Extended Oxygen Delivery from the Nerve Hemoglobin ofTellina alternata(Bivalvia)

Science ◽  
1986 ◽  
Vol 232 (4746) ◽  
pp. 90-92 ◽  
Author(s):  
DAVID W. KRAUS ◽  
JAMES M. COLACINO
Keyword(s):  
Carbon Monoxide ◽  
Oxygen Delivery ◽  
Oxygen Removal ◽  
Oxygen Binding ◽  
Considerable Time ◽  
Pure Nitrogen ◽  
Anoxic Conditions ◽  
Neural Excitability ◽  
Aerobic Activity

An oxygen-binding hemoglobin localized in the nerves ofTellina alternata(Bivalvia) required 30 minutes to unload oxygen when excised nerves were exposed to pure nitrogen. Neural excitability under these conditions could be sustained only until deoxygenation of the hemoglobin was complete. When the oxygen-combining function of the hemoglobin was abolished with carbon monoxide, the neural excitability ceased within a few minutes of oxygen removal, a response identical to that of hemoglobinless homologous nerves of other bivalves. These results demonstrate that aerobic activity can be supported by the oxygen stored on hemoglobin in microscopic tissues for a considerable time under anoxic conditions.

Whole body oxygen consumption and critical oxygen delivery in response to prolonged and severe carbon monoxide poisoning

Resuscitation ◽  
2003 ◽  
Vol 56 (1) ◽  
pp. 97-104 ◽  
Author(s):  
Howard A Smithline ◽  
Kevin R Ward ◽  
Donald A Chiulli ◽  
Heidi C Blake ◽  
Emanuel P Rivers
Keyword(s):  
Carbon Monoxide ◽  
Oxygen Consumption ◽  
Oxygen Delivery ◽  
Carbon Monoxide Poisoning ◽  
Whole Body ◽  
Critical Oxygen

Influence of carbon monoxide on hemoglobin-oxygen binding

1976 ◽  
Vol 41 (6) ◽  
pp. 893-899 ◽  
Author(s):  
M. P. Hlastala ◽  
H. P. McKenna ◽  
R. L. Franada ◽  
J. C. Detter
Keyword(s):  
Carbon Monoxide ◽  
Oxygen Affinity ◽  
Co2 Concentration ◽  
Bohr Effect ◽  
Oxygen Binding ◽  
Dissociation Curve ◽  
Low Oxygen ◽  
Oxygen Dissociation ◽  
Initial Binding ◽  
Fixed Acid

The oxygen dissociation curve and Bohr effect were measured in normal whole blood as a function of carboxyhemoglobin concentration [HbCO]. pH was changed by varying CO2 concentration (CO2 Bohr effect) or by addition of isotonic NaOH or HCl at constant PCO2 (fixed acid Bohr effect). As [HbCO] varied through the range of 2, 25, 50, and 75%, P50 was 26.3, 18.0, 11.6, and 6.5 mmHg, respectively. CO2 Bohr effect was highest at low oxygen saturations. This effect did not change as [HbCO] was increased. However, as [HbCO] was increased from 2 to 75%, the fixed acid Bohr factor increased in magnitude from -0.20 to -0.80 at very low oxygen saturations. The effect of molecular CO2 binding (carbamino) on oxygen affinity was eliminated at high [HbCO]. These results are consistent with the initial binding of O2 or CO to thealpha-chain of hemoglobin. The results also suggest that heme-heme interaction is different for oxygen than for carbon monoxide.

scholarly journals A neuroglobin-based high-affinity ligand trap reverses carbon monoxide–induced mitochondrial poisoning

2020 ◽  
Vol 295 (19) ◽  
pp. 6357-6371 ◽  
Author(s):  
Jason J. Rose ◽  
Kaitlin A. Bocian ◽  
Qinzi Xu ◽  
Ling Wang ◽  
Anthony W. DeMartino ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Mitochondrial Respiration ◽  
Oxygen Delivery ◽  
Oxygen Electrode ◽  
Heart Tissue ◽  
Tissue Respiration ◽  
Co Poisoning ◽  
Affinity Ligand

