Dextran

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Dextran
Dextran-2.png
Dextran ball-and-stick.png
Identifiers
CAS number9004-54-0 YesY
KEGGC00372 YesY
ATC codeB05AA05
Properties
Molecular formulaH(C6H10O5)xOH
Molar massVariable
Except where noted otherwise, data are given for materials in their standard state (at 25 °C (77 °F), 100 kPa)
 N (verify) (what is: YesY/N?)
Infobox references
 
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Dextran
Dextran-2.png
Dextran ball-and-stick.png
Identifiers
CAS number9004-54-0 YesY
KEGGC00372 YesY
ATC codeB05AA05
Properties
Molecular formulaH(C6H10O5)xOH
Molar massVariable
Except where noted otherwise, data are given for materials in their standard state (at 25 °C (77 °F), 100 kPa)
 N (verify) (what is: YesY/N?)
Infobox references

Dextran is a complex, branched glucan (polysaccharide made of many glucose molecules) composed of chains of varying lengths (from 3 to 2000 kilodaltons). It is used medicinally as an antithrombotic (anti-platelet), to reduce blood viscosity, and as a volume expander in hypovolaemia.[1]

The straight chain consists of α-1,6 glycosidic linkages between glucose molecules, while branches begin from α-1,3 linkages. (For information on the numbering of carbon atoms in glucose, see the glucose article.) Dextran is synthesized from sucrose by certain lactic-acid bacteria, the best-known being Leuconostoc mesenteroides and Streptococcus mutans. Dental plaque is rich in dextrans.[2] Dextran is also formed by the lactic acid bacterium Lactobacillus brevis to create the crystals of tibicos, a water kefir fermented beverage which supposedly has some health benefits.[citation needed]

Dextran was first discovered by Louis Pasteur as a microbial product in wine.[3]

Uses[edit]

Microsurgery[edit]

These agents are used commonly by microsurgeons to decrease vascular thrombosis. The antithrombotic effect of dextran is mediated through its binding of erythrocytes, platelets, and vascular endothelium, increasing their electronegativity and thus reducing erythrocyte aggregation and platelet adhesiveness. Dextrans also reduce factor VIII-Ag Von Willebrand factor, thereby decreasing platelet function. Clots formed after administration of dextrans are more easily lysed due to an altered thrombus structure (more evenly distributed platelets with coarser fibrin[citation needed]). By inhibiting α-2 antiplasmin, dextran serves as a plasminogen activator and therefore possesses thrombolytic features.

Outside from these features, larger dextrans, which do not pass out of the vessels, are potent osmotic agents, and thus have been used urgently to treat hypovolemia. The hemodilution caused by volume expansion with dextran use improves blood flow, thus further improving patency of microanastomoses and reducing thrombosis. Still, no difference has been detected in antithrombotic effectiveness in comparison of intraarterial and intravenous administration of dextran.

Dextrans are available in multiple molecular weights ranging from 3,000 Da to 2,000,000 Da. The larger dextrans (>60,000 Da) are excreted poorly from the kidney and therefore remain in the blood for as long as weeks until they are metabolized. Consequently, they have prolonged antithrombotic and colloidal effects. In this family, dextran-40 (MW: 40,000 Da), has been the most popular member for anticoagulation therapy. Close to 70% of dextran-40 is excreted in urine within the first 24 hours after intravenous infusion while the remaining 30% will be retained for several more days.

Other medical uses[edit]

Laboratory uses[edit]

Side effects[edit]

Although there are relatively few side-effects associated with dextran use, these side-effects can be very serious. These include anaphylaxis,[5] volume overload, pulmonary edema, cerebral edema, or platelet dysfunction.

An uncommon but significant complication of dextran osmotic effect is acute renal failure.[6] The pathogenesis of this renal failure is the subject of many debates with direct toxic effect on tubules and glomerulus versus intraluminal hyperviscosity being some of the proposed mechanisms .[citation needed] Patients with history of diabetes mellitus, renal insufficiency, or vascular disorders are most at risk. Brooks and others recommend the avoidance of dextran therapy in patients with chronic renal insufficiency and CrCl<40 cc per minute.

See also[edit]

References[edit]

  1. ^ Lewis, Sharon L. (2010). Medical Surgical Nursing (8th ed.). ISBN 978-0323079150. 
  2. ^ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC422963/
  3. ^ Pasteur, L. (1861). "On the viscous fermentation and the butyrous fermentation". Bull. Soc. Chim. Paris (in French) 11: 30–31. ISSN 0037-8968. 
  4. ^ http://www.medicines.org.uk/EMC/medicine/74/SPC/Tears+Naturale/#CLINICAL_PARTS
  5. ^ http://www.medicines.org.uk/emc/medicine/14139#UNDESIRABLE_EFFECTS
  6. ^ Feest, TG (1976). "Low molecular weight dextran: A continuing cause of acute renal failure". British Medical Journal 2 (6047): 1300. doi:10.1136/bmj.2.6047.1300. PMC 1689992. PMID 1000202. 

External links[edit]