Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Norepinephrine release during vasoconstriction induced by cross-linked hemoglobin

L W Hunter1, G M Tyce, D K Rorie

  • 1Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota 55905, USA.

Life Sciences
|January 1, 1996
PubMed
Summary

Hemoglobin-based blood substitutes cause blood vessel contraction partly by scavenging nitric oxide (NO), not by increasing norepinephrine (NE) release from nerve endings. This suggests NO pathway inhibition contributes to their pressor effects.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Temperature sensitivity of capillary-driven flow: application to age monitoring devices.

Journal of colloid and interface science·2012
Same author

Transform method of processing for speckle strain-rate measurements.

Applied optics·2010
Same author

L-DOPA biotransformation: correlations of dosage, erythrocyte catechol O-methyltransferase and platelet SULT1A3 activities with metabolic pathways in Parkinsonian patients.

Journal of neural transmission (Vienna, Austria : 1996)·2003
Same author

Nitric oxide modulates evoked catecholamine release from canine adrenal medulla.

Neuroscience·2001
Same author

Postoperative left vocal cord dysfunction caused by Ortner's cardiovocal syndrome.

Anesthesia and analgesia·2001
Same author

Intrarenal serotonin, dopamine, and phosphate handling in remnant kidneys.

Kidney international·2001

Area of Science:

  • Pharmacology
  • Cardiovascular Physiology
  • Biochemistry

Background:

  • Hemoglobin-based blood substitutes can cause a pressor effect, partly due to nitric oxide (NO) scavenging.
  • NO is a vasodilator and may modulate norepinephrine (NE) release from sympathetic nerves.

Purpose of the Study:

  • To investigate if alpha alpha-cross-linked hemoglobin (XL-Hb) induced contractions are due to increased NE release from vascular nerve endings.
  • To explore the role of NO in mediating the vascular effects of XL-Hb.

Main Methods:

  • Canine femoral artery strips were used in vitro.
  • Measurements included NE overflow into superfusate and contractile responses.
  • Experiments involved basal conditions, nerve stimulation, and tyramine-evoked NE release.

Related Experiment Videos

  • Treatments included XL-Hb, NG-monomethyl-L-arginine (L-NMMA), and sodium nitroprusside (SNP).

    • Main Results:

    • XL-Hb contracted unstimulated strips without altering NE overflow.
    • L-NMMA and SNP did not affect XL-Hb-induced NE overflow or contraction (SNP caused relaxation).
    • Nerve stimulation and tyramine-evoked NE release were not affected by XL-Hb.
    • XL-Hb augmented tyramine-induced contractions without changing NE release.

    Conclusions:

    • Contractions induced by XL-Hb in the canine femoral artery are not mediated by increased NE efflux from vascular nerve endings.
    • The results support the hypothesis that XL-Hb's pressor effect is related to the inhibition of NO actions.