scholarly journals The effect of inhaled nitric oxide (iNO) on bleeding time and platelet aggregation in neonates. † 886

1997 ◽  
Vol 41 ◽  
pp. 150-150 ◽  
Author(s):  
Thomas N. George ◽  
Karen J. Johnson ◽  
James N. Bates ◽  
Jeffrey L. Segar
Keyword(s):  
Nitric Oxide ◽  
Platelet Aggregation ◽  
Bleeding Time ◽  
Inhaled Nitric Oxide

Randomized, Placebo-controlled, Blinded and Cross-matched Study on the Antiplatelet Effect of Inhaled Nitric Oxide in Healthy Volunteers

2000 ◽  
Vol 83 (02) ◽  
pp. 309-315 ◽  
Author(s):  
Axel Herr ◽  
Johann Motsch ◽  
Alexandra Holzmann ◽  
Jörg Weimann ◽  
Friedemann Taut ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Platelet Aggregation ◽  
Healthy Volunteers ◽  
Bleeding Time ◽  
Inhibitory Effect ◽  
Inhaled Nitric Oxide ◽  
Men And Women ◽  
Fibrinogen Binding ◽  
Matched Study

SummaryThe platelet inhibitory effect of 0-40 ppm inhaled nitric oxide (NO) was investigated in healthy men and women. In both groups, ADPand collagen-induced platelet aggregation was significantly inhibited 20 (T20) and 40 min (T40) after the beginning of inhalation of 5, 10, and 40 ppm. Moreover, in both men and women, the in vitro bleeding time was significantly prolonged at T20 and T40 during inhalation of 40 ppm. Inhalation of NO also inhibited P-selectin expression at 5, 10, and 40 ppm and fibrinogen binding to the GPIIb/IIIa-receptor at 40 ppm. In conclusion, in healthy volunteers, the platelet inhibitory effect of inhaled NO was not dose-related, since it was significant at 5 and 10 ppm but did not increase during the administration of higher NO concentrations. In addition, gender-related differences were only observed in ADP-induced platelet aggregation at 10 ppm and in bleeding time prolongation at 40 ppm.

Inhibition of Platelet Aggregation by Inhaled Nitric Oxide in Patients with Acute Respiratory Distress Syndrome

1995 ◽  
Vol 83 (1) ◽  
pp. 56-65. ◽  
Author(s):  
Charles Marc Samama ◽  
Mohamed Diaby ◽  
Jean-Luc Fellahi ◽  
Ayoub Mdhafar ◽  
Daniel Eyraud ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Acute Respiratory Distress Syndrome ◽  
Platelet Aggregation ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Bleeding Time ◽  
Distress Syndrome ◽  
Inhaled Nitric Oxide ◽  
Arterial Oxygenation ◽  
Inhibition Of Platelet Aggregation

Background Nitric oxide inhibits platelet adhesion and aggregation in vitro. The aim of this prospective study was to assess the platelet antiaggregating activity of nitric oxide administered to patients with acute respiratory distress syndrome (ARDS) at increasing concentrations. Methods In six critically ill patients (mean age 37 +/- 16 yr) with ARDS (lung injury severity score > or = 2.2), the lungs were mechanically ventilated with inhaled nitric oxide (1, 3, 10, 30, and 100 ppm) randomly administered. Patients with cardiac dysrhythmias, septic shock, an underlying hemostasis disorder (constitutive or acquired), a platelet count less than 100 Giga/l, or a decreased platelet aggregation and those treated with antiplatelet or anticoagulant agents were excluded. Platelet aggregation was measured without nitric oxide and at each nitric oxide concentration in platelet-rich plasma issued from radial artery. Ivy bleeding time using a horizontal incision was simultaneously performed. Results After nitric oxide, a non-dose-dependent but statistically significant decrease in ex vivo platelet aggregation induced by three aggregating agents was observed: adenosine diphosphate = -56 +/- 18%, collagen = -37 +/- 18%, and ristocetin = -45 +/- 18% (P < 0.05). In each individual, Ivy bleeding time remained within normal values measured in healthy volunteers, and variations after nitric oxide did not correlate with changes in platelet aggregation. Simultaneously, arterial oxygenation improved significantly and pulmonary artery pressure decreased significantly. Conclusions In patients with ARDS and without preexisting coagulation disorders, the beneficial effects of inhaled nitric oxide on arterial oxygenation and pulmonary circulation are associated with a significant inhibition of platelet aggregation. This antithrombotic effect is not associated with a significant prolongation of the bleeding time.

