Postnatal regulation of oxygen delivery: hematologic parameters of postnatal dogs

1979 ◽  
Vol 237 (1) ◽  
pp. H71-H75 ◽  
Author(s):  
P. A. Mueggler ◽  
J. S. Peterson ◽  
R. D. Koler ◽  
J. Metcalfe ◽  
J. A. Black
Keyword(s):  
Oxygen Delivery ◽  
Cell Mass ◽  
Oxygen Affinity ◽  
Oxygen Demand ◽  
Hemoglobin Concentration ◽  
Postnatal Life ◽  
Red Cell ◽  
Tissue Oxygen ◽  
Red Cell Mass ◽  
Tissue Oxygen Delivery

Hematologic parameters influencing tissue oxygen delivery in dogs during the first 4 mo of life have been investigated. The rapid growth and increase in body temperature during this period imply an increased metabolic rate and increased tissue oxygen demand. Hemoglobin concentration and hematocrit decrease during the 1st mo following birth. The total red cell mass does not decrease during this period. The observed hemodilution can be attributed to an increasing plasma volume in the growing animal. The blood oxygen affinity decreases during this same period, resulting in a more effective tissue oxygen delivery. Erythropoiesis, as estimated from the percent circulating reticulocytes, decreases following birth and does not increase until 1 mo of postnatal life. The increase of erythropoietic activity during the 2nd mo of postnatal life coincides with an increase in red cell mass, hematocrit, and hemoglobin concentration.

Failure of prolonged exercise training to increase red cell mass in humans

1996 ◽  
Vol 270 (1) ◽  
pp. H121-H126 ◽  
Author(s):  
J. K. Shoemaker ◽  
H. J. Green ◽  
J. Coates ◽  
M. Ali ◽  
S. Grant
Keyword(s):  
Exercise Training ◽  
Prolonged Exercise ◽  
Cell Mass ◽  
Hemoglobin Concentration ◽  
Red Cell ◽  
Total Blood ◽  
Mean Cell Volume ◽  
Red Cell Mass ◽  
Mean Cell Hemoglobin

The purpose of this study was to investigate the time-dependent effects of long-term prolonged exercise training on vascular volumes and hematological status. Training using seven untrained males [age 21.1 +/- 1.4 (SE) yr] initially consisted of cycling at 68% of peak aerobic power (VO2peak) for 2 h/day, 4-5 days/wk, for 11 wk. Absolute training intensity was increased every 3 wk. Red cell mass (RCM), obtained using 51Cr, was unchanged (P > 0.05) with training (2,142 +/- 95, 2,168 +/- 86, 2,003 +/- 112, and 2,080 +/- 116 ml at 0, 3, 6, and 11 wk, respectively) as were serum erythropoietin levels (17.1 +/- 4.3, 13.9 +/- 3.5, and 17.0 +/- 2.0 U/l at 0, 6, and 11 wk, respectively). Plasma volume measured with 125I-labeled albumin and total blood volume (TBV) were also not significantly altered. The increase in mean cell volume that occurred with training (89.7 +/- 0.95 vs. 91.0 +/- 1.0 fl, 0 vs. 6 wk, P < 0.05) was not accompanied by changes in either mean cell hemoglobin or mean cell hemoglobin concentration. Serum ferritin was reduced 73% with training (67.4 +/- 13 to 17.9 +/- 1 microgram/l, 0 vs. 11 wk, P < 0.05). Total hemoglobin (HbTot) calculated as the product of hemoglobin concentration and TBV was unaltered (P > 0.05) at both 6 and 11 wk of training. The 15% increase in VO2peak (3.39 +/- 0.16 to 3.87 +/- 0.14 l/min, 0 vs. 11 wk, P < 0.05) with training occurred despite a failure of training to change TBV, RCM, or HbTot.

scholarly journals Oxygen Affinity in Hemoglobin Köln Disease

Blood ◽  
1972 ◽  
Vol 39 (3) ◽  
pp. 398-406 ◽  
Author(s):  
Frank G. de Furia ◽  
Denis R. Miller
Keyword(s):  
Whole Blood ◽  
Normal Values ◽  
Cell Mass ◽  
Oxygen Affinity ◽  
Red Cell ◽  
Blood Oxygen ◽  
Red Cell Mass ◽  
High Oxygen Affinity ◽  
Blood Oxygen Affinity

