Actions of Prostaglandins E1 and F2  on Isolated Intrapulmonary Vascular Smooth Muscle

Pd, Joiner; Pj, Kadowitz; Jp, Hughes; Al, Hyman

doi:10.3181/00379727-150-39047

Cited by 11 publications

(14 citation statements)

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“…PGF2,, induced only weak contractile responses of canine intrapulmonary arteries, even at extremely high concentrations. These findings are in contrast to the potent pulmonary arterial constrictions demonstrated for the prostaglandins in other mammals (Lewis & Eyre, 1972;Burka & Eyre, 1974;Kadowitz et al, 1975;Chand & Eyre, 1977;Chand & Altura, 1980a, c noted by others for PGF2a (Lewis & Eyre, 1972;Burka & Eyre, 1974;Joiner et al, 1975;Ketamura et al, 1976;Chand & Eyre, 1977;Gruetter et al, 1978;Dusting et al, 1979). Whether or not such findings are suggestive of a role for PGF's in the pathophysiology of the pulmonary vasculature remains unclear, especially in view of the rapid metabolism of these primary prostaglandins by the lungs (Dusting et al, 1979).…”

Section: Discussioncontrasting

confidence: 60%

“…Earlier, prostaglandins of the A and E series have been shown to induce relaxations of canine isolated intrapulmonary arteries (Joiner, Kadowitz, Hughes & Hyman, 1975;. Recently, in our laboratory, we were unable to demonstrate any relaxant effects of prostaglandins E I, E2, A1 or A2 on isolated pulmonary arteries of the 0007-1188/81/080819-09 $01.00 rat (Chand & Altura, 1980a, b, c).…”

Section: Introductionmentioning

confidence: 64%

“…The vascular effects of prostaglandins of the E series are highly variable, depending upon the concentration, species, region, blood vessels, media and spasmogen used to induce tone (Lewis & Eyre, 1972;Burka & Eyre, 1974;Joiner et al, 1975;Altura & Edgarian, 1976;Kitamura, Suzuki & Kuriyama, 1976;Chand & Eyre, 1977;Altura et al, 1980b;Chand & Altura, 1980a, c (Chand & Altura, 1980a, c Su & Bevan, 1976;Dusting et al, 1979), and variability from segment to segment of the individual (Somlyo & Somlyo, 1970;Chand & Altura, 1980a;1980c), together with the rapid pulmonary metabolism of PGE, and PGE2 (Dusting et al, 1979), it is doubtful whether either of these primary prostaglandins plays an important role. in regulating the pulmonary vasculature in either the dog or rat.…”

Section: Discussionmentioning

confidence: 99%

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Differential Effects of Prostaglandins on Canine Intrapulmonary Arteries and Veins

Altura

Chand

1981

British J Pharmacology

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1 The sensitivity and contractility of isolated canine intrapulmonary arteries and veins to a variety of primary prostaglandin compounds was studied.2 Intrapulmonary arteries produced no measurable contractile responses to prostaglandin A, (PGA,), PGA2, PGB,, PGD2, PGE,, PGE2 or to PGFI,. However, high concentrations of both PGB2 (> 10-7 M) and PGF2a (> 10-6 M) elicited concentrated-related, but weak, contractile responses, measuring only 5-25% of KCI-induced maximum contractions. 3 Intrapulmonary arteries, partially contracted by 5-hydroxytryptamine (5-HT), exhibited concentration-related relaxations in response to PGE,; PGE2, PGA, or PGA2 produced only weak superimposed con)actions. 4 In contrast to intrapulmonary arteries, intrapulmonary veins contracted in a concentrationrelated fashion to all prostaglandins tested, where the contractile sensitivity was (based on EC50 s and threshold concentrations): PGB2 > PGB, > PGD2 > PGF2a > PGA2 >> PGA, > PGFi, > PGE, > PGE,. 5 In terms of the ability to generate maximum contractile responses on intrapulmonary veins, the prostaglandins were also variable, with PGA2 and PGB2 being the most potent and PGD2 the least potent. 6 Intrapulmonary veins, partially contracted by 5-HT, exhibited concentration-related relaxations to PGE, at low concentrations, followed by secondary contractile responses at higher concentrations. 7 Neither PGA1 nor PGA2 (3.4 x 10-# to 3.4 x 10-5 M) inhibited or potentiated 5-HT responses of intrapulmonary arteries. 8 These data suggest that there are species, regional and major qualitative and quantitative, differences in the responsiveness of intrapulmonary arteries and veins to prostaglandin.

