scholarly journals Reduction of Oxygen-Carrying Capacity Weakens the Effects of Increased Plasma Viscosity on Cardiac Performance in Anesthetized Hemodilution Model

2012 ◽  
Vol 2012 ◽  
pp. 1-9
Author(s):  
Surapong Chatpun ◽  
Pedro Cabrales

We investigated the effects of reduced oxygen-carrying capacity on cardiac function during acute hemodilution, while the plasma viscosity was increased in anesthetized animals. Two levels of oxygen-carrying capacity were created by 1-step and 2-step hemodilution in male golden Syrian hamsters. In the 1-step hemodilution (1-HD), 40% of the animals' blood volume (BV) was exchanged with 6% dextran 70 kDa (Dx70) or dextran 2000 kDa (Dx2M). In the 2-step hemodilution (2-HD), 25% of the animals' BV was exchanged with Dx70 followed by 40% BV exchanged with Dx70 or Dx2M after 30 minutes of first hemodilution. Oxygen delivery in the 2-HD group consequently decreased by 17% and 38% compared to that in the 1-HD group hemodiluted with Dx70 and Dx2M, respectively. End-systolic pressure and maximum rate of pressure change in the 2-HD group significantly lowered compared with that in the 1-HD group for both Dx70 and Dx2M. Cardiac output in the 2-HD group hemodiluted with Dx2M was significantly higher compared with that hemodiluted with Dx70. In conclusion, increasing plasma viscosity associated with lowering oxygen-carrying capacity should be considerably balanced to maintain the cardiac performance, especially in the state of anesthesia.

1976 ◽  
Vol 231 (5) ◽  
pp. 1451-1456 ◽  
Author(s):  
TE Nightingale

Acute isovolemic anemia was produced in anesthetized chickens by serial exchanges of 6% dextran 70 equal to 1% of body weight to quantitate cardiovascular and metabolic parameters. When hematocrit (Hct) and hemoglobin (Hb) levels were reduced by 50% (from 33.3 to 16.3 vol %, and from 10.3 to 5.4 g/100 g, respectively, P less than 0.001), tissue oxygen delivery was maintained by increases in cardiac output (CO), stroke volume (SV), oxygen extraction, and reduced total peripheral resistance (TPR). Heart rate, right atrial pressure, and oxygen consumption (Vo2) were unchanged. Further reductions in Hct and Hb (to 10.8 vol % and 3.7 g/100 g, respectively), were accompanied by cardiovascular failure, as evidenced by falling CO, SV, tissue oxygen delivery, and Vo2. Relative apparent viscosity determinations on the exchanged blood-dextran mixtures indicated that large viscosity changes occurred with the first exchange whereas subsequent exchanges had small incremental viscosity changes. These data indicate that in acutely anemic chickens, oxygen transport capacity was maintained by increased cardiac output and decreased peripheral resistance, unless the severity of the anemia resulted in cardiovascular failure.


2019 ◽  
Vol 39 (4) ◽  
pp. 468-476 ◽  
Author(s):  
Amalia M Harrington ◽  
Heather J Hamlin

ABSTRACT Increased anthropogenic input of carbon dioxide into the atmosphere has caused widespread patterns of ocean acidification (OA) and increased the frequency of extreme warming events. We explored the sublethal effects of OA on the hemolymph chemistry and physiological response to acute thermal stress in the American lobster (Homarus americanus H. Milne Edwards, 1837). We exposed subadult lobsters to current or predicted end-century pH conditions (8.0 and 7.6, respectively) for 60 days. Following exposure, we assessed hemolymph L-lactate and calcium concentrations (as indicators of oxygen carrying capacity), ecdysterone concentrations, total protein content, and total hemocyte counts (THCs) as an indicator of immune response. We also assessed cardiac performance in the context of an acute warming event using impedance pneumography. Calcium, total protein, and ecdysterone concentrations were not significantly altered (P ≥ 0.10) by OA exposure. Control lobsters, however, had significantly higher levels of L-lactate concentrations compared to acidified lobsters, suggesting reduced oxygen carrying capacity under OA. THCs were also 61% higher in control versus acidified lobsters, suggesting immunosuppression under chronic OA. Lobsters exposed to acidified conditions exhibited reduced cardiac performance under acute warming as indicated by significantly lower (P = 0.040) Arrhenius Break Temperatures compared to control lobsters. These results suggest that although some physiological endpoints of American lobster are not impacted by OA, the stress of OA will likely be compounded by acute heat shock and may present additional physiological challenges for this species in the face of future change.


