Anesthetic induction with ketamine inhibits platelet activation before, during, and after cardiopulmonary bypass in baboons

Akif Undar, Harald C. Eichstaedt, Fred J. Clubb, Mason Lu, Joyce E. Bigley, Blake A. Deady, Aimee Porter, William K. Vaughn, Michael Fung

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

The objective of this study was to investigate the effects of antifactor D monoclonal antibody (Mab) 166-32 on platelet activation during and after hypothermic cardiopulmonary bypass (CPB) in baboons. Fourteen baboons (mean weight, 15 kg) underwent hypothermic CPB. Seven of them were treated with a single injection of antifactor D Mab 166-32 (5 mg/kg) and the other seven animals were given saline as control. Each baboon was sedated with an intramuscular injection of 10 mg/kg of ketamine hydrochloride. A 20-gauge angiocatheter was placed in the cephalic vein, and 5 mg of diazepam was administered intravenously. Anesthesia was maintained with 0.80% to 2.25% isoflurane, 100% O2, and an inspiratory tidal volume of 13 mL/kg at a rate of 13 breaths per minute throughout the surgical procedure except during CPB. Pancuronium bromide, 0.1 mg/kg, was administered to achieve adequate muscle paralysis. Blood samples were collected before CPB, during CPB, and 1,2,3, and 6 h after CPB. Assays were performed to measure platelet activation [CD62P (P-selectin)] using immunofluorocytometric methods. There were no significant differences on CD62P expression of platelets between control and antibody groups before CPB (105 ± 12% vs. 99 ± 8%, P = NS), during normothermic CPB (62 ± 6% vs. 63 ± 19%, P = NS), during hypothermic CPB (55 ± 8% vs. 54 ± 13%, P = NS), and 1, 3, or 6 h after CPB (74 ± 20% vs. 81 ± 11%, P = NS). Anesthetic induction with ketamine caused significant reduction in the platelet activation in both groups. Ketamine did not affect complement, neutrophil, and monocyte activation or cytokine production. Further studies on the mechanisms of platelet inhibition by ketamine are warranted.

Original languageEnglish (US)
Pages (from-to)959-962
Number of pages4
JournalArtificial organs
Volume28
Issue number10
DOIs
StatePublished - Oct 1 2004

Fingerprint

Anesthetics
Papio
Platelet Activation
Ketamine
Platelets
Cardiopulmonary Bypass
Chemical activation
Monoclonal antibodies
Monoclonal Antibodies
Pancuronium
P-Selectin
montirelin
Isoflurane
Diazepam
Antibodies
Gages
Muscle
Assays
Animals
Blood

All Science Journal Classification (ASJC) codes

  • Bioengineering
  • Medicine (miscellaneous)
  • Biomaterials
  • Biomedical Engineering

Cite this

Undar, Akif ; Eichstaedt, Harald C. ; Clubb, Fred J. ; Lu, Mason ; Bigley, Joyce E. ; Deady, Blake A. ; Porter, Aimee ; Vaughn, William K. ; Fung, Michael. / Anesthetic induction with ketamine inhibits platelet activation before, during, and after cardiopulmonary bypass in baboons. In: Artificial organs. 2004 ; Vol. 28, No. 10. pp. 959-962.
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title = "Anesthetic induction with ketamine inhibits platelet activation before, during, and after cardiopulmonary bypass in baboons",
abstract = "The objective of this study was to investigate the effects of antifactor D monoclonal antibody (Mab) 166-32 on platelet activation during and after hypothermic cardiopulmonary bypass (CPB) in baboons. Fourteen baboons (mean weight, 15 kg) underwent hypothermic CPB. Seven of them were treated with a single injection of antifactor D Mab 166-32 (5 mg/kg) and the other seven animals were given saline as control. Each baboon was sedated with an intramuscular injection of 10 mg/kg of ketamine hydrochloride. A 20-gauge angiocatheter was placed in the cephalic vein, and 5 mg of diazepam was administered intravenously. Anesthesia was maintained with 0.80{\%} to 2.25{\%} isoflurane, 100{\%} O2, and an inspiratory tidal volume of 13 mL/kg at a rate of 13 breaths per minute throughout the surgical procedure except during CPB. Pancuronium bromide, 0.1 mg/kg, was administered to achieve adequate muscle paralysis. Blood samples were collected before CPB, during CPB, and 1,2,3, and 6 h after CPB. Assays were performed to measure platelet activation [CD62P (P-selectin)] using immunofluorocytometric methods. There were no significant differences on CD62P expression of platelets between control and antibody groups before CPB (105 ± 12{\%} vs. 99 ± 8{\%}, P = NS), during normothermic CPB (62 ± 6{\%} vs. 63 ± 19{\%}, P = NS), during hypothermic CPB (55 ± 8{\%} vs. 54 ± 13{\%}, P = NS), and 1, 3, or 6 h after CPB (74 ± 20{\%} vs. 81 ± 11{\%}, P = NS). Anesthetic induction with ketamine caused significant reduction in the platelet activation in both groups. Ketamine did not affect complement, neutrophil, and monocyte activation or cytokine production. Further studies on the mechanisms of platelet inhibition by ketamine are warranted.",
author = "Akif Undar and Eichstaedt, {Harald C.} and Clubb, {Fred J.} and Mason Lu and Bigley, {Joyce E.} and Deady, {Blake A.} and Aimee Porter and Vaughn, {William K.} and Michael Fung",
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Undar, A, Eichstaedt, HC, Clubb, FJ, Lu, M, Bigley, JE, Deady, BA, Porter, A, Vaughn, WK & Fung, M 2004, 'Anesthetic induction with ketamine inhibits platelet activation before, during, and after cardiopulmonary bypass in baboons', Artificial organs, vol. 28, no. 10, pp. 959-962. https://doi.org/10.1111/j.1525-1594.2004.07377.x

