Lack of Release of Prostaglandins From Isolated Per-Fused Lungs During Pulmonary Hypertension and Oedema

Scott, Elizabeth; Vaage, Jarle; T, Wiberg

doi:10.1111/j.1476-5381.1979.tb07819.x

Cited by 3 publications

(2 citation statements)

References 22 publications

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“…In one of the two cases where fulminant alveolar edema developed no PGLS appeared. Recently we have found in isolated, perfused lungs that no PGLS were detected in spite of gross alveolar edema and hypertension (Scott, Vaage & Wiberg 1979), indicating that the release detected in the present work is dependent on the intact state of the animal and probably not due to direct mechanical effects on the lungs. The elevation of Pi.., is a marked strain on the animal.…”

Section: Discussionsupporting

confidence: 44%

Release of prostaglandin‐like substances during elevations of left atrial pressure in the cat

Vaage

Scott

1979

Acta Physiologica Scandinavica

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The purpose of the present work was to measure prostaglandin (PG)-like activity in arterial blood during acute pulmonary hypertension. Anesthetized cats with the chest opened and given positive pressure ventilation were used. A balloon in the left atrium was inflated to elevate hydrostatic vascular pressure in the lungs. Blood was pumped (10 ml/min) from a carotid artery to superfuse 3 smooth muscle tissues: rat stomach strip, rat colon and chick rectum: the blood was then returned to the jugular vein by gravity. The assay tissues were pretreated with antagonists against catecholamines, histamine, serotonin and acetylcholine during the experiments. They were sensitive to calibrating doses of 2 ng/ml of PGF2 alpha and 1 ng/ml of PGE2. 18 periods with elevated left atrial pressure (P LA) (21--49 mmHg), lasting 2--26 min, were applied in 9 cats. This manoevre usually also caused systemic hypotension. 14 of these PLA elevations were accompanied by increased arterial PG-like activity, which rapidly subsided when the pressure was released or when indomethacin (2 mg/kg, n = 4) was given i.v. In 3 additional experiments it was found that pulmonary degradation of PGs was unaffected during P LA elevation. I.v. infusion of angiotensin II contracted the tissues in a pattern different from that caused by pressure elevations and the PG calibrations, and these contractions were not affected by indomethacin. This indicates that the assay tissue contractions cannot be caused by angiotensin II which alone does not increase PG-like activity in arterial blood. Consequently, acute pulmonary vascular hypertension appears to stimulate PG synthesis and release in lungs of intact cats.

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Section: Discussionsupporting

confidence: 44%

Release of prostaglandin‐like substances during elevations of left atrial pressure in the cat

Vaage

Scott

1979

Acta Physiologica Scandinavica

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“…Initial efforts by other workers at demonstrating the presence of and identifying a vasodilator PG employed classical tissue cascade bioassay techniques and radioimmunoassays of PGE and PGF2,, (19,25,29). Augmentation of PG synthesis by hypoxic pulmonary vasoconstriction was not detected in these studies.…”

Section: Resultsmentioning

confidence: 99%

Hypoxia Stimulates Prostacyclin Synthesis by Neonatal Lungs

Green

Leffler

1984

Pediatr Res

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Summarysynthesis of a vasodilator PG that reduces the vasoconstriction.Inhibition of prostaglandin cyclooxygenase augments hypoxic pulmonary vasoconstriction. We used a neonatal lamb lung preparation perfused with Krebs' bicarbonate buffer to characterize and quantify prostanoids produced by the pulmonary vasculature from endogenous arachidonic acid in the absence of formed blood elements during ventilation with normoxic and hypoxic gas mixtures. Prostaglandin (PG) 12 synthesis increased from 6.4 + 2.7 ng/min (SEM) during normoxic ventilation to 14.3 f 5.4 ng/min during hypoxia and returned to 4.7 f 1.2 ng/min with resumption of normoxia. These data demonstrate that hypoxia stimulates pulmonary vascular synthesis of prostaglandin I2 from endogenous substrate in neonatal lambs and suggest that the augmentation of hypoxic pulmonary vasoconstriction by prostaglandin cyclooxygenase inhibition is due, at least in part, to interference with the synthesis of this vasodilator prostanoid. Abbreviations PG, prostanoid PG12, prostacyclin TXB2, thromboxane B2Inhibition of prostaglandin cyclooxygenase augments hypoxic pulmonary vasoconstriction in adult mammals of several species (1,12,24,27,28). A possible explanation for this observation is that hypoxia or hypoxic pulmonary vasoconstriction induces the ~nhibition of PG synthesis would remove this vasodilator PG and, thus, increase the hypoxic constriction. Indirect evidence supporting this hypothesis in the neonate includes the observations that: 1) PGIa is the most abundant PG produced by fetal bovine pulmonary arterial slices (22); 2) under normoxic conditions, PGI? is the most abundant PG produced by the newly ventilated neonatal lamb lung (10, 11); 3) PG12 is a pulmonary vasodilator in the fetal and neonatal lamb (3, 9, 13), and its vasodilatory effect on the neonatal pulmonary vasculature is more evident during hypoxic pulmonary vasoconstriction (13); and 4) hypoxic pulmonary vasoconstriction in premature and term neonatal goats is augmented by indomethacin, an inhibitor of PG synthesis (23). In the present study, we used a neonatal lamb lung preparation perfused with Krebs' bicarbonate buffer to characterize and quantify prostanoids produced by the pulmonary vasculature from endogenous arachidonic acid in the absence of formed blood elements. Pulmonary perfusate was collected during ventilation with normoxic and hypoxic gas mixtures. Analysis of these perfusates allowed determination of the effect of hypoxic pulmonary vasoconstriction on pulmonary vascular prostanoid synthesis. MATERIALS AND METHODSAnimalpreparation. Fourteen neonatal lambs [10.7 & 2.0 days old (SEM); 5.5 +. 1.6 kg) were anesthetized with 50 mg/kg achloralose IV. A tracheostomy was performed, and ventilation with room air was begun using a constant volume ventilator. A left thoracotomy was performed and the left lung was removed, leaving the mediastinum intact. Consequently, the right lung, which was to be perfused, was not exposed to the environment. The tidal volume was reduced by approximately 40%...

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