Influence of sulfinpyrazone and naproxen on infarct size in the dog

Bolli, Roberto; Goldstein, Robert E.; Davenport, Nancy J.; Epstein, Stephen E.

doi:10.1016/0002-9149(81)90183-1

Cited by 42 publications

(13 citation statements)

References 27 publications

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“…1-3). Our findings are in accordance with other studies that have shown that ibuprofen does not reduce basal blood flow to the brain (13,34) nor to other major organs (renal, cardiac, and mesenteric) (45)(46)(47)(48). PGE and PG12 are the predominant PG produced by the brain tissue and cerebral vasculature (3,4,49,50).…”

Section: -----------supporting

confidence: 93%

“…mate, and aspirin, indomethacin has been shown to reduce basal organ (mesenteric, renal, uterine, and cardiac) blood flow (45-48, 52, 53) to the same extent, regardless of its dose (53), and to constrict isolated vessels (29), probably by an action independent of the effects on PG. For instance, indomethacin has been shown to inhibit histamine release (54) and to potentiate the lipoxygenase pathway (28,55,56) in contrast to other NSAID (47,56). Several factors are involved in the regulation of basal CBF, including K+, Ca2+, glutamate, ATP, adenosine, endotheliumderived relaxing factor, endothelin, and eicosanoids, and some of them have opposing actions.…”

Section: -----------mentioning

confidence: 99%

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Differences in the Effects in the Newborn Piglet of Various Nonsteroidal Antiinflammatory Drugs on Cerebral Blood Flow but Not on Cerebrovascular Prostaglandins

et al. 1991

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ABSTRACT. To characterize the role of prostaglandins (PG) in the regulation of basal cerebral blood flow (CBF) in the newborn, we determined the effects of four nonsteroidal antiinflammatory drugs, indomethacin (3 mg/kg, n = 8 and 10 mglkg, n = 5), aspirin (65 mg/kg, n = 6), ibuprofen (30 mg/kg, n = 8), and naproxen (15 mg/kg, n = 6), on CBF, cerebral metabolism, and cerebrovascular PG in conscious 1-to 3-d-old piglets. Drugs and vehicle (n = 8) were injected i.v., and measurements were made 5 min before and 20 and 60 min after injections. Neither the vehicle nor any of the nonsteroidal antiinflammatory drugs exerted significant effects on mean arterial blood pressure and on blood gases and pH. All four drugs, with the exception of indomethacin at the lower dose (3 mg/kg), decreased PG to nearly undetectable levels within 20 min; the low dose of indomethacin caused a small decrease (18-32%) in PG at 60 min. However, the effects of these agents on CBF were diverse. CBF increased after the administration of aspirin, decreased to almost the same extent after both low and high doses of indomethacin, and did not change after the administration of ibuprofen and naproxen. Cerebral metabolic rate for oxygen was increased by aspirin but was unaltered by the other drugs. The data suggest that PG may not play a critical role in the regulation of basal CBF in the newborn animal and that certain nonsteroidal antiinflammatory drugs may have additional actions unrelated to the inhibition of PG synthesis. (Pediatr Res 30: 106-111,1991) Abbreviations PG, prostaglandin CBF, cerebral blood flow BP, blood pressure NSAID, nonsteroidal antiinflammatory drugThe role of PG in the regulation of CBF during various hemodynamic disturbances, such as hypertension, hypotension, hypoxia, and asphyxia, has been reported by various investigators (1-14). However, the significance of PG in the regulation of basal CBF remains controversial (1 5-19). In most studies ex-

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confidence: 93%

Section: -----------mentioning

confidence: 99%

Differences in the Effects in the Newborn Piglet of Various Nonsteroidal Antiinflammatory Drugs on Cerebral Blood Flow but Not on Cerebrovascular Prostaglandins

et al. 1991

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“…Sulphinpyrazone has also been shown to protect animal hearts against some but not all of the biochemical and histological consequences of coronary artery occlusion (Kelliher et al, 1980;Povalski et al, 1980;Bolli et al, 1981;Innes & Wiseman, 1981;Moschos et al, 1981;Karmazyn, 1984). It was of interest, therefore, to examine the effects of sulphinpyrazone on the electrical changes that occur within ischaemic myocardium.…”

