scholarly journals Interrelationship between cardiac output and vascular resistance as determinants of effective arterial blood volume in cirrhotic patients

1985 ◽  
Vol 28 (2) ◽  
pp. 206-211 ◽  
Author(s):  
Michael D. Shapiro ◽  
Kathleen M. Nicholls ◽  
Bertron M. Groves ◽  
Rudiger Kluge ◽  
Hsaio-Min Chung ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Arterial Blood ◽  
Cirrhotic Patients ◽  
Arterial Blood Volume

Detection of early central circulatory transits in patients with cirrhosis by gamma variate fit of indicator dilution profiles

2005 ◽  
Vol 288 (4) ◽  
pp. G677-G684 ◽  
Author(s):  
Jens H. Henriksen ◽  
Søren Møller ◽  
Stefan Fuglsang ◽  
Flemming Bendtsen
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Indicator Dilution ◽  
Arterial Oxygen ◽  
Dilution Method ◽  
Gamma Variate ◽  
Arterial Blood ◽  
Flow Circulation ◽  
Cirrhotic Patients

Patients with cirrhosis have hyperdynamic circulation with abnormally distributed blood volume and widespread arteriovenous communications. We aimed to detect possible very early (i.e., before 4 s) and early (i.e., after 4 s) central circulatory transits and their potential influence on determination of central and arterial blood volume (CBV). Thirty-six cirrhotic patients and nineteen controls without liver disease undergoing hemodynamic catheterization were given central bolus injections of albumin with different labels. Exponential and gamma variate fits were applied to the indicator dilution curves, and the relations between flow, circulation times, and volumes were established according to kinetic principles. No significant very early central circulatory transits were identified. In contrast, early (i.e., 4 s to maximal) transits corresponding to a mean of 5.1% (vs. 0.8% in controls; P < 0.005) of cardiac output (equivalent to 0.36 vs. 0.05 l/min; P < 0.01) were found in cirrhotic patients. These early transits averaged 7.7 vs. 12.7 and 17.2 s of ordinary central transits of cirrhotic patients and controls, respectively ( P < 0.001). Early transits were directly correlated to the alveolar-arterial oxygen difference in the cirrhotic patients ( r = 0.46, P < 0.01) but not in controls ( r = 0.04; not significant). There was good agreement between the CBV determined by the conventional indicator dilution method and that determined by separation of early and ordinary transits by the gamma variate fit method (1.51 vs. 1.53 liter; not significant). In conclusion, no very early central circulatory transits were identified in cirrhotic patients. A significant part of the cardiac output undergoes an early transit, probably through pulmonary shunts or areas with low ventilation-perfusion ratios in cirrhotic patients. Composite determination of CBV by the gamma variate fit method is in close agreement with established kinetic methods. The study provides further evidence of abnormal central circulation in cirrhosis.

Reflection photoplethysmography of arterial-blood-volume pulses

1977 ◽  
Vol 15 (1) ◽  
pp. 22-31 ◽  
Author(s):  
J. Weinman ◽  
A. Hayat ◽  
G. Raviv
Keyword(s):  
Blood Volume ◽  
Arterial Blood ◽  
Arterial Blood Volume

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.

Supine exercise restores arterial blood pressure and skin blood flow despite dehydration and hyperthermia

1999 ◽  
Vol 277 (2) ◽  
pp. H576-H583 ◽  
Author(s):  
José González-Alonso ◽  
Ricardo Mora-Rodríguez ◽  
Edward F. Coyle
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Blood Volume ◽  
Plasma Catecholamines ◽  
Central Blood Volume ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Cutaneous Vascular Conductance

We determined whether the deleterious effects of dehydration and hyperthermia on cardiovascular function during upright exercise were attenuated by elevating central blood volume with supine exercise. Seven trained men [maximal oxygen consumption (V˙o 2 max) 4.7 ± 0.4 l/min (mean ± SE)] cycled for 30 min in the heat (35°C) in the upright and in the supine positions (V˙o 2 2.93 ± 0.27 l/min) while maintaining euhydration by fluid ingestion or while being dehydrated by 5% of body weight after 2 h of upright exercise. When subjects were euhydrated, esophageal temperature (Tes) was 37.8–38.0°C in both body postures. Dehydration caused equal hyperthermia during both upright and supine exercise (Tes = 38.7–38.8°C). During upright exercise, dehydration lowered stroke volume (SV), cardiac output, mean arterial pressure (MAP), and cutaneous vascular conductance and increased heart rate and plasma catecholamines [30 ± 6 ml, 3.0 ± 0.7 l/min, 6 ± 2 mmHg, 22 ± 8%, 14 ± 2 beats/min, and 50–96%, respectively; all P < 0.05]. In contrast, during supine exercise, dehydration did not cause significant alterations in MAP, cutaneous vascular conductance, or plasma catecholamines. Furthermore, supine versus upright exercise attenuated the increases in heart rate (7 ± 2 vs. 9 ± 1%) and the reductions in SV (13 ± 4 vs. 21 ± 3%) and cardiac output (8 ± 3 vs. 14 ± 3%) (all P< 0.05). These results suggest that the decline in cutaneous vascular conductance and the increase in plasma norepinephrine concentration, independent of hyperthermia, are associated with a reduction in central blood volume and a lower arterial blood pressure.

