 24 h, hepatic blood flow is altered in such a manner that the damaged liver receives a higher proportion of arterial blood and a total blood flow that is not reduced in spite of a generally depressed cardiovascular system.

Salutary effects of androstenediol on cardiac function and splanchnic perfusion after trauma-hemorrhage

2004 ◽  
Vol 287 (2) ◽  
pp. R386-R390 ◽  
Author(s):  
Tomoharu Shimizu ◽  
Mashkoor A. Choudhry ◽  
Laszlo Szalay ◽  
Loring W. Rue ◽  
Kirby I. Bland ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Function ◽  
Cytokine Production ◽  
Cardiovascular Function ◽  
Organ Blood Flow ◽  
Sprague Dawley ◽  
Splanchnic Perfusion ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Circulating Levels

Recent studies have shown that dehydroepiandrosterone (DHEA) administration after trauma-hemorrhage (T-H) improves cardiovascular function and decreases cytokine production in male animals. Although androstenediol, one of the metabolites of DHEA, is reported to have estrogen-like activity, it remains unknown whether androstenediol per se has any salutary effects on cytokines and cardiovascular function after T-H. To examine this effect, male Sprague-Dawley rats underwent laparotomy and were bled to and maintained at a mean arterial blood pressure of 35–40 mmHg for ∼90 min. The animals were resuscitated with four times the volume of maximal bleedout volume in the form of Ringer lactate. Androstenediol (1 mg/kg body wt iv) or vehicle was administered at the end of resuscitation. Twenty-four hours after resuscitation, cardiac function and organ blood flow were measured by using 85Sr-microspheres. Circulating levels of nitrate/nitrite and IL-6 were also determined. Cardiovascular function and organ blood flow were significantly depressed after T-H. However, these parameters were restored by androstenediol treatment. The elevated plasma IL-6 levels after T-H were also lowered by androstenediol treatment. In contrast, plasma levels of nitrate/nitrite were the highest in the androstenediol-treated T-H animals. Because androstenediol administration after T-H decreases cytokine production and improves cardiovascular function, this agent appears to be a novel and useful adjunct for restoring the depressed cardiovascular function and for cytokine production in males after adverse circulatory conditions.

Precautions for measuring blood flow during anemia with the microsphere technique

1983 ◽  
Vol 244 (2) ◽  
pp. H308-H311 ◽  
Author(s):  
A. A. Rosenberg ◽  
M. D. Jones ◽  
R. C. Koehler ◽  
R. J. Traystman ◽  
G. Lister
Keyword(s):  
Blood Flow ◽  
Blood Cells ◽  
Standard Procedure ◽  
Reference Sample ◽  
Organ Blood Flow ◽  
Brachiocephalic Artery ◽  
Peripheral Artery ◽  
Fick Principle ◽  
Arterial Blood ◽  
The Difference

Preliminary data from a study of the effects of anemia on organ blood flow showed large discrepancies between cardiac output measured with the microsphere technique and simultaneous values calculated by the Fick principle. The most likely explanation was that the reference sample drawn according to our standard procedure underestimated the microsphere concentration in arterial blood, resulting in erroneously high blood flow values. In the present experiments we compared our usual reference sample, from a small catheter advanced from a peripheral artery into the brachiocephalic artery (withdrawal rate 1.3 ml/min), with a simultaneous sample from a larger catheter withdrawn at the much higher rate (7.89 ml/min). At hematocrits above 32%, microsphere concentrations from the two catheters were similar, but below 32% the concentration of microspheres in blood from the larger catheter was 30-50% more than from the smaller. The discrepancy was not altered by changing the injection site from left ventricle to left atrium and thus was probably not the result of poor mixing within the heart. It may have been the result of nonhomogeneous distribution of microspheres within larger vessels, perhaps as a consequence of laminar flow and axial streaming of both red blood cells and microspheres during anemia. Whatever the cause, it was possible to eliminate the difference by withdrawing from the smaller catheter at a more rapid rate (2.46 ml/min).

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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