Prostaglandins do not modulate the positive chronotropic and inotropic effects of sympathetic nerve stimulation and injected norepinephrine in the isolated blood perfused canine atrium

Shigetoshi Chiba, Kafait Malik

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

In isolated canine atrium, perfused with blood from a donor dog, the infusions of both prostaglandins (PG)I2 and E2 (0.1-1 μg/min) into the sinus node arterial cannula neither altered the sinus rate and developed tension nor the positive chronotropic and inotropic responses elicited by either electrical stimulation or by injected norepinephrine. Infusion of arachidonic acid (10-100 μg/min), a precursor of PGs, or indomethacin (15-20 μg/min), an inhibitor of PG synthesis, into the sinus node arterial cannula also failed to alter the increase in sinus rate or developed tension produced by either adrenergic stimulus in the isolated atria. When arachidonic acid, 100-300 μg/kg or PGI2, 1 μg/kg, were injected into the jugular vein of the donor dog, they produced a fall in systemic blood pressure; this effect of arachidonic acid but not of PGI2 was abolished by indomethacin, 1 mg/kg. During administration of either arachidonic acid or indomethacin to the donor dog, the positive chronotripic and inotropic responses to adrenergic stimuli in the isolated atria also remained unaltered. These data indicate that PGs do not modulate adrenergic transmission in the blood perfused canine atrium.

Original languageEnglish (US)
Pages (from-to)687-695
Number of pages9
JournalLife Sciences
Volume28
Issue number6
DOIs
StatePublished - Feb 9 1981

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Arachidonic Acid
Prostaglandins
Canidae
Norepinephrine
Blood
Epoprostenol
Indomethacin
Adrenergic Agents
Sinoatrial Node
Dogs
Tissue Donors
Prostaglandin Antagonists
Jugular Veins
Blood pressure
Blood Donors
Dinoprostone
Electric Stimulation
Blood Pressure
Cannula

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

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title = "Prostaglandins do not modulate the positive chronotropic and inotropic effects of sympathetic nerve stimulation and injected norepinephrine in the isolated blood perfused canine atrium",
abstract = "In isolated canine atrium, perfused with blood from a donor dog, the infusions of both prostaglandins (PG)I2 and E2 (0.1-1 μg/min) into the sinus node arterial cannula neither altered the sinus rate and developed tension nor the positive chronotropic and inotropic responses elicited by either electrical stimulation or by injected norepinephrine. Infusion of arachidonic acid (10-100 μg/min), a precursor of PGs, or indomethacin (15-20 μg/min), an inhibitor of PG synthesis, into the sinus node arterial cannula also failed to alter the increase in sinus rate or developed tension produced by either adrenergic stimulus in the isolated atria. When arachidonic acid, 100-300 μg/kg or PGI2, 1 μg/kg, were injected into the jugular vein of the donor dog, they produced a fall in systemic blood pressure; this effect of arachidonic acid but not of PGI2 was abolished by indomethacin, 1 mg/kg. During administration of either arachidonic acid or indomethacin to the donor dog, the positive chronotripic and inotropic responses to adrenergic stimuli in the isolated atria also remained unaltered. These data indicate that PGs do not modulate adrenergic transmission in the blood perfused canine atrium.",
author = "Shigetoshi Chiba and Kafait Malik",
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AB - In isolated canine atrium, perfused with blood from a donor dog, the infusions of both prostaglandins (PG)I2 and E2 (0.1-1 μg/min) into the sinus node arterial cannula neither altered the sinus rate and developed tension nor the positive chronotropic and inotropic responses elicited by either electrical stimulation or by injected norepinephrine. Infusion of arachidonic acid (10-100 μg/min), a precursor of PGs, or indomethacin (15-20 μg/min), an inhibitor of PG synthesis, into the sinus node arterial cannula also failed to alter the increase in sinus rate or developed tension produced by either adrenergic stimulus in the isolated atria. When arachidonic acid, 100-300 μg/kg or PGI2, 1 μg/kg, were injected into the jugular vein of the donor dog, they produced a fall in systemic blood pressure; this effect of arachidonic acid but not of PGI2 was abolished by indomethacin, 1 mg/kg. During administration of either arachidonic acid or indomethacin to the donor dog, the positive chronotripic and inotropic responses to adrenergic stimuli in the isolated atria also remained unaltered. These data indicate that PGs do not modulate adrenergic transmission in the blood perfused canine atrium.

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