Abstract Oxygen affinity studies in a splenectomized patient with sporadically occurring Hb Köln disease revealed high whole blood oxygen affinity (P50 O2 17.6 mm Hg) with increased 2, 3-diphosphoglycerate (DPG), low ATP, and normal RBC ΔpH. Isolated electrophoretically slow migrating Hb Köln had a high oxygen affinity, decreased Hill’s number, and normal DPG reactivity. Functional evidence for hybrid tetramers with normal mobility is presented. Partial deoxygenation may play a role in the denaturation of the Hb Köln molecule and thus account for a higher oxygen affinity (low P50 O2), measured by the mixing technique, than the actual values for P50 that exist in vivo. Increased oxygen affinity and decreased P50 O2 would result in increased erythropoiesis and account for a well-compensated hemolytic process in this patient with a normal red cell mass and normal values of hemoglobin.

Acute hypervolemia, cardiac performance, and aerobic power during exercise

1982 ◽  
Vol 52 (5) ◽  
pp. 1186-1191 ◽  
Author(s):  
I. L. Kanstrup ◽  
B. Ekblom
Keyword(s):  
Blood Volume ◽  
Aerobic Power ◽  
Cell Mass ◽  
Hemoglobin Concentration ◽  
Cardiac Performance ◽  
Red Cell ◽  
Vo2 Max ◽  
Plasma Volume Expansion ◽  
Arterial Blood ◽  
Red Cell Mass

The relative importance of blood volume (BV) for the maximum aerobic power (VO2 max) was evaluated in healthy subjects by sequential measurements without intervention under two conditions: 1) after hemodilution with a plasma expander, thus increasing BV but keeping red cell mass constant and lowering hemoglobin concentration [Hb], and 2) after whole blood withdrawal, which restored BV to control conditions but reduced red cell mass and [Hb] to equal conditions under 1. After BV expansion (avg 700 ml), we found an unchanged VO2 max compared with control data despite lowered [Hb]. Cardiac output (Q) was increased after BV expansion at rest and during all exercise levels (maximum 27.4 and 29.5 l . min-1, respectively). Peak stroke volume was increased from 144 to 173 ml. Arterial blood pressures were either unchanged or lowered. In contrast, after blood letting to a similar [Hb], we found a significantly reduced VO2 max. These findings indicate a significant influence of the size of the blood volume on cardiac performance. The increased Qmax is discussed in relation to preload, inotropic state, heart rate, and afterload. Plasma volume expansion causes increased preload which may explain this primary effect on the central circulation (Frank-Starling effect).

Hydroxyurea Induces Expression of HbF and Increase of P50 in High Oxygen Affinity Hemoglobinopathy.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3730-3730
Author(s):  
Ghislain Cournoyer ◽  
Harry Bard ◽  
Xiaoduan Weng ◽  
Louise Robin ◽  
Carmen Gagnon ◽  
...  
Keyword(s):  
Cell Mass ◽  
Oxygen Affinity ◽  
High Oxygen ◽  
Red Cell ◽  
Subsequent Increase ◽  
Exon 2 ◽  
Red Cell Mass ◽  
High Oxygen Affinity ◽  
High O2 ◽  
2,3 Dpg

