Arachidonic Acid Causes Sudden Death in Rabbits

Silver, Melvin J.; Hoch, Willis S.; Kocsis, James J.; Ingerman, Carol M.; Smith, J B

doi:10.1126/science.183.4129.1085

Cited by 246 publications

(66 citation statements)

References 10 publications

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“…AA has been conclusively shown to induce platelet aggregation both in vitro (Silver, Smith, Ingerman & Kocsis, 1973;Vargaftig & Zirins, 1973;Rose et al 1974) and in vivo preparations (Silver et al, 1974;Furlow & Bass, 1975) in several different species. The results of experiments using the platelet-free perfusate strongly suggest that the increased perfusion pressure is independent of the release of vasoactive platelet products or mechanical obstruction of small vessels by platelet aggregates.…”

Section: Methodsmentioning

confidence: 99%

“…These authors have suggested that conversion of a vasoconstrictor intermediate to its degradation products, particularly prostaglandin E2, produces a longer lasting reduction in blood pressure due to peripheral vasodilatation. The well-known enhancement of platelet aggregation by AA (Silver, Hoch, Kocsis, Ingerman & Smith, 1974) suggests that another possible mechanism for acute systemic hypotension could be momentary obstruction of the pulmonary vasculature.…”

Section: Introductionmentioning

confidence: 99%

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Vasoconstrictor Response to Arachidonic Acid in the Isolated Hind Limb of the Dog

Fitzpatrick

Johnson

Kot

et al. 1977

British J Pharmacology

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1Arachidonic acid (AA) (25‐200 μg/kg) produced a dose‐related increase in perfusion pressure in dog isolated hind limbs perfused with either blood or a platelet‐free perfusate. 2Prostaglandin E2 produced vasodilatation while prostaglandin produced no vascular change at these administered doses. 3Phentolamine did not alter the arachidonic acid response, eliminating possible α‐adrenoceptor mediation. 4Aspirin and indomethacin blocked the vasoconstrictor response to AA. 5This study indicates that a vasoactive intermediate in prostaglandin synthesis can be elaborated in the absence of platelets.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Vasoconstrictor Response to Arachidonic Acid in the Isolated Hind Limb of the Dog

Fitzpatrick

Johnson

Kot

et al. 1977

British J Pharmacology

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“…Effect on AA-induced death in rabbits AA (1.7 mg/kg) was injected into the marginal ear vein of rabbits at a rate of 0.1 ml/sec, and the mortality was observed 30 min thereafter (10). The AA was dissolved in saline and adjusted to a final concentration of 3.4 mg/ml.…”

Section: Drugs and Chemicalsmentioning

confidence: 99%

Anti-thrombotic Activity of KBT-3022 in Experimental Models of Thrombosis

Yokota¹,

Yamashita²,

Oda³

1995

Japanese Journal of Pharmacology

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ABSTRACT-In this study, we investigated the effects of KBT-3022 (ethyl 2-[4,5-bis(4-methoxyphenyl)-thiazol-2-yl]pyrrol-1-ylacetate), a potent and long-lasting anti-platelet agent, in several experimental thrombosis models and compared them with those of other anti-platelet drugs. Oral administration of KBT-3022 prevented arachidonic acid-induced death due to pulmonary embolism in mice and rabbits with respective ED50 values of 0.29 and 0.12 mg/kg. The protective effect of acetylsalicylic acid (ASA) against mortality was weaker than that of KBT-3022, and ticlopidine hydrochloride (TP) showed no such effect in these models. In a guinea pig arterio-venous shunt model, the inhibition by KBT-3022 of thrombus formation on a silk thread inserted into the shunt was dose-dependent and 300 and 30 times more potent than the inhibition obtained with ASA and indomethacin, respectively. In a model of aortic thrombosis induced by perivascular application of 20% silver nitrate solution, KBT-3022 (1 mg/kg, p.o.) inhibited thrombus formation significantly, ASA (100 mg/kg, p.o.) tended to inhibit it, and TP had no effect. However, in a stasisinduced venous thrombosis model in guinea pigs, TP inhibited thrombus formation significantly, but KBT-3022 and ASA were ineffective. These results suggest that KBT-3022 may be a useful drug for the treatment and/or prophylaxis of thrombus formation in shunts and aortic thrombosis.

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“…Effect of NSAI D and SAID on acute death by arachidonic acid in rabbits: The i.v. injection of 1.4 mg/kg of arachidonic acid in rabbits causes acute death within a few min (15). Male rabbits weighing 2.5-3.0 kg received p.o.…”

Section: Abstract-prostaglandinsmentioning

confidence: 99%

Effect of anti-inflammatory drugs on endotoxin-induced diarrhea in mice.

Tsurumi

Fujimura

1983

Jpn.J.Pharmacol

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Abstract-Prostaglandins(PGs) increase the intestinal fluid to result in diarrhea. Some laxatives are known to exert their actions partially by stimulating the PGs biosynthesis. On the other hand, it is well documented that nonsteroidal anti-inflammatory drugs (NSAID) inhibit markedly the PGs biosynthesis. Since endotoxin (ETX) also produces diarrhea similarly in all species of experimental animals, we investigated the effect of various NSAID and steroidal anti-inflammatory drugs (SAID) on ETX-induced diarrhea in mice. ETX given p.o. did not produce diarrhea, but it could induce it after parenteral administration, especially intravenous injection. All NSAID and SAID tested inhibited ETX-induced diarrhea at dose levels similar to or lower than those commonly producing an acute anti-inflammatory effect. The anti-diarrheal effects were found in not only acidic NSAID, but also in basic NSAID and SAID which did not inhibit ultraviolet erythema, acute death induced by arachidonic acid injection and PGs biosynthesis. Therefore, this test using ETX-induced diarrhea in mice may be used as a new and desirable method for screening or evaluating anti-inflammatory drugs. The mechanism of diarrhogenic action of ETX is poorly understood, but may be attributed to inhibition of PGs biosynthesis besides other unknown actions.

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Arachidonic Acid Causes Sudden Death in Rabbits

Cited by 246 publications

References 10 publications

Vasoconstrictor Response to Arachidonic Acid in the Isolated Hind Limb of the Dog

Vasoconstrictor Response to Arachidonic Acid in the Isolated Hind Limb of the Dog

Anti-thrombotic Activity of KBT-3022 in Experimental Models of Thrombosis

Effect of anti-inflammatory drugs on endotoxin-induced diarrhea in mice.

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