Regional Blood Flow by Fractional Distribution of Indicators

1958 ◽  
Vol 193 (1) ◽  
pp. 161-168 ◽  
Author(s):  
Leo A. Sapirstein
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Regional Blood Flow ◽  
The Body ◽  
Arterial System ◽  
Whole Body ◽  
Blood Concentrations ◽  
Arterial Blood ◽  
The Brain ◽  
Fractional Uptake

K42 Cl, Rb86Cl and iodoantipyrine (I131) were given in single intravenous injections to rats. The isotope content of the organs and the arterial blood concentrations were studied as a function of time. K42Cl and Rb86Cl reached a stable level in all organs other than the brain in 6–9 seconds and maintained this level until 64 seconds. The arterial concentration curves for the isotopes showed that the injected dose was almost completely transferred into the arterial system at about 6–8 seconds. The isotopes showed subsequent recirculation amounting to about 40% of the original dose between the first recirculation and 64 seconds. The organs which displayed stability during the period of recirculation must have had extraction ratios from zero time less than 1.00 but equal to that of the whole body. The fractional uptake of indicator by such organs must therefore have been equal to their blood flow fraction of the cardiac output. The brain reached its maximum content of Rb86 and K42 in 5–6 seconds; both isotopes then disappeared rapidly. The brain was thus shown to have a lower extraction ratio toward these isotopes than the body as a whole; its flow fraction could not therefore be measured by their use. Most organs failed to show stability of their iodoantipyrine content between 9 and 64 seconds; this indicator is not suitable for the measurement of the flow fraction of such organs. By combining values for the cardiac output and the fractional uptake of K42 in dog organs, regional blood flow values were obtained. For those other organs where flow values by other methods are available, the agreement was good. The following blood flow values were obtained in the major organs of the dog: Heart (coronary flow), 1.0 ml/gm/min.; kidney, 3.0 ml/gm/min.; liver, 1.2 ml/gm/min. (0.4 ml/gm/min. hepatic artery, 0.8 ml/gm/min. portal vein); skin, 0.07 ml/gm/min.

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.

Whole body and splanchnic oxygen consumption and blood flow after oral ingestion of fructose or glucose

1993 ◽  
Vol 264 (4) ◽  
pp. E504-E513 ◽  
Author(s):  
T. Brundin ◽  
J. Wahren
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Oxygen Uptake ◽  
The Body ◽  
Splanchnic Blood Flow ◽  
Whole Body ◽  
Co2 Production ◽  
Arterial Blood ◽  
Splanchnic Oxygen

The contribution of the splanchnic tissues to the initial 2-h rise in whole body energy expenditure after ingestion of glucose or fructose was examined in healthy subjects. Indirect calorimetry and catheter techniques were employed to determine pulmonary gas exchange, cardiac output, splanchnic blood flow, splanchnic oxygen uptake, and blood temperatures before and for 2 h after ingestion of 75 g of either fructose or glucose in water solution or of water only. Fructose ingestion was found to increase total oxygen uptake by an average of 9.5% above basal levels; the corresponding increase for glucose was 8.8% and for water only 2.5%. The respiratory exchange ratio increased from 0.84 in the basal state to 0.97 at 45 min after fructose ingestion and rose gradually after glucose to 0.86 after 120 min. The average 2-h thermic effect, expressed as percent of ingested energy, was 5.0% for fructose and 3.7% for glucose (not significant). Splanchnic oxygen consumption did not increase measurably after ingestion of either fructose or glucose. The arterial concentration of lactate rose, arterial pH fell, and PCO2 remained essentially unchanged after fructose ingestion. Glucose, but not fructose, elicited increases in cardiac output (28%) and splanchnic blood flow (56%). Fructose, but not glucose, increased arterial blood temperature significantly. It is concluded that both fructose and glucose-induced thermogenesis occurs exclusively in extrasplanchnic tissues. Compared with glucose, fructose ingestion is accompanied by a more marked rise in CO2 production, possibly reflecting an increased extrasplanchnic oxidation of lactate and an accumulation of heat in the body.

