Haemodynamic changes induced by prostacyclin in man.

Szczeklik, J; Szczeklik, Andrzej; Niżankowski, Rafał

doi:10.1136/hrt.44.3.254

Cited by 63 publications

(21 citation statements)

References 13 publications

(1 reference statement)

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“…Although PGI2 has also been reported to relieve rest pain in ischaemic limbs most investigators who have used intra-arterial injections of PGI2 have produced limb pains at times (Szczeklik et al, , 1980dOlsson & Nilsson, 1981;Machin et al, 1981b;Vermylen et al, 1980). Machin et al (1981b) also report one case of intolerable burning sensation in the toes.…”

Section: Pain In Limbs and Jawmentioning

confidence: 99%

Side effects occurring during administration of epoprostenol (prostacyclin, PGI2), in man.

Pickles¹,

O’Grady²

1982

Brit J Clinical Pharma

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1 Fifty infusions of epoprostenol (PGI2) were made, usually increasing the infusion rate until adverse effects were encountered. The volunteers were appraised that they might experience headache and facial flushing. 2 Facial flushing, headache, tachycardia and decrease in diastolic blood pressure were seen in almost all subjects. Erythema over the venous infusing site was also encountered in 13 infusions. Less common effects were sudden bradycardia, pallor and sweating-the vagal reflex-(seven times) and chest pain (twice). Other complaints included restlessness, abdominal discomfort, nausea and drowsiness.3 The literature on side effects reported during PGI2 infusion is reviewed and recommendations are made concerning administration of PGI2.

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Section: Pain In Limbs and Jawmentioning

confidence: 99%

Side effects occurring during administration of epoprostenol (prostacyclin, PGI2), in man.

Pickles¹,

O’Grady²

1982

Brit J Clinical Pharma

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“…Systemic hypotension has blocked the wide use of PGI2 in the treatment of chronic pulmonary hypertension (Kadowitz et al 1978;Szczeklik et al 1980). With the dose of BPS tested in the present study, systemic arterial pressure was not suppressed in a dose-dependent manner.…”

Section: Resultsmentioning

confidence: 60%

Orally Administered Beraprost Sodium Inhibits Pulmonary Hypertension Induced by Monocrotaline in Rats.

Yuki

Sato

Arisaka

et al. 1994

Tohoku J. Exp. Med.

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Rats were fed on distilled water (DW) or DW containing beraprost sodium (BPS). BPS concentration was 1.5 or 3.0 ,u /ml in DW for the low BPS groups and 6.0 or 10.0 p /ml in DW for the high BPS group. Monocrotaline (MCT) was subcutaneously given (60 mg/kg), and saline was injected as control. Data were analyzed among the following groups; Groups (Saline+DW), (Saline+Low BPS), (MCT+DW), (MCT+Low BPS) and (MCT+High BPS). Three weeks later, pulmonary (Ppa) and systemic (Psa) arterial pressure were measured under anesthesia. MCT caused significant elevation of Ppa { 18.3 ±0.6 cmH2 0 for Group ( Saline + DW) vs. 27.2 ± 1.2 cmH2O for Group (MCT+DW), p<0.001, mean±s.E.} and Ppa was significantly and dose-dependently suppressed by BPS; Group (MCT+DW) vs. Groups (MCT+Low BPS), 23.4±0.7 cmH2O and (MCT+High BPS), 22.5+0.5 cmH2O, p <0.05, mean±s.E.). Psa was not lowered dose-dependently by BPS. We conclude that oral beraprost sodium suppresses pulmonary hypertension produced by monocrotaline in rat.monocrotaline, beraprost sodium, pulmonary hypertension A single subcutaneous injection of the monocrotaline (MCT) results in pulmonary hypertension (Kay et al. 1967). It has been known that platelets are responsible for the development of pulmonary arterial injury in this model. MCT induces pulmonary sequestration of platelets and thrombocytopenia (Hilliker et al. 1982(Hilliker et al. , 1984. A single intravenous injection of prostacyclin (PGI2) at the time of MCT administration inhibits MCT-induced immediate pulmonary hypertension (Czer et al. 1986). To test the hypothesis that a long-term administration of a PGI2 derivative, beraprost sodium (BPS), suppresses MCT-induced pulmonary hypertension, we measured pulmonary arterial pressure (Ppa) three weeks after MCT-treatment in rats fed on distilled water (DW) with or without BPS.

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“…It is known to cause a tachycardia and lower in particular the diastolic blood pressure, but its effects on cardiac output are controversial; it has been reported as doubling it (Eklund et al, 1981) or having no effect (Szczeklik et al, 1980;Cook et al, 1983).…”

Section: Introductionmentioning

confidence: 99%

Time course of the effects of epoprostenol on effective pulmonary blood flow in normal volunteers.

Bush

Busst

Millar

et al. 1988

Brit J Clinical Pharma

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1 Epoprostenol (prostacyclin) has been widely used as a vasodilator, but its effects on cardiac output are controversial and the time course of its effects little studied.2 We report its cardiovascular effects in doses of 5 and 10 ng kg-' min-' in six healthy volunteers. 3 Each of the two doses caused a mean 20% rise in effective pulmonary blood flow and a 15% rise in heart rate. These effects appeared to reach a maximum within 10 min of starting or increasing the rate of infusion, with no evidence of a rebound effect. 4 When the dose was reduced, heart rate and effective pulmonary blood flow appeared to reach a new steady state within 5 min of reducing or stopping the infusion. Only minor side-effects were encountered, and they were rapidly reversed on stopping the drug. 5 These results should be applied to the therapeutic use of epoprostenol as a vasodilator, particularly when titrating the optimum dose for a given individual.

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Haemodynamic changes induced by prostacyclin in man.

Cited by 63 publications

References 13 publications

Side effects occurring during administration of epoprostenol (prostacyclin, PGI2), in man.

Side effects occurring during administration of epoprostenol (prostacyclin, PGI2), in man.

Orally Administered Beraprost Sodium Inhibits Pulmonary Hypertension Induced by Monocrotaline in Rats.

Time course of the effects of epoprostenol on effective pulmonary blood flow in normal volunteers.

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