The Release of Prostaglandins From Lung and Other Tissues

Piper, Priscilla J.; Vane, John R.

doi:10.1111/j.1749-6632.1971.tb53205.x

Cited by 634 publications

(189 citation statements)

References 36 publications

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“…from any part of the ventricular surface, and even into the subarachnoid space from the surface of the brain stem. Further, Piper & Vane (1971) have pointed W. FELDBERG AND K. P. GUPTA out that 'mammalian cells seem to disgorge prostaglandins at the slightest provocation' and the fever produced by the intraventricular injection of pyrogen may constitute such a slight provocation exerted locally at the ventricular surface and may thus not have been an exact reproduction of the mechanism by which fever is produced on i.v. injection.…”

Section: Discussionmentioning

confidence: 99%

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Pyrogen fever and prostaglandin‐like activity in cerebrospinal fluid

Feldberg¹,

Gupta²

1973

The Journal of Physiology

186

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1. In the unanaesthetized cat, rectal temperature was recorded and c.s.f. was collected from a Collison cannula implanted into the third ventricle with its opening lying in close proximity to the anterior hypothalamus. Samples of c.s.f. were collected from the same cat, during normal temperature, during fever produced by Shigella dysenteriae injected into the third ventricle and during the fall in temperature which occurred when the antipyretic paracetamol was injected intraperitoneally during the pyrogen fever. 2. The samples of c.s.f., when tested on the rat stomach fundus preparation, caused contractions which were not due, or at most to a small degree only, to 5‐hydroxytryptamine, as they were resistant to BOL. They were therefore probably due to a prostaglandin‐like substance. 3. When assayed against PGE1, the activity of c.s.f. collected from cats when their body temperature was normal corresponded to between 1·3 and 10 ng/ml. The values, whether low or high, rose over 2·5‐4 times to between 4 and 35 ng/ml. in c.s.f. collected during pyrogen fever; they were again low, between 1·5 and 6 ng/ml., in samples collected when the fever had been brought down by paracetamol, but rose again with the return of fever. 4. The results provide direct evidence for the theory that fever produced by pyrogens results from their ability to increase synthesis and release of prostaglandins, and that antipyretics bring down the fever because they inhibit the increased synthesis.

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Section: Discussionmentioning

confidence: 99%

“…This suggested rapid synthesis (Ramwell, Shaw, Douglas & Poisner, 1966; Davies, Horton & Withrington, 1968). In fact, as expressed by Piper & Vane (1971) prostaglandin release can often be equated with prostaglandin synthesis.…”

Section: Introductionmentioning

confidence: 99%

Pyrogen fever and prostaglandin‐like activity in cerebrospinal fluid

Feldberg¹,

Gupta²

1973

The Journal of Physiology

186

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“…In our experiments, the intramyocardial cell synthesis of PGL would be activated by the exogenous administration of its substrate, AA, while the release of PGL from the heart, although it may be an indication of de novo synthesis of PGL (Piper & Vane, 1971) could also indicate that a severe disturbance had affected the myocardium as a consequence of which the release of prostaglandin would take place; this opinion led Block et al (1974) to suggest...'that a local prostaglandin release does not contribute to the maintenance of coronary flow or the genesis of the anoxic-induced vasodilator response' beca tise the prerequisite for prostaglandin release in the heart is some form of cellular distortion produced for instance by traumatic stimuli, anoxia or embolization (Block et al, 1974). This opinion is supported by the observation that experimentally induced myocardial ischaemia is followed by the increase in prostaglandin release into the venous effluent of the coronaries in dogs (Berger, Zaret, Speroff, Cohen & Wolfson, 1976;Kraemer, Phernetton & Folts, 1976) and in humans with myocardial alterations induced by myocardial ischaemia (Berger, Zaret, Speroff, Cohen & Wolfson, 1977).…”

Section: Effect Of Non-steroidal Anti-inflammatory Agents On the Reacmentioning

confidence: 99%

Myocardial Synthesis of Prostaglandin‐like Substances and Coronary Reactions to Cardiostimulation and to Hypoxia