Isoflurane Alters the Recirculatory Pharmacokinetics of Physiologic Markers

2000 ◽  
Vol 92 (6) ◽  
pp. 1757-1768 ◽  
Author(s):  
Michael J. Avram ◽  
Tom C. Krejcie ◽  
Claus U. Niemann ◽  
Cheri Enders-Klein ◽  
Colin A. Shanks ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Drug Disposition ◽  
Regional Blood Flow ◽  
Flow Distribution ◽  
Maximum Effect ◽  
Blood Flow Distribution ◽  
Blood Concentrations ◽  
Isoflurane Anesthesia ◽  
Arterial Blood

Background Earlier studies have demonstrated that physiologic marker blood concentrations in the first minutes after administration, when intravenous anesthetics exert their maximum effect, are determined by both cardiac output and its distribution. Given the reported vasodilating properties of isoflurane, we studied the effects of isoflurane anesthesia on marker disposition as another paradigm of altered cardiac output and regional blood flow distribution. Methods The dispositions of markers of intravascular space and blood flow (indocyanine green), extracellular space and free water diffusion (inulin), and total body water and tissue perfusion (antipyrine) were determined in four purpose-bred coonhounds. The dogs were studied while awake and while anesthetized with 1.7%, 2.6%, and 3.5% isoflurane (1.15, 1.7, and 2.3 minimum alveolar concentration, respectively) in a randomized order determined by a Latin square experimental design. Marker dispositions were described by recirculatory pharmacokinetic models based on very frequent early, and less frequent later, arterial blood samples. These models characterize the role of cardiac output and regional blood flow distribution on drug disposition. Results Isoflurane caused a significant and dose-dependent decrease in cardiac output. Antipyrine disposition was profoundly affected by isoflurane anesthesia, during which nondistributive blood flow was maintained despite decreases in cardiac output, and the balance between fast and slow tissue volumes and blood flows was altered. Conclusions The isoflurane-induced changes in marker disposition were different than those the authors reported previously for halothane anesthesia, volume loading, or hypovolemia. These data provide further evidence that not only cardiac output but also its peripheral distribution affect early drug concentration history after rapid intravenous administration.

Regional blood flow in the brain and spinal cord of hypothermic rats

1989 ◽  
Vol 257 (3) ◽  
pp. H785-H790
Author(s):  
T. Sakamoto ◽  
W. W. Monafo
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Brain Stem ◽  
Regional Blood Flow ◽  
Experimental Conditions ◽  
Pentobarbital Sodium ◽  
Arterial Blood ◽  
Group A ◽  
Group B ◽  
The Brain

[14C]butanol tissue uptake was used to measure simultaneously regional blood flow in three regions of the brain (cerebral and cerebellar hemispheres and brain stem) and in five levels of the spinal cord in 10 normothermic rats (group A) and in 10 rats in which rectal temperature had been lowered to 27.7 +/- 0.3 degrees C by applying ice to the torso (group B). Pentobarbital sodium anesthesia was used. Mean arterial blood pressure varied minimally between groups as did arterial pH, PO2, and PCO2. In group A, regional spinal cord blood flow (rSCBF) varied from 49.7 +/- 1.6 to 62.6 +/- 2.1 ml.min-1.100 g-1; in brain, regional blood flow (rBBF) averaged 74.4 +/- 2.3 ml.min-1.100 g-1 in the whole brain and was highest in the brain stem. rSCBF in group B was elevated in all levels of the cord by 21-34% (P less than 0.05). rBBF, however, was lowered by 21% in the cerebral hemispheres (P less than 0.001) and by 14% in the brain as a whole (P less than 0.05). The changes in calculated vascular resistance tended to be inversely related to blood flow in all tissues. We conclude that rBBF is depressed in acutely hypothermic pentobarbital sodium-anesthetized rats, as has been noted before, but that rSCBF rises under these experimental conditions. The elevation of rSCBF in hypothermic rats confirms our previous observations.

