Thromboxane and Prostacyclin (Epoprostenol) During Exercise in Diffuse Pulmonary Fibrosis

Risk, Clifford G.; Peterson, Myron B.; Woods, Bartholomew; Rie, Michael; Kong, Derek Kai; Watkins, W. D.

doi:10.1016/s0140-6736(82)91202-8

Cited by 20 publications

(7 citation statements)

References 11 publications

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“…In keeping with findings from previous studies in healthy humans, short-term exercise increased the platelets' capacity to release TXB 2 (7). The response was similar in the diabetic and control subjects, indicating normal TXA 2 production in our diabetic patients.…”

Section: Discussionsupporting

confidence: 91%

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Stimulation of Prostacyclin Synthesis by Physical Exercise in Type I Diabetes

et al. 1989

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We examined the effect of short- and long-term exercise on prostacyclin (prostaglandin I2 [PGI2]) and thromboxane A2 (TXA2) synthesis in type I (insulin-dependent) diabetic patients and healthy control subjects. PGI2 synthesis was assessed by determining the urinary excretion of 6-keto-PGF1 alpha and 2,3-dinor-6-keto-PGF1 alpha and TX synthesis by measuring TXB2 in serum and urine. In the resting state, prostanoid excretion and concentrations were similar in diabetic and control subjects. During 40 min of ergometric cycling exercise, the urinary excretion of 6-keto-PGF1 alpha (a hydration product of vasodilatory PGI2) increased 5.8-fold more in the 12 control subjects than in the 15 diabetic patients (P less than .02). Serum TXB2 concentration rose similarly in diabetic patients and control subjects (P less than .05). During a 75-km competitive cross-country ski race (7 h, 30 min), urinary excretion of 6-keto-PGF1 alpha rose 1.9-fold in 7 diabetic (P less than .05) and 3.3-fold in 10 control (P less than .001) subjects, whereas urinary dinor excretion, reflecting vascular PGI2 synthesis more closely, increased only in the control subjects (P less than .01). Urinary TXB2 excretion remained unchanged in both groups during long-term exercise. These data suggest that diabetic patients have normal PGI2 and TXA2 synthesis in the resting state but diminished PGI2 response to both acute and prolonged exercise.

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Section: Discussionsupporting

confidence: 91%

“…Plasma concentration of TXB 2 , a metabolite of TXA 2 , is shown to increase (7) or remain the same (4,8,9) during exercise in healthy people.…”

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confidence: 99%

Stimulation of Prostacyclin Synthesis by Physical Exercise in Type I Diabetes

et al. 1989

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“…We have found no change in platelet aggregation following strenuous exercise which made our original hypothesis, that (3-blockade could prevent exercise-induced hyperaggregability, impos sible to test. In normal subjects following exercise PGI2 levels have been shown to re main unchanged [39] or to increase [15]. We have found that PGI2 levels increase with exercise which could explain why no increase in platelet aggregation responses occurred in our study.…”

Section: Discussionsupporting

confidence: 46%

“…PGI2 results, however, were not available from all the exercise studies and the lack of significance may be due to smaller numbers in each group. In vivo platelet ag gregation, as measured by (3-TG levels, has been reported to increase [38] or remain un changed [39] in normal males following exer cise. In our study the lack of change in P-TG levels noted is in keeping with the failure to demonstrate enhanced platelet responses by standard aggregometry.…”

Section: Discussionmentioning

confidence: 99%

Blood Coagulation and Platelet Function following Maximal Exercise: Effects of Beta-Adrenoceptor Blockade

Small¹,

Tweddel

Rankin

et al. 1984

Pathophysiol Haemos Thromb

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Alterations of platelet function and blood coagulation may occur with exercise or β-adrenoceptor blockade. To determine if β-blockade could modify exercise-induced changes in haemostatic factors we performed a double-blind study of actue strenuous exercise in normal males with and without β-blockade. Exercise increased prostacyclin and plasminogen activator levels but there was no evidence of thrombin generation as indicated by unchanged platelet aggregation responses, β-thromboglobulin and íibrinopeptide A levels. The only alteration in coagulation by β-blockade was a reduction in the factor VIII:C and VIII:RAg rise after exercise and this modification may be relevant to the protective effect of these drugs in patients with coronary artery disease.

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“…In fact, real improvements in exercise tolerance with oxygen administration seem to be com moner in patients with restrictive disease than in those with obstructive pulmonary disease [16][17][18]. Since short-term administration of var ious vasodilators appears to improve pul monary hemodynamics in patients with chronic cor pulmonale secondary to other pulmonary diseases [19][20][21][22][23][24][25], we examined the response of pulmonary circulation to the vasodilator nifedipine in patients with IPF. This drug has been shown experi mentally [26][27][28] and clinically [19][20][21][22] to reduce pulmonary vasoconstriction with out adverse effects [19,29,30].…”

Section: Introductionmentioning

confidence: 99%

Pulmonary Vascular Responsiveness at Rest and during Exercise in Idiopathic Pulmonary Fibrosis: Effects of Oxygen and Nifedipine

Sturani¹,

Papiris²,

Galavotti³

et al. 1986

Respiration

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To detect whether pulmonary vascular responsiveness is a factor which can aggravate the pulmonary hypertension induced by irreversible pulmonary fibrosis, we examined the acute hemodynamic effects of low-flow oxygen and of nifedipine both at rest and during exercise in 8 patients with idiopathic pulmonary fibrosis (IPF). During exercise, the increments in pulmonary artery pressure, pulmonary vascular resistance (PVR), and right ventricular stroke work index relative to resting values were blunted by both treatments. During exercise, both systemic vascular resistance and PVR decreased more significantly after nifedipine than on oxygen (p < 0.001). At exercise, nifedipine administration induced a greater increment in oxygen delivery (CaO₂ × CI) than that produced by oxygen breathing (p < 0.01). Our results in patients with IPF seem to confirm that active vasoconstriction of pulmonary vessels may contribute to the pulmonary hypertension during exercise. The evaluation of reversibility of pulmonary hypertension by nifedipine in IPF deserves further long-term studies

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Thromboxane and Prostacyclin (Epoprostenol) During Exercise in Diffuse Pulmonary Fibrosis

Cited by 20 publications

References 11 publications

Stimulation of Prostacyclin Synthesis by Physical Exercise in Type I Diabetes

Stimulation of Prostacyclin Synthesis by Physical Exercise in Type I Diabetes

Blood Coagulation and Platelet Function following Maximal Exercise: Effects of Beta-Adrenoceptor Blockade

Pulmonary Vascular Responsiveness at Rest and during Exercise in Idiopathic Pulmonary Fibrosis: Effects of Oxygen and Nifedipine

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