Abstract Introduction: A 38-year-old causasian male with hepatomegaly, splenomegaly and erythrocytosis (Ht 69.2%, Hb 217 g/L, MCV 76fl, normal WBC and platelets counts) presented with flank pain found to be a renal artery thrombosis. He had a history of increased Ht since birth without bone marrow (BM), cardiac, pulmonary, renal or cerebral anomalies and for which a diagnosis of a high oxygen affinity hemoglobinopathy was made. The disease had previously been uncomplicated without therapy. Initial evaluation in our center revealed a normal BM morphology, a normal karyotype and an abnormal Hb HPLC (elevated HbF (4.9%) and an abnormal Hb eluting after normal HbA1). The red cell mass was increased at 74.9 ml/kg (normal = 26.5 ml/kg). The oxygen (O2) P50 saturation determined from the Hb-O2 dissociation curve using an Hemox-Analyser was markedly decreased at 6 mmHg (normal = 27 mmHg). α and β globins (gb) HPLC demonstrated normal α, but 100% abnormal β-gb. A diagnosis of a double heterozygote for β-gb gene was established: an allele with mutation causing high affinity for O2 and an allele causing β-thalassemia (thal) minor. Anticoagulation and serial phlebotomies did not improve the erythrocytosis. Therapy with hydroxyurea (HU) was therefore proposed to the patient. Objectives: To determine the β-gb genotype and to evaluate the effect of HU therapy at maximally tolerated dose (MTD) on induction of HbF and its effect on Ht, P50, red cell mass, 2,3-DPG and total HbNO concentrations. Methods and results: Sequencing of the β-gb locus was done by RT-PCR amplified mRNA and by PCR amplified DNA, using primers spanning almost the entire gene (−450 to 601 bp, excluding a small portion of IVS2). Two mutations were identified: Leu96→Val (339C→G) in exon 2, producing Hb Regina, a high O2 affinity hemoglobin variant, and IVS1-110 G/A, a frequent mutation causing β-thal minor. Therapy with HU was initiated at 7 mg/kg/day. Dose was increased to MTD resulting in a dose of 25 mg/kg/day. Table 1 summarizes variations in relevant parameters while on HU therapy. Conclusion: HU rapidly induced HgF and improved measured parameters in this patient with a high O2 affinity Hb/β-thal minor. HU’s effect in this case did not seem to be strictly related to its anti-proliferation properties. Induction of HbF and subsequent increase in P50 probably reduced Epo production (data pending) and erythropoiesis. Modifications in other mediators of O2 release were also modified by HU. The changes in HbNO are not totally consistant with the rest of the data, being increased at 3 months but decreased at 6 months. While on HU therapy, the patient did not present any new complications (thrombotic or other) and clinically reported an improved exercise tolerance. Further evaluation will focus on epigenetic factors affecting HbF expression and correlation of NO level with plasma L-arginine concentration. Time HU dose (mg/kg) Ht (%) HbF (%) P50 (mm/Hg) 2,3-DPG (umol/g Hb) Total HbNO (nM) Red cell mass (ml/kg) NA: not available, TBD: to be determined Baseline 0 61.1 3.6 6 21.3 242.7 74.9 3 months 21 69.4 9.1 6 19.0 694.3 NA 6 months 25 56.9 15.1 9 21.4 105.8 NA 8 months 25 46.7 25.4 TBD TBD TBD 51.7

Anemia of spaceflight

Blood ◽  
1982 ◽  
Vol 60 (5) ◽  
pp. 1059-1067 ◽  
Author(s):  
M Tavassoli
Keyword(s):  
Bone Formation ◽  
Plasma Volume ◽  
Cell Mass ◽  
Hemoglobin Concentration ◽  
Red Cell ◽  
Space Flights ◽  
Total Inhibition ◽  
Red Cell Mass ◽  
Orbital Space ◽  
Normal Ambient

Abstract A consistent deficit in the red cell mass has been observed during both the American and Soviet orbital space flights and is sometimes referred to as “astronaut anemia.” This may be associated with a reduction in plasma volume so that the hematocrit and the hemoglobin concentration remain unchanged. During the Gemini program, the hypobaric hyperoxic atmosphere of the spacecraft led to oxidative injury to the red cells, causing hemolysis. Thus, the atmosphere proved to be, in part, responsible for the deficit. However, a similar deficit of a lesser magnitude was again observed in subsequent flights with normal ambient PO2 as well as in the Soviet flights in which an atmosphere essentially of see level air is used. The cause of this deficit seems to be suppression of erythropoiesis, as indicated by reticulocytopenia and erythroid hypoplasia of the marrow. No suppression of erythropoiesis has been observed in ground-based experiments carried out under almost identical conditions. Thus, the suppression of erythropoiesis is thought to be related to weightlessness. The reason for the suppression is not known but may be related to total inhibition of bone formation.

scholarly journals Effect of Smoking on Tissue Oxygen Supply

Blood ◽  
1973 ◽  
Vol 41 (6) ◽  
pp. 845-851 ◽  
Author(s):  
Arthur L. Sagone ◽  
Thomas Lawrence ◽  
Stanley P. Balcerzak
Keyword(s):  
Oxygen Delivery ◽  
Chronic Exposure ◽  
Oxygen Supply ◽  
Cell Mass ◽  
Tissue Hypoxia ◽  
Red Cell ◽  
Tissue Oxygen ◽  
Low Levels ◽  
Oxygen Carrying Capacity ◽  
Tissue Oxygen Supply