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Section: Discussioncontrasting

confidence: 60%

Section: Introductionmentioning

confidence: 64%

Section: Discussionmentioning

confidence: 99%

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Differential Effects of Prostaglandins on Canine Intrapulmonary Arteries and Veins

Altura

Chand

1981

British J Pharmacology

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“…Of numerous experimental models used to simulate acute pulmonary hyperten sion, arachidonic by-products have been shown to elicit transient vasoconstrictive states mimicking pulmonary hypertension [4]. Previous studies revealed that PGF2(I con stricts both pulmonary veins and arteries [ 17,18]. In our investigation, PGF?« elicited sig nificant changes in PAP without affecting SAP.…”

Section: Discussionmentioning

confidence: 62%

Effects of PGE<sub>1</sub> in Experimental Vasoconstrictive Pulmonary Hypertension

Dagher

Dumont²,

Chartrand³

et al. 1993

Eur Surg Res

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The pulmonary vascular and systemic effects of PGE₁ were studied in a canine model of pulmonary hypertension. Systemic arterial, central venous and pulmonary arterial pressures were monitored and an electromagnetic flow probe was placed around the ascending aorta for continuous cardiac index (CI) measurements. Through a laparotomy, an arteriovenous fistula was created between the abdominal aorta and inferior vena cava. Gradual opening of this fistula significantly affected CI and these values were used to generate pressure-flow curves (pulmonary arterial pressure (PAP)/Cl). Following PGF_2α infusion (5–10 µg/kg/min) significant pulmonary hypertension was observed (2- to 3-fold increase in PAP). PGF_2α infusion also resulted in a significant rise in heart rate and systemic vascular resistance (SVR) while CI was reduced. PGF_2α significantly increased both the line slope (vascular resistance) and intercept (outflow pressure) of the pressure-flow curves. Intravenous PGE₁ infusion in doses ranging from 40 to 320 ng/ml/min elicited a dose-dependent reduction of both pulmonary and systemic vascular resistances, the former being slightly more affected. With PGE₁ infusions only the intercept of the pressure-flow curve was affected suggesting that specific components of the pulmonary vascular bed modulating the outflow pressure were involved. High doses of PGE₁ significantly decreased arterial Po₂, indicating that this prostaglandin derivative deteriorates pulmonary gas exchanges.

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“…The effects of different prostaglandins on isolated vascular smooth muscles have been reported to vary greatly with the species, vascular bed and tone of the vessels (Joiner, Kadowitz, Hughes & Hyman, 1975).…”

Section: Discussionmentioning

confidence: 99%

Anaphylactic Contraction of Pulmonary Blood Vessels of Chicken

Chand

Eyre

1977

British J Pharmacology

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1Isolated pulmonary arterial and vein strips from sensitized or non-sensitized chickens exhibited dose-dependent contractions to adrenaline>, noradrenaline>, 5-hydroxytryptamine>, histamine>, dopamine. Individual variability in the responsiveness of the vessels to agonists was marked. In general veins were 2 to 25 times more sensitive to agonists than arterial strips. 2 Isoprenaline (a relatively specific ,B-adrenoceptor agonist) induced relaxations of the submaximally contracted pulmonary vein and arteries at low doses and contractions at high concentrations. 3 Contractile responses to acetylcholine or carbachol were not regularly recorded; only 50% of the vessels reacted to cholinoceptor agonists over a wide threshold dose range. 4 Chicken pulmonary vessels were found relatively insensitive to bradykinin. 5Effects of prostaglandins were variable. Prostaglandin Fm induced dose-related contractions of the vein and arterial strips; prostaglandins E1 and E2 at low doses relaxed partially contracted pulmonary artery irrespective of the spasmogen used and further increase in doses induced either no effect or contractions. Prostaglandin E1 induced marked and rapid contractions of the vein.Prostaglandin E2 induced relaxations of the prostaglandin Fm-contracted vein only, but produced no effect or slight contractions of the veins partially contracted to other spasmogens. 6 Pulmonary arterial and vein strips obtained from chickens sensitized to horse plasma exhibited Schultz-Dale contractions of variable magnitude and duration to specific antigenic challenge only. In many vessels, antigen-induced contractions were associated with marked increase in spontaneous activity. 7 The importance of the Schultz-Dale reaction in avian pulmonary vessels is discussed in relation to the right heart dilatation associated with anaphylaxis in the chicken.

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Actions of Prostaglandins E1 and F2 on Isolated Intrapulmonary Vascular Smooth Muscle

Cited by 11 publications

References 0 publications

Differential Effects of Prostaglandins on Canine Intrapulmonary Arteries and Veins

Differential Effects of Prostaglandins on Canine Intrapulmonary Arteries and Veins

Effects of PGE<sub>1</sub> in Experimental Vasoconstrictive Pulmonary Hypertension

Anaphylactic Contraction of Pulmonary Blood Vessels of Chicken

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