Modulation of cardiovascular function and platelet survival by endogenous prostacyclin released during surgery

Michael M. Krausz, Takayoshi Utsunomiya, Andrew J. McIrvine, Paul D. Allen, Lawrence Levine, John A. Mannick, David Shepro, Herbert B. Hechtman

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


Surgery has been reported to stimulate production of the potent vasodilating and antiaggregating agent prostacyclin (PGI2). The consequences of this metabolic event were studied in 21 patients, with and without aspirin pretreatment, who underwent abdominal aortic aneurysmectomy. In eight patients who received a placebo, plasma concentration of 6-keto-PGF, the PGI2 degradation product rose from 35 to 950 pg/ml (P < 0.01) 30 minutes after the start of surgery. This was related to a decrease in mean arterial pressure (MAP), which averaged 12 torr (r = 0.73, P < 0.01), and an increase in cardiac index (CI), which averaged 0.5 l/min · m2 (r = 0.69, P < 0.01). Ex vivo adenosine diphosphate-induced platelet aggregation decreased 28% (P < 0.001). After aortic clamping, the stable degradation product of thromboxane (Tx) A2, TxB2, increased from 68 to 111 pg/ml (P < 0.025), and the platelet count decreased from 190,000 to 147,000/mm3 (P < 0.025). In contrast, the concentrations of 6-keto-PGF and TxB2 were unchanged during surgery in 13 patients who received 650 mg aspirin 12 hours before operation. After the incision, the MAP increased 25 torr (P < 0.05); the CI and platelet aggregation were unchanged. The preoperative platelet counts were 211,000/mm3 in controls and 190,000/mm3 in aspirin-treated patients, whereas after 24 hours platelet counts averaged 156,000 and 105,000/mm3, respectively (P < 0.01). In vitro incubation of sections from the aneurysm wall in Ringer's solution led to a 60-fold greater production of 6-keto-PGF in controls as compared to aspirin-treated patients. In a parallel experiment with ten dogs, barbiturate anesthesia and mechanical ventilation led to a small increase in 6-keto-PFG from 23 to 56 pg/ml, whereas 10 minutes after the start of surgery, the levels increased to 257 pg/ml (P < 0.005) without a change in TxB2. Arterial concentrations of 6-keto-PFG were higher in every animal (P < 0.05), suggesting that the lungs were at least partially responsible for the increased prostaglandin synthesis. A decrease in ex vivo platelet aggregation and MAP and a rise in cardiac output were noted, events prevented in five dogs pretreated with indomethacin (5 mg/kg). These data indicate that surgery stimulates production of PGI2, a metabolic event associated with systemic hemodynamic and antiaggregatory consequences.

Original languageEnglish (US)
Pages (from-to)554-559
Number of pages6
Issue number4
StatePublished - 1983
Externally publishedYes

ASJC Scopus subject areas

  • Surgery


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