Sunahara

Talesnik

1979

British J Pharmacology

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1Continuous recording of cardiac contractions and coronary flow from isolated perfused hearts of rats permitted the study of coronary reactions to: (a) cardiostimulation induced by single doses or slow infusions of noradrenaline, CaCl2, glucagon or electrically induced tachycardia; (b) short interruptions of coronary inflow (hypoxia). 2 Except during tachycardia the heart rate was kept constant at 210 beats/min by electrical pacing. 3 Metabolic coronary vasodilatation (MCD) resulting from cardiac hyperactivity induced by noradrenaline, Ca2 +, tachycardia or glucagon was inhibited by administration of prostaglandin E2. Reactive hyperaemia response to hypoxia was unaffected by prostaglandin administration. 4 Inhibition of MCD could also be obtained by prolonged infusion with arachidonic acid (1.6 x 10'-M), presumably by its conversion into prostaglandin-like substance since arachidonic acid failed to block MCD in hearts from rats pretreated with non-steroidal anti-inflammatory drugs (indomethacin, naproxen, phenylbutazone). 5 Reactive hyperaemia was unaffected either by arachidonic acid or by blockade of the synthesis of prostaglandin-like substances by anti-inflammatory drugs. 6 Since prostaglandin synthetase inhibition does not prevent but may enhance MCD, we do not adtocate prostaglandin-like substances as agents directly responsible for the coronary vasodilatation that follows cardiac hyperactivity. 7 We postulate that cardiac overproduction of prostaglandins may lead to a failure in the adaptive coronary flow response to cardiac hyperactivity (coronary insufficiency?).

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“…Effects on the guinea-pig ileum could be due to PCPA methyl ester affecting calcium influx. In experiments using the superfused RSS and rat colon (Piper & Vane, 1971) Previously it has been shown that in the cat depletion of brain 5-hydroxytryptamine (5-HT) reduces the hyperthermic response to both bacterial pyrogen and prostaglandin El (PGE1) (Harvey & Milton, 1974). As both noradrenaline (NA) and 5-HT are thought to be concerned with temperature regulation in this species it was of interest, therefore, to determine whether depletion of brain catecholamines would also affect the response to hyperthermic agents.…”

Section: ) and Prostaglandinsmentioning

confidence: 99%

“…Inhibition of prostaglandin biosynthesis by aspirin-like drugs (Ferreira, Moncada & Vane, 1971; Smith & Willis, 1971;Vane, 1971) abolishes this sensitization and thereby produces analgesia.…”

Section: ) and Prostaglandinsmentioning

confidence: 99%

PROCEEDINGS OF THE British Pharmacological Society

1974

British J Pharmacology

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Guinea pigs were sensitized with ovalbumin (100 mg i.p. and s.c.) 3 weeks before the lungs were removed and perfused free of blood with Tyrode solution (Brocklehurst, 1960 author, an asterisk (*) denotes the one who mepyramine (5 x 10-7 g/ml) and the remainder extracted with two volumes of diethyl ether at pH 3. The organic extracts were examined in various thin layer chromatographic systems using parent vrostaglandins (PGs) as standards.Six radio-labelled peaks were seen on scanning the TLC plates, two major and four minor. Two peaks had similar RF values to PGE2 and PGF2a and a minor peak had the same RF as arachidonate. The other peaks are as yet unidentified but probably include 13-14 dihydro PGE2 and 13-14 dihydro 15-keto PGE2 (Anggard and Samuelsson, 1965) and possibly similar metabolic products of PGF2o, Eicosatetraynoic acid (TYA, 10 jg/ml), a competitive inhibitor of PG synthesis, or disodium cromoglycate (10 jug/ml) were added to the closed circuit perfusion system 60 min after the [14CI -arachidonate, thus reducing the possibility that these compounds may interfere with uptake rather than PG synthesis. The lungs were then challenged and samples collected and processed as before. Each experiment was repeated at least three times and similar results were obtained on each occasion.TYA reduced all the radio-labelled peaks whilst cromoglycate had no effect.

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The Release of Prostaglandins From Lung and Other Tissues

Cited by 634 publications

References 36 publications

Pyrogen fever and prostaglandin‐like activity in cerebrospinal fluid

Pyrogen fever and prostaglandin‐like activity in cerebrospinal fluid

Myocardial Synthesis of Prostaglandin‐like Substances and Coronary Reactions to Cardiostimulation and to Hypoxia

PROCEEDINGS OF THE British Pharmacological Society

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