Nitroglycerin prolongs the bleeding time in healthy males

Ring, Troels; Knudsen, Flemming; Kristensen, Steen Dalby; Larsen, Carsten E.

doi:10.1016/0049-3848(83)90210-4

Cited by 52 publications

(13 citation statements)

References 14 publications

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“…On the basis of our findings, the use of ketorolac and ketoprofen as analgesics in the early postoperative period should be carefully considered, particularly in patients undergoing surgery with a high risk of bleeding or with possible minor coagulation defects or if treated with agents known to prolong bleeding time [26,27]. In these conditions, ketorolac and ketoprofen treatment should be considered as a cause of increased postoperative bleeding and nefopam might be regarded as a safer drug with regard to bleeding tendency.…”

Section: Discussionmentioning

confidence: 99%

Effect of ketorolac, ketoprofen and nefopam on platelet function

Pl¹,

Ventura²,

Stefanelli³

et al. 1994

Anaesthesia

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Section: Discussionmentioning

confidence: 99%

Effect of ketorolac, ketoprofen and nefopam on platelet function

Pl¹,

Ventura²,

Stefanelli³

et al. 1994

Anaesthesia

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“…4 tory effects of high-or low-dose nitrates are mediated by stimulation of prostacyclin biosynthesis in vivo.…”

Section: Discussionmentioning

confidence: 99%

The effects of organic nitrates on prostacyclin biosynthesis and platelet function in humans.

Fitzgerald¹,

Roy²,

Robertson³

et al. 1984

Circulation

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The results of prior studies indicate that nitroglycerin stimulates prostacyclin release by cultured endothelium and by the coronary vasculature in vivo. However, the accuracy of these findings in coronary vasculature relies on plasma samples obtained from the circulation via cardiac catheters, a procedure we have shown to stimulate prostacyclin release, thereby confounding'interpretation of drug action. We studied the effects of short-acting (nitroglycerin) and long-acting (isosorbide dinitrate) nitrates on a noninvasive index of prostacyclin synthesis, excretion of urinary 2,3-dinor-6-keto-PGF,,. Nitroglycerin was infused into six subjects to either a maximum of 480 gg/min or until mean arterial pressure fell by 20 mm Hg. Urine was collected for negative ion chemical ionization gas chromatographic, mass spectrometric analysis before and during the nitroglycerin infusion and for two 2 hr periods after nitroglycerin. The 297-302, 1984. NITROGLYCERIN is a potent vasodilator that is widely used in 'the treatment of angina pectoris.' Despite its availability for over 100 years, the basis of its effect on vascular smooth muscle is poorly understood. Nitroglycerin also inhibits platelet function in vitro2 3 and has been reported to prolong the bleeding time in human beings.4 5 In view of these biological properties, it has been postulated that nitroglycerin mediates these effects by enhancing generation of the arachidonic acid metabolite prostacyclin in vivo. Formed From the Divisions of Clinical Pharmacology and Cardiology, Van-

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“…Ring et al (1983) found that bleeding time in 15 healthy young men was prolonged approximately 50% by GTN (0.5 mg sublingually). This effect was abolished 2-3.5 h after aspirin, and they argued that it might be due to stimulation by GTN of prostacyclin synthesis.…”

Section: Resultsmentioning

confidence: 99%

“…GTN has been reported to inhibit platelet aggregation in vitro (Hampton et al, 1967;Schafer et al, 1980;Synek et al, 1970) and to prolong bleeding time (Lichtenthal et al, 1985;Ring et al, 1983). Nitric oxide is generated when GTN is metabolised and increases intracellular cyclic GMP (cGMP) (Feelisch & Noack, 1987;Mellion et al, 1981), thereby mediating some of the effects of GTN.…”

Section: Introductionmentioning

confidence: 99%

Effects of a selective thromboxane receptor antagonist (GR32191B) and of glyceryl trinitrate on bleeding time in man.

Ritter¹,

Benjamin²,

Doktor³

et al. 1990

Brit J Clinical Pharma

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1. GR32191B is a potent and selective thromboxane receptor antagonist. Glyceryl trinitrate (GTN) also inhibits platelet function in vitro. Both have been reported to prolong bleeding time. Since they may be used together in patients with coronary artery disease, we have investigated the possibility of an interaction between them. 2. Twenty‐ four healthy male volunteers were treated with GR32191B using a double‐ blind placebo‐controlled crossover design. Bleeding times were determined before and after GR32191B or placebo and during co‐ administration of GTN. Plasma GR32191B concentration was measured. Platelet aggregation in response to adenosine diphosphate and to a thromboxane mimetic, U46619, was measured ex vivo. Urinary excretion of thromboxane (TX)B2 and 2,3‐dinor‐TXB2 was determined in 24 h urine samples. 3. Twelve hours after GR32191B (80 mg; p.o.), the plasma concentration was 36.6 +/− 2.7 nM (mean +/− s.e. mean) and bleeding time was increased by 66%. Ninety minutes after a second dose (40 mg; p.o.) the plasma concentration was 431.9 +/− 23.6 nM but bleeding time was not further prolonged. 4. Responses of platelets to U46619 were selectively antagonised following GR32191B. Urinary excretion rates of TXB2 and 2,3‐dinor TXB2 were similar after treatment with GR32191B or placebo. 5. GTN (1 mg sub‐lingually) had no significant effect on bleeding time 90‐100 min following either placebo or GR32191B. 6. We conclude that GR32191B, in a dose that causes profound yet specific blockade of thromboxane receptors, causes only a modest prolongation of bleeding time that is unaffected by a therapeutic dose of GTN. This may prove advantageous when GR32191B is used in patients with ischaemic heart disease.

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Nitroglycerin prolongs the bleeding time in healthy males

Cited by 52 publications

References 14 publications

Effect of ketorolac, ketoprofen and nefopam on platelet function

Effect of ketorolac, ketoprofen and nefopam on platelet function

The effects of organic nitrates on prostacyclin biosynthesis and platelet function in humans.

Effects of a selective thromboxane receptor antagonist (GR32191B) and of glyceryl trinitrate on bleeding time in man.

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