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definition - Carboxyhemoglobin

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Wikipedia

Carboxyhemoglobin

                   
  A heme unit of human carboxyhemoglobin, showing the carbonyl ligand at the apical position, trans to the histidine residue.[1]

Carboxyhemoglobin (British English: Carboxyhaemoglobin) (COHb) is a stable complex of carbon monoxide and hemoglobin that forms in red blood cells when carbon monoxide is inhaled or produced in normal metabolism. Large quantities of it hinder delivery of oxygen to the body. Tobacco smoking (through carbon monoxide inhalation) raises the blood levels of COHb by a factor of several times from its normal concentrations. It is bright, cherry red.

Contents

  Carbon monoxide as poison

Hemoglobin binds to carbon monoxide preferentially compared to oxygen (approx 240:1),[2] so effectively, COHb will not release the carbon monoxide, and therefore hemoglobin will not be available to transport oxygen from the lungs to the rest of the body.

In large quantities, the effect of COHb is death - known medically as carboxyhemoglobinemia[3] or carbon monoxide poisoning.[4] However in smaller quantities COHb leads to oxygen deprivation of the body causing tiredness, dizziness and unconsciousness.

COHb has a half-life in the blood of 4 to 6 hours, but in cases of poisoning, this can be reduced to 70 to 35 minutes with administration of pure oxygen (the lower number applying when oxygen is administered with 4 to 5% CO2 to cause hyperventilation).

COHb increases risk of blood clot. It is thought that through this mechanism smoking increases the risk of having an ischemic stroke.

Pregnant smokers may give birth to babies of a lower birth mass. One theory is that, since fetal hemoglobin takes up carbon monoxide more readily than in an adult, therefore the fetus of a smoker will suffer from mild hypoxia, potentially retarding its development.

  Carbon monoxide as normal biological metabolite

In biology, carbon monoxide is naturally produced by the action of heme oxygenase 1 and 2 on the heme from hemoglobin breakdown. This process produces a certain amount of carboxyhemoglobin in normal persons, even if they do not breathe any carbon monoxide.

Following the first report that carbon monoxide is a normal neurotransmitter in 1993,[5] as well as one of three gasses which naturally modulate inflammatory responses in the body (the other two being nitric oxide and hydrogen sulfide), carbon monoxide has received a great deal of clinical attention as a biological regulator. In many tissues, all three gases are known to act as anti-inflammatories, vasodilators and encouragers of neovascular growth.[6] However, the issues are complex, as neovascular growth is not always beneficial, since it plays a role in tumor growth, and also the damage from wet macular degeneration, a disease for which smoking (a major source of carbon monoxide in the blood, several times more than natural production) increases the risk from 4 to 6 times.

  Carbon monoxide as beneficially active substance, and potential pharmaceutical

Studies involving carbon monoxide have been conducted in many laboratories throughout the world for its anti-inflammatory and cytoprotective properties. These properties could potentially be used to prevent the development of a series of pathological conditions including ischemia reperfusion injury, transplant rejection, atherosclerosis, severe sepsis, severe malaria or autoimmunity. Clinical tests involving humans have been performed, however the results have not yet been released.[7]

  References

  1. ^ Gregory B. Vásquez, Xinhua Ji, Clara Fronticelli, Gary L. Gilliland (1998). "Human Carboxyhemoglobin at 2.2 Å Resolution: Structure and Solvent Comparisons of R-State, R2-State and T-State Hemoglobins". Acta Crys. D 54 (3): 355–366. DOI:10.1107/S0907444997012250. 
  2. ^ West JB: Respiratory Physiology -the essentials, 5th Ed. Williams & Wilkins, 1995, p. 76
  3. ^ López-Herce J, Borrego R, Bustinza A, Carrillo A (September 2005). "Elevated carboxyhemoglobin associated with sodium nitroprusside treatment". Intensive Care Med 31 (9): 1235–8. DOI:10.1007/s00134-005-2718-x. PMID 16041521. 
  4. ^ Roth D, Hubmann N, Havel C, Herkner H, Schreiber W, Laggner A (July 2009). "Victim of Carbon Monoxide Poisoning Identified by Carbon Monoxide Oximetry". J Emerg Med 40 (6): 640–2. DOI:10.1016/j.jemermed.2009.05.017. PMID 19615844. http://linkinghub.elsevier.com/retrieve/pii/S0736-4679(09)00407-7. 
  5. ^ New York Times article. Accessed May 2, 2010
  6. ^ Li L, Hsu A, Moore PK. Actions and interactions of nitric oxide, carbon monoxide and hydrogen sulphide in the cardiovascular system and in inflammation--a tale of three gases! Pharmacol Ther. 2009 Sep;123(3):386-400. PMID 19486912
  7. ^ Johnson, Carolyn Y. (October 16, 2009). "Poison gas may carry a medical benefit". The Boston Globe. http://www.boston.com/news/local/massachusetts/articles/2009/10/16/poison_gas_may_carry_a_medical_benefit/?page=full. Retrieved October 16, 2009. 

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