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Study of the effects of nitric oxide...

Xu, Xiuli.

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Study of the effects of nitric oxide on sickle cell disease.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Study of the effects of nitric oxide on sickle cell disease./
作者:	Xu, Xiuli.
面頁冊數:	84 p.
附註:	Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1201.
Contained By:	Dissertation Abstracts International65-03B.
標題:	Biophysics, General. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3125140
ISBN:	0496724304

Study of the effects of nitric oxide on sickle cell disease.
Xu, Xiuli.

Study of the effects of nitric oxide on sickle cell disease. - 84 p.

Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1201.

Thesis (Ph.D.)--Wake Forest University, 2004.

Sickle cell disease (SCD) is a serious vascular disorder that affects one of every six hundred African Americans. The disease is caused by a single point mutation within hemoglobin (Hb), which causes polymerization of Hb, leading to abnormally-shaped and rigid red cells that cause obstruction of small blood vessels and decreased oxygen-carrying capacity.

ISBN: 0496724304Subjects--Topical Terms:

1019105
Biophysics, General.

Study of the effects of nitric oxide on sickle cell disease.
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245 1 0 $a Study of the effects of nitric oxide on sickle cell disease.
300 $a 84 p.
500 $a Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1201.
500 $a Adviser: Daniel B. Kim-Shapiro.
502 $a Thesis (Ph.D.)--Wake Forest University, 2004.
520 $a Sickle cell disease (SCD) is a serious vascular disorder that affects one of every six hundred African Americans. The disease is caused by a single point mutation within hemoglobin (Hb), which causes polymerization of Hb, leading to abnormally-shaped and rigid red cells that cause obstruction of small blood vessels and decreased oxygen-carrying capacity.
520 $a Inhalation of nitric oxide (NO) in acceptable amounts by the human body has been tried as a treatment of SCD. The basis of NO therapy is that NO functions as a vaso-dilator in human circulation by initiating reactions that result in relaxation of smooth muscle. On the other hand, NO is an active molecule that reacts very fast with oxygen, deoxygenated and oxygenated Hb. Given so many reactions that could take place within seconds, how could the biological function of NO as a vaso-dilator be preserved?
520 $a Stamler and coworkers proposed a controversial NO transport model to answer this question. In this model, NO is preserved in the form of s-nitroso-Hb in arterial blood and can be transferred to the heme groups on the same Hb molecule to form iron-nitrosyl-Hb in venous blood. Some of this NO escapes the intramolecular transfer and is exported from the erythrocyte to trigger dilation of blood vessels.
520 $a This research focuses on the biophysical aspects of NO therapy for patients with SCD. We examined the solubilizing effect, the ability to reduce polymerization, of partially NO-ligated sickle Hb and the ability of NO to undergo the intramolecular transfer. Our results showed that NO therapy doesn't benefit patients through solubilizing effect and no evidence for intramolecular transfer of NO was found. Contaminating nitrite could play a key role in previous reports of intramolecular transfer due to the reaction between Hb and nitrite producing NO. Simulations of the diffusion of NO produced by this reaction within erythrocytes showed that the amount of NO diffusing out is not high enough to function as a vaso-dilator. An intermediate species in this reaction might play an important role in the delivery and preservation of biological activity of NO in the human body.
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792 $a 2004
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