Carbon monoxide (CO) remains the most common cause of human poisoning. The consequences of CO poisoning include cardiac dysfunction, brain injury, and death. CO causes toxicity by binding to hemoglobin and by inhibiting mitochondrial cytochrome c oxidase (CcO), thereby decreasing oxygen delivery and inhibiting oxidative phosphorylation. We have recently developed a CO antidote based on human neuroglobin (Ngb-H64Q-CCC). This molecule enhances clearance of CO from red blood cells in vitro and in vivo. Herein, we tested whether Ngb-H64Q-CCC can also scavenge CO from CcO and attenuate CO-induced inhibition of mitochondrial respiration. Heart tissue from mice exposed to 3% CO exhibited a 42 ± 19% reduction in tissue respiration rate and a 33 ± 38% reduction in CcO activity compared with unexposed mice. Intravenous infusion of Ngb-H64Q-CCC restored respiration rates to that of control mice correlating with higher electron transport chain CcO activity in Ngb-H64Q-CCC–treated compared with PBS-treated, CO-poisoned mice. Further, using a Clark-type oxygen electrode, we measured isolated rat liver mitochondrial respiration in the presence and absence of saturating solutions of CO (160 μm) and nitric oxide (100 μm). Both CO and NO inhibited respiration, and treatment with Ngb-H64Q-CCC (100 and 50 μm, respectively) significantly reversed this inhibition. These results suggest that Ngb-H64Q-CCC mitigates CO toxicity by scavenging CO from carboxyhemoglobin, improving systemic oxygen delivery and reversing the inhibitory effects of CO on mitochondria. We conclude that Ngb-H64Q-CCC or other CO scavengers demonstrate potential as antidotes that reverse the clinical and molecular effects of CO poisoning.

scholarly journals Allosteric kinetics and equilibria differ for carbon monoxide and oxygen binding to hemoglobin

1990 ◽  
Vol 58 (2) ◽  
pp. 333-340 ◽  
Author(s):  
N.Q. Zhang ◽  
F.A. Ferrone ◽  
A.J. Martino
Keyword(s):  
Carbon Monoxide ◽  
Oxygen Binding

scholarly journals The velocity with which carbon monoxide displaces oxygen from combination with hœmoglobin.—Part I

1923 ◽  
Vol 94 (662) ◽  
pp. 336-367 ◽  
Keyword(s):  
Carbon Monoxide ◽  
Gas Analysis ◽  
Considerable Time ◽  
Successful Method ◽  
Physico Chemical ◽  
Chemical Behaviour

The object of the work described in this paper was to determine the velocity of the reaction CO + O 2 Hb ⇌ O 2 + COHb, in the hope thereby of throwing further light upon the physico-chemical behaviour of hæmoglobin. There are two reasons which make it specially difficult to devise a successful method of making this measurement. (a) The reaction was found by preliminary experiments to be a swift one, lasting not more than a few seconds ; this made it necessary to estimate the respective concentrations of the different reacting substances instantaneously. This puts out of court the usual methods by gas analysis because of the considerable time taken by such methods.

scholarly journals Role of Nitric Oxide Carried by Hemoglobin in Cardiovascular Physiology

2020 ◽  
Vol 126 (1) ◽  
pp. 129-158 ◽  
Author(s):  
Richard T. Premont ◽  
James D. Reynolds ◽  
Rongli Zhang ◽  
Jonathan S. Stamler
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Oxygen Delivery ◽  
Tissue Oxygenation ◽  
Common Factor ◽  
Well Being ◽  
Therapeutic Interventions ◽  
Oxygen Binding ◽  
Metabolic Demand ◽  
Hypoxic Vasodilation

A continuous supply of oxygen is essential for the survival of multicellular organisms. The understanding of how this supply is regulated in the microvasculature has evolved from viewing erythrocytes (red blood cells [RBCs]) as passive carriers of oxygen to recognizing the complex interplay between Hb (hemoglobin) and oxygen, carbon dioxide, and nitric oxide—the three-gas respiratory cycle—that insures adequate oxygen and nutrient delivery to meet local metabolic demand. In this context, it is blood flow and not blood oxygen content that is the main driver of tissue oxygenation by RBCs. Herein, we review the lines of experimentation that led to this understanding of RBC function; from the foundational understanding of allosteric regulation of oxygen binding in Hb in the stereochemical model of Perutz, to blood flow autoregulation (hypoxic vasodilation governing oxygen delivery) observed by Guyton, to current understanding that centers on S-nitrosylation of Hb (ie, S-nitrosohemoglobin; SNO-Hb) as a purveyor of oxygen-dependent vasodilatory activity. Notably, hypoxic vasodilation is recapitulated by native S-nitrosothiol (SNO)–replete RBCs and by SNO-Hb itself, whereby SNO is released from Hb and RBCs during deoxygenation, in proportion to the degree of Hb deoxygenation, to regulate vessels directly. In addition, we discuss how dysregulation of this system through genetic mutation in Hb or through disease is a common factor in oxygenation pathologies resulting from microcirculatory impairment, including sickle cell disease, ischemic heart disease, and heart failure. We then conclude by identifying potential therapeutic interventions to correct deficits in RBC-mediated vasodilation to improve oxygen delivery—steps toward effective microvasculature-targeted therapies. To the extent that diseases of the heart, lungs, and blood are associated with impaired tissue oxygenation, the development of new therapies based on the three-gas respiratory system have the potential to improve the well-being of millions of patients.

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