Section: Introductionmentioning

confidence: 99%

A protective effect of sulphinpyrazone against coronary occlusion‐induced shortening of myocardial refractory periods in the rat

Northover

1986

British J Pharmacology

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1 The hearts of anaesthetized, artificially ventilated rats were exposed, and the left coronary artery occluded. The diastolic threshold voltage for stimulation (DTV), the duration of the bipolar electrogram (DBE) and the functional refractory period (FRP) of the ischaemic area were measured at minute intervals for an hour after occlusion. 2 Coronary occlusion caused a rise in DTV, a prolongation of the DBE and a biphasic change in the FRP, with an initial prolongation phase (1-4 min) followed by a decline to below pre-occlusion values (5-15 min). 3 Episodes ofventricular tachyarrhythmia (VT) were most frequent during the period 5-15 min after the onset of occlusion of the coronary artery. This coincided with the period when FRP was minimal and the difference between DBE and FRP was maximal. 4 Pretreatment of rats with sulphinpyrazone (2.5-40mgkg-') or indomethacin (5-20mgkg-') protected against the episodes of coronary occlusion-induced VT and against the associated decline in FRP of the ischaemic muscle. Sulphinpyrazone was more effective than indomethacin in this respect and a combination of the two drugs was approximately as effective as sulphinpyrazone alone. 5 It was concluded that sulphinpyrazone protects rats against coronary occlusion-induced episodes of VT by reducing the risk of ventricular action potential re-entry. This effect is probably due to protection against the ischaemia-induced shortening of the myocardial FRP.

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“…In spite of these findings the mechanism for the protective effects of sulphinpyrazone still remains obscure. Although inhibition of platelet aggregation may be a contributory factor, a recent study has demonstrated that sulphinpyrazone fails to protect the ischaemic myocardium of dog at concentrations that inhibit the aggregation of platelets (Bolli et al, 1981) suggesting the involvement of other mechanisms.…”

Section: Heart Perfusionmentioning

confidence: 99%

A direct protective effect of sulphinpyrazone on ischaemic and reperfused rat hearts

Karmazyn¹

1984

British J Pharmacology

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4H71 Initiation of 60 min ischaemia to rat isolated hearts produced a depression in developed tension and heart rate. Subsequent reperfusion caused a greatly exacerbated creatine phosphokinase (CPK) efflux and limited functional recovery.2 Sulphinpyrazone (100 ng ml-1 and lyg ml) significantly reduced CPK release, particularly after reperfusion, the lower concentration being more effective. 3 A reduction in the mechanical depression during ischaemia and enhanced recovery after reperfusion were seen only with 100 ng ml-I sulphinpyrazone. Heart rate and coronary perfusion pressure were unaffected by drug treatment. 4 The reduction in reperfusion-induced CPK efflux by 100 ng ml-sulphinpyrazone was maximal when the drug was present throughout the perfusion period although some protection was evident when sulphinpyrazone was present either during ischaemia or reperfusion only. An enhanced recovery in contractility was seen only when the drug was present throughout all phases of perfusion. 5 It is suggested that sulphinpyrazone exerts a direct protective effect on the heart particularly during reperfusion. The degree of protection is critically dependent on the concentration of sulphinpyrazone.

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Influence of sulfinpyrazone and naproxen on infarct size in the dog

Cited by 42 publications

References 27 publications

Differences in the Effects in the Newborn Piglet of Various Nonsteroidal Antiinflammatory Drugs on Cerebral Blood Flow but Not on Cerebrovascular Prostaglandins

Differences in the Effects in the Newborn Piglet of Various Nonsteroidal Antiinflammatory Drugs on Cerebral Blood Flow but Not on Cerebrovascular Prostaglandins

A protective effect of sulphinpyrazone against coronary occlusion‐induced shortening of myocardial refractory periods in the rat

A direct protective effect of sulphinpyrazone on ischaemic and reperfused rat hearts

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