The effect of inhaled nitric oxide therapy on bleeding time and platelet aggregation in neonates

1998 ◽  
Vol 132 (4) ◽  
pp. 731-734 ◽  
Author(s):  
Thomas N. George ◽  
Karen J. Johnson ◽  
James N. Bates ◽  
Jeffrey L. Segar
Keyword(s):  
Nitric Oxide ◽  
Platelet Aggregation ◽  
Bleeding Time ◽  
Inhaled Nitric Oxide ◽  
Nitric Oxide Therapy

scholarly journals A.360 Inhibition of platelet aggregation by inhaled nitric oxide in ARDS patients: a dose—effect study

1996 ◽  
Vol 76 ◽  
pp. 112
Author(s):  
G.S. Umamaheswara Rao ◽  
QIn Lu ◽  
M. Diaby ◽  
E. Mourgeon ◽  
J.D. Law Koune ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Platelet Aggregation ◽  
Effect Study ◽  
Inhaled Nitric Oxide ◽  
Dose Effect ◽  
Inhibition Of Platelet Aggregation

scholarly journals Inhaled Nitric Oxide Inhibits Human Platelet Aggregation, P-Selectin Expression, and Fibrinogen Binding In Vitro and In Vivo

Circulation ◽  
1998 ◽  
Vol 97 (15) ◽  
pp. 1481-1487 ◽  
Author(s):  
André Gries ◽  
Christoph Bode ◽  
Karlheinz Peter ◽  
Axel Herr ◽  
Hubert Böhrer ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Platelet Aggregation ◽  
Human Platelet ◽  
Inhaled Nitric Oxide ◽  
Human Platelet Aggregation ◽  
Fibrinogen Binding

Inhaled Nitric Oxide Inhibits Platelet Aggregation after Pulmonary Embolism in Pigs

1997 ◽  
Vol 86 (2) ◽  
pp. 387-393 ◽  
Author(s):  
Andre Gries ◽  
Bernd W. Bottiger ◽  
Joachim Dorsam ◽  
Harry Bauer ◽  
Jorg Weimann ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Embolism ◽  
Platelet Aggregation ◽  
Thrombus Formation ◽  
Carbon Dioxide Concentration ◽  
Right Ventricular Dysfunction ◽  
Inhaled Nitric Oxide ◽  
Control Group ◽  
Maximum Decrease ◽  
Inhaled No

Background Inhaled nitric oxide (NO) is reported to prolong bleeding time in animals and humans and to inhibit platelet aggregation in persons with acute respiratory distress syndrome. In pulmonary embolism (PE), inhibition of platelet aggregation appears useful because further thrombus formation may lead to right ventricular dysfunction that results in circulatory failure. In the present study, the effect of inhaled NO on platelet aggregation after acute massive PE was investigated. Methods After acute massive PE was induced in 25 anesthetized pigs by injecting microspheres, 5, 20, 40, and 80 parts per million inhaled NO were administered stepwise for 10 min each in 11 animals (NO group). In the control group (n = 14). NO was not administered. Adenosine diphosphate-induced initial and maximal platelet aggregation were measured before PE (10), immediately after induction of PE (PE), at the end of each 10-min NO inhalation interval (t10-t40), and 15 min after cessation of NO inhalation (t55) in the NO group, and at corresponding times in the control group, respectively. Results Two animals in the control group and one in the NO group died within 10 min after PE induction and were excluded from analysis. Peaking at t40 and t55, respectively, initial (-13 +/- 6%; P < 0.05) and maximal (+44 +/- 17%; P < 0.05) platelet aggregation increased significantly after PE in the control group. In contrast, NO administration after PE led to a significant decrease in initial (maximum decrease, -9 +/- 3% at t40; P < 0.05) and maximal (maximum decrease, -15 +/- 7% at t30; P < 0.05) platelet aggregation. In the NO group, platelet aggregation had returned to baseline levels again at t55. In addition, NO administration significantly decreased mean pulmonary artery pressure and significantly increased end-tidal carbon dioxide concentration and mean systemic blood pressure. Conclusions Inhaled NO has a systemic and rapidly reversible inhibitory effect on platelet aggregation after acute massive PE in pigs. This may be beneficial in treating acute massive PE.

Prolongation of bleeding time by acute hemolysis in rats: a role for nitric oxide

1997 ◽  
Vol 272 (6) ◽  
pp. H2875-H2884 ◽  
Author(s):  
T. Wollny ◽  
L. Iacoviello ◽  
W. Buczko ◽  
G. de Gaetano ◽  
M. B. Donati
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Platelet Aggregation ◽  
Blood Cell ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Platelet Adhesion ◽  
Bleeding Time ◽  
Ex Vivo ◽  
White Blood Cells