Anesthetic induction with ketamine inhibits platelet activation before, during, and after cardiopulmonary bypass in baboons. / Undar, Akif; Eichstaedt, Harald C.; Clubb, Fred J.; Lu, Mason; Bigley, Joyce E.; Deady, Blake A.; Porter, Aimee; Vaughn, William K.; Fung, Michael.

In: Artificial organs, Vol. 28, No. 10, 01.10.2004, p. 959-962.

Research output: Contribution to journalArticle

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T1 - Anesthetic induction with ketamine inhibits platelet activation before, during, and after cardiopulmonary bypass in baboons

AU - Undar, Akif

AU - Eichstaedt, Harald C.

AU - Clubb, Fred J.

AU - Lu, Mason

AU - Bigley, Joyce E.

AU - Deady, Blake A.

AU - Porter, Aimee

AU - Vaughn, William K.

AU - Fung, Michael

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N2 - The objective of this study was to investigate the effects of antifactor D monoclonal antibody (Mab) 166-32 on platelet activation during and after hypothermic cardiopulmonary bypass (CPB) in baboons. Fourteen baboons (mean weight, 15 kg) underwent hypothermic CPB. Seven of them were treated with a single injection of antifactor D Mab 166-32 (5 mg/kg) and the other seven animals were given saline as control. Each baboon was sedated with an intramuscular injection of 10 mg/kg of ketamine hydrochloride. A 20-gauge angiocatheter was placed in the cephalic vein, and 5 mg of diazepam was administered intravenously. Anesthesia was maintained with 0.80% to 2.25% isoflurane, 100% O2, and an inspiratory tidal volume of 13 mL/kg at a rate of 13 breaths per minute throughout the surgical procedure except during CPB. Pancuronium bromide, 0.1 mg/kg, was administered to achieve adequate muscle paralysis. Blood samples were collected before CPB, during CPB, and 1,2,3, and 6 h after CPB. Assays were performed to measure platelet activation [CD62P (P-selectin)] using immunofluorocytometric methods. There were no significant differences on CD62P expression of platelets between control and antibody groups before CPB (105 ± 12% vs. 99 ± 8%, P = NS), during normothermic CPB (62 ± 6% vs. 63 ± 19%, P = NS), during hypothermic CPB (55 ± 8% vs. 54 ± 13%, P = NS), and 1, 3, or 6 h after CPB (74 ± 20% vs. 81 ± 11%, P = NS). Anesthetic induction with ketamine caused significant reduction in the platelet activation in both groups. Ketamine did not affect complement, neutrophil, and monocyte activation or cytokine production. Further studies on the mechanisms of platelet inhibition by ketamine are warranted.

AB - The objective of this study was to investigate the effects of antifactor D monoclonal antibody (Mab) 166-32 on platelet activation during and after hypothermic cardiopulmonary bypass (CPB) in baboons. Fourteen baboons (mean weight, 15 kg) underwent hypothermic CPB. Seven of them were treated with a single injection of antifactor D Mab 166-32 (5 mg/kg) and the other seven animals were given saline as control. Each baboon was sedated with an intramuscular injection of 10 mg/kg of ketamine hydrochloride. A 20-gauge angiocatheter was placed in the cephalic vein, and 5 mg of diazepam was administered intravenously. Anesthesia was maintained with 0.80% to 2.25% isoflurane, 100% O2, and an inspiratory tidal volume of 13 mL/kg at a rate of 13 breaths per minute throughout the surgical procedure except during CPB. Pancuronium bromide, 0.1 mg/kg, was administered to achieve adequate muscle paralysis. Blood samples were collected before CPB, during CPB, and 1,2,3, and 6 h after CPB. Assays were performed to measure platelet activation [CD62P (P-selectin)] using immunofluorocytometric methods. There were no significant differences on CD62P expression of platelets between control and antibody groups before CPB (105 ± 12% vs. 99 ± 8%, P = NS), during normothermic CPB (62 ± 6% vs. 63 ± 19%, P = NS), during hypothermic CPB (55 ± 8% vs. 54 ± 13%, P = NS), and 1, 3, or 6 h after CPB (74 ± 20% vs. 81 ± 11%, P = NS). Anesthetic induction with ketamine caused significant reduction in the platelet activation in both groups. Ketamine did not affect complement, neutrophil, and monocyte activation or cytokine production. Further studies on the mechanisms of platelet inhibition by ketamine are warranted.

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