Nitric oxide decreases coagulation protein function in rabbits as assessed by thromboelastography

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Nitric oxide (NO) is administered via infusion of donors such as nitroglycerin or in inhaled form for treatment of ischemia and pulmonary hypertension, respectively. In rabbits, the NO donor, DETANONOate, decreases whole blood clotting function as assessed by thromboelastographic variables (R, reaction time; α, angle; and G, a measure of clot strength). I hypothesized that DETANONOate-derived NO would adversely affect coagulation protein and platelet function. Blood obtained from ear arteries of conscious rabbits (n = 8) anticoagulated with sodium citrate. The blood was then incubated with 0 or 10mM DETANONOate for 30 min. After incubation and recalcification, thromboelastography was performed for 60 min under four conditions: 1) 0mM DETANONOate, 2) 0mM DETANONOate with platelet inhibition with cytochalasin D, 3) 10mM DETANONOate, and 4) 10mM DETANONOate with platelet inhibition. DETANONOate significantly (P < 0.05) increased R and decreased α and G in samples with or without platelet inhibition, compared with samples not exposed to DETANONOate. Lastly, the percentage of total G (GT) attributable to platelet function (GP) was significantly more in the absence of DETANONOate (GP = 92.3% ± 1.6%; mean ± SD) than after exposure to DETANONOate (GP = 90.2% ± 2.3%). DETANONOate-derived NO significantly decreased coagulation protein function and platelet function. Coagulation protein function may be similarly affected in clinical situations involving the administration of NO or NO donors.

Original languageEnglish (US)
Pages (from-to)320-323
Number of pages4
JournalAnesthesia and Analgesia
Volume92
Issue number2
StatePublished - 2001
Externally publishedYes

Fingerprint

Thrombelastography
Nitric Oxide
Rabbits
Proteins
Blood Platelets
Nitric Oxide Donors
2,2'-(hydroxynitrosohydrazono)bis-ethanamine
Cytochalasin D
Nitroglycerin
Blood Coagulation
Pulmonary Hypertension
Ear

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Nitric oxide decreases coagulation protein function in rabbits as assessed by thromboelastography. / Nielsen, Vance G.

In: Anesthesia and Analgesia, Vol. 92, No. 2, 2001, p. 320-323.

Research output: Contribution to journalArticle

@article{c9facfa4eaee4a54b05ad3737e54de1c,
title = "Nitric oxide decreases coagulation protein function in rabbits as assessed by thromboelastography",
abstract = "Nitric oxide (NO) is administered via infusion of donors such as nitroglycerin or in inhaled form for treatment of ischemia and pulmonary hypertension, respectively. In rabbits, the NO donor, DETANONOate, decreases whole blood clotting function as assessed by thromboelastographic variables (R, reaction time; α, angle; and G, a measure of clot strength). I hypothesized that DETANONOate-derived NO would adversely affect coagulation protein and platelet function. Blood obtained from ear arteries of conscious rabbits (n = 8) anticoagulated with sodium citrate. The blood was then incubated with 0 or 10mM DETANONOate for 30 min. After incubation and recalcification, thromboelastography was performed for 60 min under four conditions: 1) 0mM DETANONOate, 2) 0mM DETANONOate with platelet inhibition with cytochalasin D, 3) 10mM DETANONOate, and 4) 10mM DETANONOate with platelet inhibition. DETANONOate significantly (P < 0.05) increased R and decreased α and G in samples with or without platelet inhibition, compared with samples not exposed to DETANONOate. Lastly, the percentage of total G (GT) attributable to platelet function (GP) was significantly more in the absence of DETANONOate (GP = 92.3{\%} ± 1.6{\%}; mean ± SD) than after exposure to DETANONOate (GP = 90.2{\%} ± 2.3{\%}). DETANONOate-derived NO significantly decreased coagulation protein function and platelet function. Coagulation protein function may be similarly affected in clinical situations involving the administration of NO or NO donors.",
author = "Nielsen, {Vance G}",
year = "2001",
language = "English (US)",
volume = "92",
pages = "320--323",
journal = "Anesthesia and Analgesia",
issn = "0003-2999",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

TY - JOUR

T1 - Nitric oxide decreases coagulation protein function in rabbits as assessed by thromboelastography

AU - Nielsen, Vance G

PY - 2001

Y1 - 2001

N2 - Nitric oxide (NO) is administered via infusion of donors such as nitroglycerin or in inhaled form for treatment of ischemia and pulmonary hypertension, respectively. In rabbits, the NO donor, DETANONOate, decreases whole blood clotting function as assessed by thromboelastographic variables (R, reaction time; α, angle; and G, a measure of clot strength). I hypothesized that DETANONOate-derived NO would adversely affect coagulation protein and platelet function. Blood obtained from ear arteries of conscious rabbits (n = 8) anticoagulated with sodium citrate. The blood was then incubated with 0 or 10mM DETANONOate for 30 min. After incubation and recalcification, thromboelastography was performed for 60 min under four conditions: 1) 0mM DETANONOate, 2) 0mM DETANONOate with platelet inhibition with cytochalasin D, 3) 10mM DETANONOate, and 4) 10mM DETANONOate with platelet inhibition. DETANONOate significantly (P < 0.05) increased R and decreased α and G in samples with or without platelet inhibition, compared with samples not exposed to DETANONOate. Lastly, the percentage of total G (GT) attributable to platelet function (GP) was significantly more in the absence of DETANONOate (GP = 92.3% ± 1.6%; mean ± SD) than after exposure to DETANONOate (GP = 90.2% ± 2.3%). DETANONOate-derived NO significantly decreased coagulation protein function and platelet function. Coagulation protein function may be similarly affected in clinical situations involving the administration of NO or NO donors.

AB - Nitric oxide (NO) is administered via infusion of donors such as nitroglycerin or in inhaled form for treatment of ischemia and pulmonary hypertension, respectively. In rabbits, the NO donor, DETANONOate, decreases whole blood clotting function as assessed by thromboelastographic variables (R, reaction time; α, angle; and G, a measure of clot strength). I hypothesized that DETANONOate-derived NO would adversely affect coagulation protein and platelet function. Blood obtained from ear arteries of conscious rabbits (n = 8) anticoagulated with sodium citrate. The blood was then incubated with 0 or 10mM DETANONOate for 30 min. After incubation and recalcification, thromboelastography was performed for 60 min under four conditions: 1) 0mM DETANONOate, 2) 0mM DETANONOate with platelet inhibition with cytochalasin D, 3) 10mM DETANONOate, and 4) 10mM DETANONOate with platelet inhibition. DETANONOate significantly (P < 0.05) increased R and decreased α and G in samples with or without platelet inhibition, compared with samples not exposed to DETANONOate. Lastly, the percentage of total G (GT) attributable to platelet function (GP) was significantly more in the absence of DETANONOate (GP = 92.3% ± 1.6%; mean ± SD) than after exposure to DETANONOate (GP = 90.2% ± 2.3%). DETANONOate-derived NO significantly decreased coagulation protein function and platelet function. Coagulation protein function may be similarly affected in clinical situations involving the administration of NO or NO donors.

UR - http://www.scopus.com/inward/record.url?scp=0035140405&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035140405&partnerID=8YFLogxK

M3 - Article

VL - 92

SP - 320

EP - 323

JO - Anesthesia and Analgesia

JF - Anesthesia and Analgesia

SN - 0003-2999

IS - 2

ER -