The present study was aimed at clarifying the interaction between red blood cell trauma and bleeding observed in some clinical conditions. Acute hemolysis provoked by distilled water injection was followed by a significant prolongation of the "template" bleeding time in rats. Comparable effects were observed after injection of an isotonic lysate of washed red blood cells. N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) formation from L-arginine, normalized bleeding time when given to rats before hemolysis induction. The occurrence of hemolysis decreased ex vivo platelet adhesion to collagen without affecting platelet aggregation and induced a transient drop in blood pressure, the latter occurring during the first minute after injection. L-NAME pretreatment increased ex vivo platelet adhesion but did not affect either platelet aggregation or fall in blood pressure. All the effects of L-NAME were blunted by treating the animals with the NO precursor L-arginine but not D-arginine. Incubation of the erythrocyte lysate with apyrase prevented the prolongation of bleeding time induced by the hemolysate. Moreover, ADP administration, at doses that did not increase hemoglobin levels, induced effects similar to those observed after hemolysis (on template bleeding time and ex vivo platelet adhesion), which were also reversed by L-NAME and restored by L-arginine. ADP is abundantly released from (hemo)lysed red blood cells and is known to stimulate release of NO, a potent vasodilator and inhibitor of platelet adhesion. ADP-dependent NO release could be responsible for bleeding time prolongation, due to abnormalities in platelet-vessel wall interaction, during acute hemolysis. Lysis of white blood cells may also contribute to prolongation of bleeding time. Because ADP could not be detected in these cells, we postulate that other mechanisms also can be involved in bleeding time prolongation after blood cell activation in vivo.

Inhibitory role of capsaicin-sensitive afferent neurons and nitric oxide in hemostasis

1993 ◽  
Vol 265 (6) ◽  
pp. H1864-H1868 ◽  
Author(s):  
I. T. Lippe ◽  
W. Sametz ◽  
K. Sabin ◽  
P. Holzer
Keyword(s):  
Nitric Oxide ◽  
Platelet Aggregation ◽  
Bleeding Time ◽  
Antithrombin Iii ◽  
Mesenteric Arteries ◽  
Thrombin Time ◽  
Afferent Neurons ◽  
No Formation ◽  
Inhibitory Role

Capsaicin-sensitive afferent neurons control blood flow via release of peptide transmitters and formation of nitric oxide (NO). The present study examined whether capsaicin-sensitive afferent neurons and NO interact in the control of hemostasis. Afferent nerve ablation by pretreating rats with a neurotoxic dose of capsaicin (125 mg/kg) led to a 26% reduction of the time of bleeding from punctured small mesenteric arteries in pentobarbital-anesthetized animals. Blockade of NO formation by NG-nitro-L-arginine methyl ester (L-NAME; 10 mg/kg) attenuated the bleeding time in capsaicin-pretreated rats but had no effect in vehicle-pretreated rats. Platelet aggregation induced by ADP was significantly augmented by 12% in capsaicin-pretreated rats. L-NAME did not alter platelet aggregation in vehicle-pretreated rats but enhanced it in capsaicin-pretreated animals. The prothrombin and partial thromboplastin time and the plasma levels of fibrinogen and antithrombin III remained unchanged by capsaicin or L-NAME, whereas the thrombin time was reduced in capsaicin-pretreated rats. These data indicate that capsaicin-sensitive afferent neurons play an inhibitory role in platelet aggregation and hemostasis, a function in which they interact with the NO system.

Effects of Inhaled Nitric Oxide Compared with Aspirin on Platelet Function in Vivo in Healthy Subjects

1996 ◽  
Vol 91 (2) ◽  
pp. 225-231 ◽  
Author(s):  
Johanna Albert ◽  
N. Håkan Wallén ◽  
Anders Bröijersén ◽  
Claes Frostell ◽  
Paul Hjemdahl
Keyword(s):  
Nitric Oxide ◽  
Platelet Function ◽  
Healthy Subjects ◽  
Bleeding Time ◽  
Ex Vivo ◽  
Inhaled Nitric Oxide ◽  
Platelet Aggregability ◽  
Nitric Oxide Inhalation ◽  
Platelet Secretion

1. Nitric oxide has platelet-stabilizing effects. Inhaled nitric oxide is used to treat pulmonary disorders, and may prolong bleeding times, suggesting that it has effects on haemostasis. We therefore examined if inhaled nitric oxide influences platelet function in vivo in healthy subjects. 2. Platelet aggregability (filtragometry ex vivo, which reflects aggregability in vivo), bleeding time and platelet secretion products and cGMP in plasma were studied during inhalation of two different doses of nitric oxide (30 and 80 p.p.m.; 15 min at each dose level; n = 19) and during prolonged (55 min; n = 18) inhalation of 30p.p.m. nitric oxide. For comparison, studies were also performed before and after ingestion of 640 mg aspirin in 13 of the healthy subjects. 3. Plasma cGMP increased dose dependently during nitric oxide inhalation, suggesting guanylate cyclase activation in vivo. Platelet aggregability was, however, little affected and platelet secretion was not attenuated by nitric oxide inhalation. Bleeding time tended to increase (by 16–33%), but was significantly increased only after prolonged inhalation of nitric oxide at 30 p.p.m. 4. Aspirin (640 mg orally) caused pronounced and significant prolongations of filtragometry readings and bleeding time. Thus, the methods used were able to reveal platelet stabilization. 5. We conclude that nitric oxide inhalation causes only mild, if any, attenuation of platelet function in healthy subjects with a normal endogenous nitric oxide production. The effects may be different in disease states.

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