Interaction between nitric oxide and red blood cells /
Although intensive rematch has uncovered the diverse roles of nitric oxide (NO) in physiology and pathophysiology, relatively little attention has tun paid to the transfer of NO from the producing cell to the target. The commonly accepted mechanism suggests that NO, being a free radical, is intrinsi...
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| Format: | Thesis Book |
| Language: | English |
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[Place of publication not identified] :
[publisher not identified] ;
1999.
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| Subjects: | |
| Online Access: | http://proxy.library.tamu.edu/login?url=http://proquest.umi.com/pqdweb?did=731681501&sid=1&Fmt=2&clientId=2945&RQT=309&VName=PQD |
| Summary: | Although intensive rematch has uncovered the diverse roles of nitric oxide (NO) in physiology and pathophysiology, relatively little attention has tun paid to the transfer of NO from the producing cell to the target. The commonly accepted mechanism suggests that NO, being a free radical, is intrinsically unstable and thus its consumption cannot and does not need to lie regulated. However, our mathematical analysis shows that if endothelium-produced NO reacted with blood as rapidly as it does with free Hb, the NO concentrations in vascular smooth muscle would lie too low to activate soluble granulate cyclase the primary target of NO. Indeed, in vivo and in vitro evidence show that free hemoglobin (Hb) is an effective NO scavenger that depletes NO. In addition, infusion of a free Hb solution (in the micromolar range) into experimental animals or human subjects results in hypertension. It is unclear how NO can exert its vasoregulatory function with 12- to 15-mM Hb (based on heme) concentration in the blood. In order to resolve this paradox, a competition experiment based on the derived kinetic model was designed to determine the NO consumption by red blood cells (RBCs) at high hematocrit without the influence of an external diffusion barrier. Interestingly, the NO consumption rate by RBCs, which was determined from the competition experiments, is much slower than that by free oxyHb at the same overall concentration. The result suggests that the existence of intrinsic factors in the erythrocytes controls the overall NO consumption. Indeed, some mechanisms such as membrane properties and redox status of RBCs can modulate the RBC-NO consumption rate. The decrease of the RBC-NO consumption rate by the presentment of NO gas and bis(sulfosuccinimidyl)suberate suggests the involvement of membrane properties. On the other hand, the increase of RBC-NO consumption rate by the pretreatment with hypoxanthine/xanthine/sodium azide suggests the involvement of RBC redox status. The finding of the modulation of the MC-NO consumption rate will directly impact NO inhalation therapy and design of blood substitutes. |
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| Item Description: | Vita. "Major Subject: Chemical Engineering". |
| Physical Description: | xi, 113 leaves : illustrations ; 28 cm. Issued also on microfiche from University Microfilm Inc. |
| Bibliography: | Includes bibliographical references (leaves 108-110). |