Mechanism of circulatory responses to systemic hypoxia in the anesthetized dog

1965 ◽  
Vol 209 (2) ◽  
pp. 397-403 ◽  
Author(s):  
Hermes A. Kontos ◽  
H. Page Mauck ◽  
David W. Richardson ◽  
John L. Patterson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
The Other ◽  
Arterial Flow ◽  
Arterial Blood ◽  
Systemic Hypoxia ◽  
Anesthetized Dogs ◽  
Spontaneously Breathing

The possibility that mechanisms secondary to the increased ventilation may contribute significantly to the circulatory responses to systemic hypoxia was explored in anesthetized dogs. In 14 spontaneously breathing dogs systemic hypoxia induced by breathing 7.5% oxygen in nitrogen increased cardiac output, heart rate, mean arterial blood pressure, and femoral arterial flow, and decreased systemic and hindlimb vascular resistances. In 14 dogs whose ventilation was kept constant by means of a respirator pump and intravenous decamethonium, systemic hypoxia did not change cardiac output, femoral arterial flow, or limb vascular resistance; it significantly decreased heart rate and significantly increased systemic vascular resistance. In seven spontaneously breathing dogs arterial blood pCO2 was maintained at the resting level during systemic hypoxia. The increase in heart rate was significantly less pronounced but the other circulatory findings were not different from those found during hypocapnic hypoxia. Thus, mechanisms secondary to increased ventilation contribute significantly to the circulatory responses to systemic hypoxia. Hypocapnia accounts partly for the increased heart rate, but not for the other circulatory responses.

Coevolution of the rennin–angiotensin system and the nervous control of blood circulation

1984 ◽  
Vol 62 (2) ◽  
pp. 137-147 ◽  
Author(s):  
John X. Wilson
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Renin Angiotensin System ◽  
Peripheral Vascular Resistance ◽  
Peripheral Vascular ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood

The mammalian renin–angiotensin system appears to be involved in the maintenance of blood volume and pressure because (i) sodium depletion, hypovolemia, and hypotension increase renin levels, and (ii) administration of exogenous angiotensin II rapidly increases mineralocorticoid and antidiuretic hormone production, transepithelial ion transport, drinking behavior, and peripheral vascular resistance. Are these also the physiological properties of the renin–angiotensin system in nonmammalian species? Signals for altered levels of renin activity have yet to be conclusively identified in nonmammalian vertebrates, but circulating renin levels are elevated by hypotension in teleost fish and birds. Systemic injection of angiotensin II causes an increase in arterial blood pressure in all the vertebrates studied, suggesting that barostatic control is a universal function of this hormone. Angiotensin II alters vascular tone by direct action on arteriolar muscles in some species, but at concentrations of the hormone which probably are unphysiological. More generally, angiotensin II increases blood pressure indirectly, by acting on the sympathetic nervous system. Catecholamines, derived from chromaffin cells and (or) from peripheral adrenergic nerves, mediate some portion of the vasopressor response to angiotensin II in cyclostomes, elasmobranchs, teleosts, amphibians, reptiles, mammals, and birds. Alteration of sympathetic outflow is a prevalent mechanism through which the renin–angiotensin system may integrate blood volume, cardiac output, and peripheral vascular resistance to achieve control of blood pressure and adequate perfusion of tissues.

scholarly journals The VEGF gene polymorphism impacts brain volume and arterial blood volume

2017 ◽  
Author(s):  
Hikaru Takeuchi ◽  
Hiroaki Tomita ◽  
Yasuyuki Taki ◽  
Yoshie Kikuchi ◽  
Chiaki Ono ◽  
...  
Keyword(s):  
Gene Polymorphism ◽  
Blood Volume ◽  
Brain Volume ◽  
Vegf Gene ◽  
Arterial Blood ◽  
Arterial Blood Volume ◽  
Vegf Gene Polymorphism

Effects of serotonin on pulmonary blood volume in the dog

1962 ◽  
Vol 202 (5) ◽  
pp. 957-960 ◽  
Author(s):  
Charles J. McGaff ◽  
William R. Milnor
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Transit Time ◽  
Mean Transit Time ◽  
Dilution Method ◽  
Continuous Intravenous Infusion ◽  
Pulmonary Blood Volume ◽  
Control Value ◽  
Vascular Bed