Glucose and fatty acid metabolism in cows producing milk of low fat content

1974 ◽  
Vol 82 (1) ◽  
pp. 87-95 ◽  
Author(s):  
E. F. Annison ◽  
R. Bickerstaffe ◽  
J. L. Linzell
Keyword(s):  
Blood Flow ◽  
Milk Fat ◽  
The Body ◽  
Whole Body ◽  
Acetate Production ◽  
Entry Rate ◽  
Blood Concentrations ◽  
Body Tissues ◽  
High Starch ◽  
Starch Diet

SUMMARYThe effects of changing to a high starch: low roughage diet have been studied in two Friesian and two Jersey cows, surgically prepared for the simultaneous study of udder metabolism (arteriovenous difference x udder blood flow) and whole body turnover of milk precursors (isotope dilution).In the Friesian cows milk fat concentration was lower on the high starch diet but in the Jerseys fell only slightly in one animal. In both Friesians and in the one Jersey these changes were accompanied by an increase in total rumen VFA concentration. Rumen acetate concentration did not change but propionate doubled. Thus this confirms that the usually reported fall in ‘acetate:propionate ratio’ is due to a rise in propionate production rather than due to a fall in acetate production.There were significant falls in the blood concentrations of acetate and β-hydroxy-butyrate. The rate of extraction by the udder of acetate and β-hydroxybutyrate did not change but triglyceride extraction fell. Therefore since udder blood flow did not alter the uptake of all three fat precursors fell.The entry rate of glucose into the circulation and its contribution to total body CO2 increased. The entry rate and contribution to CO2 of acetate decreased but this was probably mainly due to a fall in endogenous acetate production by the body tissues. Plasma FFA concentration showed little change but the entry rate of palmitate fell on the high starch diet. There was also an increased proportion of unsaturated and trans fatty acids in the plasma and milk triglycerides.

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.

Whole body and hindlimb cardiovascular responses of the anesthetized dog during CO hypoxia

1984 ◽  
Vol 62 (7) ◽  
pp. 769-774 ◽  
Author(s):  
C. E. King ◽  
S. M. Cain ◽  
C. K. Chapler
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Cardiac Output ◽  
Sympathetic Innervation ◽  
Cardiovascular Responses ◽  
The Body ◽  
Whole Body ◽  
Total Resistance ◽  
Intact Group ◽  
Anesthetized Dogs

To compare with earlier studies of anemic hypoxia obtained by hemodilution, O2 carring capacity was decreased by carbon monoxide (CO) hypoxia. Arterial O2 content was reduced either 50% (moderate CO) or 65% (severe CO). In two groups of anesthetized dogs (moderate and severe CO) hindlimb innervation remained intact while in a third group (moderate CO) the hindlimb was denervated. Measurements were obtained prior to and at 30 and 60 min of CO hypoxia. Cardiac output was elevated at 30 min of CO hypoxia in all groups (p < 0.01) and in the severe CO group at 60 min (p < 0.01). Hindlimb blood flow remained unchanged during CO hypoxia in the intact groups. In the denervated group, hindlimb blood flow was greater (p < 0.05) than that in the intact groups throughout the experiment. A decrease in mean arterial pressure (p < 0.01) in all groups was associated with a fall in total resistance (p < 0.01). Hindlimb resistance remained unchanged during moderate CO hypoxia in the intact group but increased (p < 0.05) in the denervated group. In the severe CO group hindlimb resistance was decreased (p < 0.05) at 60 min. The results indicate that the increase in cardiac output during CO hypoxia was directed to nonmuscle areas of the body and that intact sympathetic innervation was required to achieve this redistribution.

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.

