Formation of prostacyclin and thromboxane in man as measured by the main urinary metabolites

Fischer, Sven; Bernutz, C.; Meier, Hubert; Weber, Peter

doi:10.1016/0005-2760(86)90274-2

Cited by 53 publications

(15 citation statements)

References 22 publications

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“…[6][7][8][9] Thus, the present study is the first to demonstrate that women who smoke cigarettes, in analogy with men, excrete more Tx-M than those who do not smoke. Note, however, that in women 18-19 years old, there was no difference in the median excretion of Tx-M, whereas in men of the same age group, an excretion almost 50% higher in smokers than in nonsmokers was reported previously.9 Statistical analysis revealed that the current excretion of Tx-M was positively related to the number of cigarettes smoked per day.…”

Section: Discussionsupporting

confidence: 58%

Tobacco use and urinary excretion of thromboxane A2 and prostacyclin metabolites in women stratified by age.

et al. 1992

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Background. Activated platelets have been implicated in both acute thrombus formation and atherogenesis. Because smoking is a risk factor for cardiovascular disease in men and women and male smokers have biochemical evidence of increased platelet activation, we found it of interest to study whether smoking augments platelet activity in women as well.Methods and Results. Data on smoking habits and a urinary sample were obtained from 125 healthy female nonsmokers and an equal number of smokers, stratified by age in five groups from 18 to 59 years

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Section: Discussionsupporting

confidence: 58%

Tobacco use and urinary excretion of thromboxane A2 and prostacyclin metabolites in women stratified by age.

et al. 1992

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“…Smokers have been reported to display biochemical evidence of increased activation of platelets in vivo. 12 " 15 These data may indicate facilitation of platelet aggregability as a significant etiologic factor in smoking-associated cardiovascular disease.…”

mentioning

confidence: 95%

Excretion of thromboxane metabolites in healthy women after cessation of smoking.

Rångemark

Ciabattoni

Wennmalm

1993

Arterioscler Thromb

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Cigarette smokers, but not former smokers, excrete more thromboxane A 2 (TxA 2 ) metabolites in the urine than do lifelong nonsmokers, which suggests chronic activation of their platelets. To further characterize the effect elicited by smoking on platelet function, we followed the change in urinary excretion of the 2,3-dinor (Tx-M) and 11-dehydro (dTx) metabolites of TxAj, analyzed by gas chromatography/mass spectrometry and radioimmunoassay, respectively, in eight healthy women who quit habitual smoking and compared it with the recovery of these metabolites after a single dose of acetylsalicylic acid (ASA). Tx-M and dTx before cessation of smoking were approximately 550 and 600 pg/mg creatinine, respectively. Within 3 days after quitting smoking, Tx-M and dTx had dropped to stable levels of approximately 300 and 350 pg/mg, respectively. The rates of change in excretion of Tx-M and dTx after smoking cessation were more rapid (p<0.02 and 0.02, respectively) than those observed during the recovery of platelet function after a single dose of ASA. The excretion of 2,3-dinor-6-keto-prostaglandin ¥ l a , a metabolite of prostacyclin, was not affected by smoking cessation. We conclude that cigarette smoking elicits an increase in platelet activity in the absence of vascular injury. This increase is reversible within the life span of the platelets. {Arteriosclerosis and Thrombosis 1993;13:777-782) KEY WORDS • acetylsalicylic acid • cardiovascular risk factors • cigarette smoking • platelets • prostacyclin • thromboxanes • urineC igarette smoking is a major risk factor for cardiovascular disease; the risk increases progressively as daily cigarette consumption increases.1 " 5 After cessation of smoking the risk drops rather rapidly toward the level observed in nonsmokers. 6 -9 Platelets are thought to play an important role in cardiovascular disease, 10 ' 11 but the effect of smoking on platelet function is poorly understood. Smokers have been reported to display biochemical evidence of increased activation of platelets in vivo. "15 These data may indicate facilitation of platelet aggregability as a significant etiologic factor in smoking-associated cardiovascular disease.Thromboxane A 2 (TxA 2 ) is formed in platelets from arachidonic acid.16 TxA 2 has platelet proaggregatory and proadhesive properties and is also a strong vasoconstrictor. The administration of acetylsalicylic acid (ASA) in doses that inhibit cyclooxygenase-dependent formation of TxA 2 in platelets has proven efficient in the primary 17 and secondary 18 prevention of acute myocardial infarction. These data indicate that TxA 2 formed in platelets is etiologically involved in certain acute cardio- Received November 18, 1992; revision accepted February 12, 1993. vascular disorders as well as being a marker for platelet activity.Cigarette smoking is linked to an increased incidence of cardiovascular disease in women.19 " 22 Although women seem to develop cardiovascular disease 10-15 years later than men, 23 it is a leading cause of death among women. ...

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“…The picture may be partly unclear due to difficulties in assessing PGI2 and TxA2 production in vivo. Currently, in vivo PGI2 and TxA2 synthesis is usually studied by measuring their urinary products Fischer et al, 1986;Ylikorkala et al, 1986). Urinary 2,3-dinor-6-keto-PGFIr.…”

Section: Discussionmentioning

confidence: 99%

“…Because interindividual variations in prostanoid excretion are large (Fischer et al, 1986), we studied the effect of repetitive courses of cytostatics. Previously we found increased urinary excretion of 6-keto-PGF1,, in patients with ovarian malignancy (Aitokallio-Tallberg et al, 1987).…”

Section: Discussionmentioning

confidence: 99%

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Urinary excretion of prostacyclin and thromboxane degradation products in patients with ovarian malignancy: effect of cytostatic treatment

Aitokallio-Tallberg

Viinikka²,

Ylikorkala³

1989

Br J Cancer

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Summary We studied the effect of ovarian cancer and its chemotherapy on the urinary excretion of prostacyclin (PGI2) and thromboxane A2 (TxA2) hydration and metabolic products. In six patients we measured 6-keto-PGF,a and 2,3-dinor-6-keto-PGF,. (PGI2 products) and thromboxane B2 (TxB2) and 2,3-dinor-TxB2 (TxA2 products) by HPLC followed by radioimmunoassay before, during and after the combined infusion of cisplatin, 4'epi-adriamycin and cyclophosphamide. Before the first cytostatic infusion, the urinary excretion of prostanoids was on average 4.4-5.8 times higher than in patients with ovarian endometriosis (n= 19). The infusion of cytostatics led to a 50-120% rise in the excretion of prostanoids during the first post-infusion 9 hours, but in the subsequent 10 hours their ouput was 25-45% below the initial value and remained low for at least 2 weeks. Following repetitive courses of cytostatics (2-4 per patient), prostanoid excretion tended to normalise. These data suggest that ovarian cancer is associated with increased production of PGI2 and TxA2, and that cytostatics suppress this production. This may be of biological significance in tumour behaviour and in the effect of cytostatics.

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Formation of prostacyclin and thromboxane in man as measured by the main urinary metabolites

Cited by 53 publications

References 22 publications

Tobacco use and urinary excretion of thromboxane A2 and prostacyclin metabolites in women stratified by age.

Tobacco use and urinary excretion of thromboxane A2 and prostacyclin metabolites in women stratified by age.

Excretion of thromboxane metabolites in healthy women after cessation of smoking.

Urinary excretion of prostacyclin and thromboxane degradation products in patients with ovarian malignancy: effect of cytostatic treatment

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