Author(s):  
M. H. Depledge

The oxygen-carrying capacity of the blood of decapod crustaceans fluctuates widely. Salinity stress results in doubling of haemocyanin concentration within 24–48 h in Carcinus maenas (Boone & Schoeffeniels, 1979) while in the lobster, Homarus gammarus respiratory pigment levels are very low prior to and following moulting (Spoek, 1974). In general, however, the most important factor regulating haemocyanin concentration is nutritional state. Following starvation low values are recorded (Wieser, 1965; Uglow, 1969; Djangmah, 1970) and there are concomitant reductions in ventilation, oxygen consumption and cardiac output (Ansell, 1973; Marsden, Newell & Ahsanullah, 1973; Wallace, 1973). The interrelationships between these events are poorly understood.


2016 ◽  
Vol 35 (4) ◽  
pp. 192-203 ◽  
Author(s):  
Yasser N. Elsayed ◽  
Debbie Fraser

AbstractIntact hemodynamics results when there is adequate oxygen uptake by the respiratory system, normal cardiac output, sufficient oxygen-carrying capacity of blood, and intact autoregulatory mechanisms to maintain enough oxygenation for normal end-organ function. The current routine monitoring of cardiovascular dynamics in sick preterm and term infants has been based on incomplete evaluation and relies on nonspecific and sometimes misleading clinical markers such as blood pressure. A thorough understanding of perinatal and neonatal cardiovascular, respiratory, oxygen, and other specific end-organ physiology is also mandatory for proper targeted interpretation.


1988 ◽  
Vol 33 (4) ◽  
pp. 298-299 ◽  
Author(s):  
A.R. Turner ◽  
G.D.O. Lowe ◽  
C.D. Forbes ◽  
J. G. Pollock

Patients with intermittent claudication frequently have high-normal levels of haematocrit and hence blood viscosity, which may contribute to decreased calf blood flow on exercise, and hence to the symptom of claudication. Reduction in haematocrit and viscosity by serial venesection in eight patients with stable claudication and high-normal haematocrit (mean 0.50) was performed, and the effects on claudication, calf blood flow, and calf oxygen delivery were studied. Following reduction in haematocrit to low-normal levels (mean 0.44), resting calf blood flow was unchanged; peak flow after ischaemic exercise increased slightly (+17%), but peak oxygen delivery (peak flow × haemoglobin concentration) was unchanged. Hence any increase in calf blood flow in the symptomatic leg is balanced by a decrease in oxygen-carrying capacity after venesection. No increase in claudication time would therefore be expected, and none was observed in the present study.


1992 ◽  
Vol 13 (10) ◽  
pp. 379-380
Author(s):  
William B. Strong

What is the likely pathophysiology of this event? What are the more common complications of hypoxemia in the older infant and young child? This clinical scenario is uncommon, but it represents one of the two feared central nervous system complications of cyanotic congenital heart disease, (ie, cerebrovascular accident and brain abscess). A uniform response to hypoxemia of cardiac etiology is the production of erythropoietin to produce more red blood cells. This is a compensatory mechanism to maintain oxygen delivery to the peripheral tissues. Normally, hemoglobin is about 96% saturated with oxygen. Therefore, the oxygen-carrying capacity of blood with a normal hemoglobin concentration of 15 g/dL is approximately 20.3 mL of oxygen per 100 mL of blood (ie, 15 g of hemoglobin x 1.35 mL of O2 per g of hemoglobin = 20.3). The oxygen content of blood equals the oxygen-carrying capacity multiplied by the oxygen saturation. At a normal oxygen saturation of 96%, the O2 content of arterial blood (Hgb 15 g/dL) equals 19.5 mL/dL (96% x 20.3 mm3/dL) or 195 mL per liter of cardiac output. The arterial O2 content of this child, assuming an average arterial saturation of 85%, will be 11.1 mL/dL. Therefore, every liter (10 dL) of cardiac output will carry 111 mL of O2 or 84 mL of O2 less than the child with a 15 g/dL hemoglobin level.


Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 2138-2138
Author(s):  
Jon Detterich ◽  
Roberta Miyeko Kato ◽  
Ani Dongelyan ◽  
Adam Bush ◽  
Herbert J. Meiselman ◽  
...  

Abstract Abstract 2138 Chronic transfusion therapy (CTT) is a mainstay for stroke prophylaxis in sickle cell anemia. Long-term changes with transfusion include decreased hemoglobin S% and hemolysis resulting in decreased plasma free hemoglobin. Long-term benefits are well documented, however, patients on CTT continue to suffer from acute crises. The acute effects of each transfusion are not well known but might include improved oxygen carrying capacity secondary to increased hematocrit, reducing demands for high cardiac output. But, the increased hematocrit and oxygen carrying capacity is at the cost of increased viscosity and resistance to blood flow. Despite long-term benefits, acute complications continue to plague this patient population and could be due to acute rheologic changes with transfusion. We hypothesized that transfusion would acutely improve tissue oxygen delivery despite increasing blood viscosity and vascular resistance. To test this hypothesis, we prospectively examined patients on CTT immediately pre transfusion and again 12–120 hours post transfusion. Hemodynamics were tested by measuring blood pressure, heart rate and cardiac function by echocardiography. Tissue oxygen delivery was assessed using echocardiographic estimates of cardiac output, pulse oximetry and oxygen carrying capacity as well as near infrared spectroscopy (NIRS). We obtained basic hematology and metabolic labs in addition to markers of inflammation, hemolysis and amino acid profile at both visits. Male and female patients were equally represented with similar average age. The reasons for starting transfusion as well as medication profiles were similar between sexes. Comparable changes in hemoglobin, hematocrit, reticulocyte count and hemoglobin S with transfusion were observed in all patients. However, when pre transfusion levels of free hemoglobin, hemoglobin S%, platelet count and reticulocyte count were examined with regard to timing from the previous transfusion, males had faster recovery of endogenous marrow activity and increased hemolysis, producing higher average hemoglobin S%, reticulocyte count, platelet count and free hemoglobin levels (figure 1). In males, transfusion decreased heart rate, stroke volume, and cardiac index while estimates for pulmonary and systemic vascular resistance rose, culminating in decreased oxygen delivery. In contrast, stroke volume and cardiac index were preserved in women following transfusion, while systemic and pulmonary vascular resistance did not change such that oxygen delivery improved 16%. NIRS measurements assessing tissue oxygenation confirmed the differences seen using echocardiography and oxygen carrying capacity estimates(figure 2).Figure 1Figure 1. Figure 2Figure 2. Increased endogenous marrow activity in males, resulting in higher pre-transfusion reticulocyte count, hemoglobin S%, platelet count and free hemoglobin might account for the exaggerated reduction in cardiac index, as well as increased systemic and pulmonary vascular resistance with transfusion. In addition, the faster recovery of hemoglobin S% and hemolysis likely confers increased risk of vascular complications in male patients despite chronic transfusion therapy. Disclosures: Wood: Novartis: Research Funding; Ferrokin Biosciences: Consultancy; Cooleys Anemia Foundation: Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding.


