Abstract
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-PGF1α, 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-PGF1α 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-PGF1α 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-PFG1α 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-PFG1α 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 language | English (US) |
|---|---|
| Pages (from-to) | 554-559 |
| Number of pages | 6 |
| Journal | Surgery |
| Volume | 93 |
| Issue number | 4 |
| State | Published - 1983 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Surgery
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Modulation of cardiovascular function and platelet survival by endogenous prostacyclin released during surgery. / Krausz, Michael M.; Utsunomiya, Takayoshi; McIrvine, Andrew J.; Allen, Paul D.; Levine, Lawrence; Mannick, John A.; Shepro, David; Hechtman, Herbert B.
In: Surgery, Vol. 93, No. 4, 1983, p. 554-559.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Modulation of cardiovascular function and platelet survival by endogenous prostacyclin released during surgery
AU - Krausz, Michael M.
AU - Utsunomiya, Takayoshi
AU - McIrvine, Andrew J.
AU - Allen, Paul D.
AU - Levine, Lawrence
AU - Mannick, John A.
AU - Shepro, David
AU - Hechtman, Herbert B.
PY - 1983
Y1 - 1983
N2 - 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-PGF1α, 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-PGF1α 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-PGF1α 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-PFG1α 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-PFG1α 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.
AB - 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-PGF1α, 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-PGF1α 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-PGF1α 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-PFG1α 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-PFG1α 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.
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M3 - Article
C2 - 6340233
AN - SCOPUS:0020522278
VL - 93
SP - 554
EP - 559
JO - Surgery (United States)
JF - Surgery (United States)
SN - 0039-6060
IS - 4
ER -