The physiologic reserve in oxygen carrying capacity: studies in experimental hemodilution

1986 ◽  
Vol 64 (1) ◽  
pp. 7-12 ◽  
Author(s):  
C. K. Chapler ◽  
S. M. Cain
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Supply ◽  
The Body ◽  
Extraction Ratio ◽  
Oxygen Extraction ◽  
Whole Body ◽  
Oxygen Extraction Ratio ◽  
Acute Anemia ◽  
Total Body Oxygen

The mechanisms by which the body attempts to avoid tissue hypoxia when total body oxygen delivery is compromised during acute anemia are reviewed. When the hematocrit is reduced by isovolemic hemodilution the compensatory adjustments include an increase in cardiac output, redistribution of blood flow to some tissues, and an increase in the whole body oxygen extraction ratio. These responses permit whole body oxygen uptake to be maintained until the hematocrit has been lowered to about 10%. Several factors are discussed which contribute to the increase in cardiac output during acute anemia including the reduction in blood viscosity, sympathetic innervation of the heart, and increased venomotor tone. The latter has been shown to be dependent on intact aortic chemoreceptors. With respect to peripheral vascular responses, the rise in coronary and cerebral blood flows which occur following hemodilution is proportionally greater than the increase in cardiac output while the opposite is true for kidney, liver, spleen, and intestine. Skeletal muscle does not contribute to a redistribution of blood flow to more vital areas during acute anemia despite its relatively large anaerobic capacity. Overall, peripheral compensatory adjustments result in an increased oxygen extraction ratio during acute anemia which reflects a better matching of the limited oxygen supply to tissue oxygen demands. However, some areas such as muscle are relatively overperfused which limits an even more efficient utilization of the reduced oxygen supply. Studies of the response of the microcirculation and the extent to which sympathetic vascular controls are involved in peripheral blood flow regulation are necessary to further appreciate the complex pattern of physiological responses which help ensure survival of the organism during acute anemia.

Effects of insulin-like growth factor-I and LR3IGF-I on regional blood flow in normal rats

1997 ◽  
Vol 155 (2) ◽  
pp. 351-358 ◽  
Author(s):  
CM Gillespie ◽  
AL Merkel ◽  
AA Martin
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Arterial Blood ◽  
Cardiovascular Side Effects ◽  
Igf I ◽  
The Central Nervous System ◽  
The Brain ◽  
Infusion Period

Two studies were conducted to investigate the haemodynamic effects of IGF-I and its analogue LR3IGF-I in normal anaesthetised rats. Infusion of IGF-I intravenously, at a dose of 125 micrograms/kg/h, for 20 min in the first study resulted in renal blood flow being significantly elevated by 35% above baseline. Mean arterial blood pressure (MABP) at this IGF-I dose fell by 18% of baseline, with LR3IGF-I also causing a significant decline in MABP (by 15%) at the dose of 125 micrograms/kg/h. In the second study the intravenous administration of IGF-I or LR3IGF-I, at a dose of 125 micrograms/kg/h, over a period of 60 min, resulted in MABP being significantly lowered by 25% of baseline values. Regional blood flow rates were determined using radioactive microspheres, 15 microns in diameter, injected systemically at the end of the peptide infusion period. The gastrocnemius, a representative skeletal muscle, was the only vascular region to show a significant increase in blood flow after IGF-I (by 58%) or LR3IGF-1 (by 308%) infusion. Vascular resistance in the brain was significantly reduced after infusion of IGF-I (by 60%) or LR3IGF-I (by 48%) as compared with vehicle. Skeletal muscle vascular resistance was also reduced by IGF-I (by 41%) and more particularly by LR3IGF-I (by 77%) in comparison to vehicle. These alterations to vascular tone produced by IGF infusion may be related to the central nervous system and systemic cardiovascular side-effects that have been reported during IGF-I administration in humans.

Sign in / Sign up

Export Citation Format

Share Document