2002 ◽  
Vol 50 (3) ◽  
pp. 313 ◽  
Author(s):  
J. Box ◽  
A. Lill ◽  
J. Baldwin

The responses of small birds to many seasonal energy challenges include enhancement of aspects of aerobic metabolism, sometimes involving an increase in the rate of oxygen delivery to the metabolising tissues. One such mechanism that enhances oxygen delivery seasonally is an increase in blood oxygen carrying capacity. This response is enhanced in birds because of their rapid erythrocyte turnover rate. Some small birds have also evolved winter fattening, which helps them to meet the energy challenge presented by winter conditions. Such adaptations, while well documented for North Temperate birds, have received little attention in birds inhabiting temperate Australia. Over a two-year period, we examined seasonal changes in mass, an approximate indicator of fattening, and the parameters determining blood oxygen carrying capacity in a population of superb fairy-wrens (Malurus cyaneus) in outer Melbourne, Australia. Body mass did not vary significantly seasonally, but haematocrit and whole blood haemoglobin were significantly higher in the breeding season than at other times of year and the erythrocyte count was significantly higher in spring than in autumn. We conclude that the failure of the fairy-wrens to increase mass in winter (i.e. show marked winter fattening) was probably due to the comparative mildness of the climate and to the known fitness costs of fat storage. The significant 18% increase in blood oxygen carrying capacity in spring probably helped the birds to meet the additional energy requirements of breeding, particularly the likely increase in flight activity. However, given the magnitude of the increase, other mechanisms must have been involved in meeting breeding costs. The seasonal peak in blood oxygen carrying capacity did not coincide with the time when moulting was most pronounced.


1996 ◽  
Vol 80 (1) ◽  
pp. 291-297 ◽  
Author(s):  
T. Tveita ◽  
M. Skandfer ◽  
H. Refsum ◽  
K. Ytrehus

Rewarming from accidental hypothermia is associated with fatal circulatory derangements. To investigate potential pathophysiological mechanisms involved, we examined heart function and metabolism in a rat model rewarmed after 4 h at 15-13 degrees C. Hypothermia resulted in a significant reduction of left ventricular (LV) systolic pressure, cardiac output, and heart rate, whereas stroke volume increased. The maximum rate of LV pressure rise decreased to 191 +/- 28 mmHg/s from a control value of 9,060 +/- 500 mmHg/s. Myocardial tissue content of ATP, ADP, and glycogen was significantly reduced, whereas lactate content remained unchanged. After rewarming, heart rate returned to control value, whereas LV systolic pressure, cardiac output, and stroke volume all remained significantly depressed. The posthypothermic maximum rate of LV pressure rise was 5,966 +/- 1.643 mmHg/s. The posthypothermic myocardial lactate content was significantly increased (to 13.3 +/- 3.2 nmol/mg from control value of 5.7 +/- 1.9 nmol/mg), and ATP and glycogen remained significantly lowered. Creatine phosphate or energy charge did not change significantly during the experiment. The finding of deteriorated myocardial mechanical function and a shift in energy metabolism shows that the heart could be an important target during hypothermia and rewarming in vivo, thus contributing to the development of a posthypothermic circulatory collapse.


1977 ◽  
Vol 43 (5) ◽  
pp. 784-789 ◽  
Author(s):  
J. F. Borgia ◽  
S. M. Horvath

Intact anesthetized dogs were exposed for 75 min to either 5.75, 9.0, or 12.0% oxygen in nitrogen. Although pulmonary artery pressures were significantly elevated in all hypoxic exposures, systemic hypertension occurred only at the onset of severe hypoxia(5.75% O2). Coronary blood flow increased from an average of 130 during normoxia to a peak of 400 ml/100 g per min during inhalation of 5.75% O2, and coronary sinus oxygen tensions of 8 Torr and oxygen contents of 1.1 ml/100 ml were sustained for 75 min without biochemical, functional, or electrophysiological evidence of myocardial ischemia. Cardiac index (CI) increased significantly only during severe hypoxia (5.75% O2) with the greatest elevation after 30 min. Subsequently, CI decreased concomitantly with a 27% elevation in arterial hemoglobin concentration and oxygen-carrying capacity. It is concluded that the hypoxic threshold for significant elevations of cardiac output is between 6.0 and 9.0% O2.


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