Abstract The purpose of this study was to determine if chronic exposure to low levels of carbon monoxide (CO) in man results in tissue hypoxia. For this reason, nine smokers (more than one pack of cigarettes per day) were studied. The presence of hypoxia was assessed by measurement of red cell mass (RCM). The effect of CO on intraerythrocytic factors involved with oxygen delivery was determined by measurement of oxygen-hemoglobin affinity (P50) and of red cell 2,3-diphosphoglycerate (DPG) and adenosine triphosphate (ATP). Values were compared to those of 18 nonsmokers of similar age, sex, and race. Values for carboxyhemoglobin (COHb), RCM, hemoglobin, hematocrit, and red cell count were significantly higher in the smokers. DPG levels were unaltered, while P50 and ATP levels were significantly lower in smokers. These data suggest that chronic exposure to low levels of CO results in tissue hypoxia, probably as a result of decreased blood oxygen carrying capacity and increased blood-O2 affinity. Adaption is reflected in an increased RCM and not by intraerythrocytic changes. The response in RCM may be to levels seen in polycythemia vera, as evidenced by a value of 37.6 in one smoker whose RCM fell to normal after discontinuing cigarettes. This study indicates that smoking causes mild erythrocytosis comparable to that seen in spurious or stress polycythemia. It also suggests that chronic exposure to low levels of CO may further embarrass tissue oxygen supply in patients with anemia, heart disease, chronic lung disease, and cerebral vascular disease in whom oxygen delivery to tissues is already marginal.

Perinatal Blood Loss

1990 ◽  
Vol 12 (2) ◽  
pp. 47-53
Author(s):  
Richard A. Molteni
Keyword(s):  
Blood Cell ◽  
Red Blood Cell ◽  
Oxygen Delivery ◽  
Cell Mass ◽  
Hypovolemic Shock ◽  
Fetal Life ◽  
Tissue Oxygen ◽  
Screening Process ◽  
Cell Numbers ◽  
Tissue Oxygen Delivery

In recent years a great deal of attention has been paid to the evaluation and treatment of conditions characterized by red blood cell excess (polycythemia). The debatable practice of routine newborn hematocrit screening was initiated and perpetuated by the still uncertain short-term and long-term complications of polycythemia and its commonly associated state of hyperviscosity. Previously unsuspected anemia is often identified during this same screening process. Unless profound (leading to hypovolemic shock) or associated with more visible signs of hemolysis (jaundice), the etiology of this state of diminished red blood cell mass is often ignored or evaluated incompletely. This review focuses on the effects of anemia in the fetus and neonate, discusses mechanisms of fetal red blood cell production, and provides a basic diagnostic approach for the clinician when anemia is recognized in the neonatal period. PHYSIOLOGIC EFFECTS OF RED CELL REDUCTION Tissue Oxygen Delivery Maintenance of adequate red blood cell numbers can be even more critical during fetal life than during the postnatal period. The fetus, dependent upon maternal oxygen sources, cannot raise tissue oxygen delivery acutely by increasing placental oxygen transfer, even when its red blood cell numbers are decreased. Total oxygen content (sum of oxygen dissolved in plasma and bound to hemoglobin) of the blood is dependent upon both the partial pressure of oxygen (Pao2) and the quantity of hemoglobin available.

scholarly journals Anemia of spaceflight

Blood ◽  
1982 ◽  
Vol 60 (5) ◽  
pp. 1059-1067 ◽  
Author(s):  
M Tavassoli
Keyword(s):  
Bone Formation ◽  
Plasma Volume ◽  
Cell Mass ◽  
Hemoglobin Concentration ◽  
Red Cell ◽  
Space Flights ◽  
Total Inhibition ◽  
Red Cell Mass ◽  
Orbital Space ◽  
Normal Ambient

A consistent deficit in the red cell mass has been observed during both the American and Soviet orbital space flights and is sometimes referred to as “astronaut anemia.” This may be associated with a reduction in plasma volume so that the hematocrit and the hemoglobin concentration remain unchanged. During the Gemini program, the hypobaric hyperoxic atmosphere of the spacecraft led to oxidative injury to the red cells, causing hemolysis. Thus, the atmosphere proved to be, in part, responsible for the deficit. However, a similar deficit of a lesser magnitude was again observed in subsequent flights with normal ambient PO2 as well as in the Soviet flights in which an atmosphere essentially of see level air is used. The cause of this deficit seems to be suppression of erythropoiesis, as indicated by reticulocytopenia and erythroid hypoplasia of the marrow. No suppression of erythropoiesis has been observed in ground-based experiments carried out under almost identical conditions. Thus, the suppression of erythropoiesis is thought to be related to weightlessness. The reason for the suppression is not known but may be related to total inhibition of bone formation.

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