Changes in pulmonary blood volume produced by continuous intravenous infusion of serotonin (5-hydroxytryptamine) were measured in 16 experiments on ten dogs. Pulmonary mean transit time was measured by the dye dilution method, using consecutive injections into pulmonary artery and left atrium; pulmonary blood volume was calculated by multiplying this mean transit time by the cardiac output. Serotonin lowered pulmonary blood volume by an average of 2.9 ml/kg, or 26% of the control value ( P <0.001). Pulmonary vascular resistance increased 94 ru (resistance units) kg, and systemic vascular resistance fell 294 ru kg, effects similar to those reported by other investigators. The magnitude of the decrease in pulmonary blood volume indicates that a relatively large part of the pulmonary vascular bed is constricted by serotonin, and provides an example of shifting of blood from pulmonic to systemic circuits by reciprocal changes in the distensibility of these beds.

scholarly journals Dynamics of Concatenation between Cardiac Output and Indices of Arterial Blood Presure during Graded Exercise Stress in Endurance Cohort

2018 ◽  
Vol 1 (88) ◽  
Author(s):  
Vilma Papievienė ◽  
Eugenijus Trinkūnas ◽  
Alfonsas Buliuolis ◽  
Albinas Grūnovas ◽  
Jonas Poderys
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Matrix Theory ◽  
Blood Pressure Reduction ◽  
Peripheral Resistance ◽  
Exercise Stress ◽  
Bicycle Ergometry ◽  
Linear Type ◽  
Arterial Blood

Research background and hypothesis. Potential mechanisms through which muscle perfusion is altered during prolonged exercise are not fully understood. The methods applied in the  analysis of human data are very important  because  many crucial variables are not directly measureble or even identifiable.Research aim  was to  find out the peculiarities in concatenation between  central and peripheral cardiovascular changes under conditions of increasing fatigue.Research methods. Well-trained endurance runners underwent a 50 W increase in workload (bicycle ergometry) every 6 minutes and they exercised until inability to continue the task. Dynamics of concatenation between cardiac output and systolic arterial blood pressure (ABP), diastolic ABP and total peripheral resistance were assessed using a method based on matrix theory proposed by Lithuanian scientists.Research results. The increase of cardiac output during exercising has the same tendency of stepwise increase of workload, but changes of systolic and diastolic ABP with accumulation of fatigue could be characterized as linear type dependent with the time of exercising. The concatenation between the changes in cardiac performance and behaviour of peripheral vasculature increased at onset of exercising and the decrease or loss of the concatenation led up to inability to continue exercising.Discussion and conclusions. The importance of peripheral factors, i. e. decrease of diastolic blood pressure, reduction  of  total  peripheral  vascular  resistance  plays  an  increasingly  significant  role  for  cardiac  output  during continuous exercising. The concatenations between the changes of these indices and cardiac output increase and in the case of high-grade fatigue concatenations begin to decline.Keywords: cardiac output, periferal vascular resistance, concatenation.

scholarly journals Pathogenesis and Treatment of Refractory Oedema in Nephrotic Syndrome

EMJ Urology ◽  
2021 ◽  
pp. 107-117
Author(s):  
Priyanka Jethwani ◽  
Namrata Krishnan
Keyword(s):  
Clinical Trials ◽  
Nephrotic Syndrome ◽  
Blood Volume ◽  
Loop Diuretics ◽  
Primary Role ◽  
Sodium Retention ◽  
Oedema Formation ◽  
Arterial Blood ◽  
Filtration Barrier ◽  
Arterial Blood Volume

Oedema is a hallmark feature of nephrotic syndrome (NS) and can cause significant patient morbidity. The pathogenesis of oedema formation is complex and results from abnormalities in sodium retention, inter-play of neurohormonal factors, and changes in capillary filtration barrier. Salt retention is often primary (‘overfill’ theory) because of increased sodium-potassium adenosine triphosphatase activity in the collecting duct cells, increased direct epithelial sodium channel activation (ENaC) by urinary proteases (independent of aldosterone), and an overall increased effective arterial blood volume. However, a subset of patients with NS, especially children, demonstrate decreased effective arterial blood volume (‘underfill’ theory) and secondary sodium retention as the primary mechanism of oedema formation. Increased capillary permeability and vascular inflammation contributes as well. Loop diuretics with or without salt-poor albumin are the mainstay of therapy in adults, although no large clinical trials exist to guide diuretic choice or dosage. Combination diuretic therapy is recommended to achieve multi-site nephron blockade and overcome diuretic resistance, which is a frequent challenge. Use of direct ENaC inhibitors (amiloride) in combination with loop diuretics may be especially beneficial given the primary role of ENaC in sodium retention. Aquaretics such as vasopressin receptor antagonists may have a role in treatment as well. Well-designed clinical trials are essential to guide therapy of refractory oedema in NS. In this review, the authors discuss the pathogenesis of oedema formation in patients with NS and propose a treatment algorithm for management of resistant oedema based on the limited available evidence.

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