Pulmonary and systemic vasodilator effect of the newly discovered prostaglandin PGI 2

P. J. Kadowitz, B. M. Chapnick, L. P. Feigen, A. L. Hyman, P. K. Nelson, E. W. Spannhake

Research output: Contribution to journalArticlepeer-review

Abstract

The effects of the newly discovered bicyclic prostaglandin, prostacyclin (PGI 2), on the pulmonary and systemic vascular beds were investigated in the anesthetized dog. PGI 2 decreased systemic and pulmonary arterial pressures in a dose-related manner when injected into the vena cava in doses of 1-30 μg. Since left ventricular end-diastolic, left atrial, and right atrial pressures were unchanged, and since cardiac output was increased or unchanged, pulmonary and systemic vascular resistances were decreased. PGI 2 was 10 times more potent than prostaglandins E 1 or E 2 in decreasing aortic pressure when injected intravenously, and the effects of PGI 2 on the systemic vascular bed were similar when injected into the vena cava or the left atrium. These data indicate that inactivation of PGI 2 is minimal in the lung. The stable prostacyclin metabolite, 6-keto-PGF1α, had little hemodynamic efects, suggesting that responses to PGI 2 were not due to formation of this metabolite. PGI 2 produced dose-dependent increases in blood flow in the mesenteric and renal vascular beds. These data demonstrate that PGI 2 has marked vasodilator activity in the pulmonary and systemic vascular beds and suggest that prostacyclin is the only known metabolite of arachidonic acid that dilates the pulmonary and systemic circulations.

Original languageEnglish (US)
Pages (from-to)408-413
Number of pages6
JournalJournal of Applied Physiology Respiratory Environmental and Exercise Physiology
Volume45
Issue number3
StatePublished - Dec 1 1978
Externally publishedYes

ASJC Scopus subject areas

  • Physiology
  • Endocrinology

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