Platelet aggregation is impaired during anaesthesia with sevoflurane but not with isoflurane

Hirakata, Hideo; Nakamura, Kumi; Sai, Satoko; Okuda, Hiroto; Hatano, Yoshio; Urabe, Nobukata; Mori, Kenjiro

doi:10.1007/bf03013337

Cited by 36 publications

(26 citation statements)

References 20 publications

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“…12 Similar results were also obtained by Hirakata et al as they demonstrated that in patients anesthetized with sevoflurane, but not isoflurane, secondary platelet aggregation could not be induced by adenosine diphosphate (ADP) and epinephrine. 13 However, the same group demonstrated in vitro that although isoflurane was less potent than halothane and enflurane, it could inhibit thromboxane A 2 induced platelet aggregation in a dose-dependent manner. There was a 50% inhibition with a concentration of 15.7 mM (corresponding to 24 minimum alveolar anesthetic concentration, roughly 20 times the usual concentration in humans) added in the platelet preparation.…”

Section: Discussionmentioning

confidence: 99%

La technique anesthésique n’affecte pas la performance d’un modèle de réductions cycliques de flot chez le lapin : une étude pilote

Charbonneau

Girard

Boudreault

et al. 2007

Can J Anesth/J Can Anesth

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Purpose: Pentobarbital anesthesia is, typically, used in an experimental model of cyclic flow reductions (CFR) in rabbits. Our initial observations, using a more complete and effective isoflurane-based anesthetic technique, failed to reproduce findings reported previously. Consequently, we compared the effects of these two anesthetic techniques in the model. Methods:A modified Folts' model of carotid artery lesion and stenosis was used. Twelve rabbits completed the experimental protocol: five in the pentobarbital group (P) and seven in the isoflurane group (I). The carotid artery was exposed and flow was reduced by application of a clamp. A standardized injury was performed by cross clamping the artery with a needle forceps and this produced CFR. The number of CFR and the duration of their occurrence were noted. The incidence of thrombosis was compared in each group as well as hemodynamic, hematologic and bleeding time values. Results:The hematocrit value, platelet count and bleeding time were similar in both groups. The median number and range of CFR [group P: 9 (4-16) ; group I: 9 (5-14)] and the time span of effective CFR formation (group P: 39 ± 17; group I: 38 ± 25 min) were comparable in both groups. The incidence of complete thrombosis of the carotid artery was similar in both groups. Conclusions:The stability of the model is of short duration, but the occurrence of CFR is not affected by the type of anesthesia. Our findings suggest that the ideal duration of the experimental protocol should be between 30 and 45 min in order to maximize the number of animals still developing CFR. [groupe P : 9 (4-16) ; groupe I : 9 (5-14)] ainsi que la durée pendant laquelle les CFR avaient lieu (groupe P : 39 ±17 ; groupe I : 38 ± 25 min) Méthode : Un modèle de Folts modifié de lésion de l'artère carotide et de sténose a été utilisé. Douze lapins ont pris part au protocole expérimental : cinq dans le groupe pentobarbital (P), et sept dans le groupe isoflurane (I). L'artère carotide a été exposée et le

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Section: Discussionmentioning

confidence: 99%

La technique anesthésique n’affecte pas la performance d’un modèle de réductions cycliques de flot chez le lapin : une étude pilote

Charbonneau

Girard

Boudreault

et al. 2007

Can J Anesth/J Can Anesth

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“…We are unable to comment on the clinical value of these changes due to our limited sample size, but further study is merited as sevoflurane has been shown to inhibit platelet aggregation induced by adenosine diphosphate [9,10].…”

Section: Discussionmentioning

confidence: 93%

Platelet Function as Affected by Total Intravenous and Inhalational Anesthesia

Cattano

Gomez-Rivera

Seitan

et al. 2013

J Anesthe Clinic Res

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Propofol is a frequent choice of hypnotic anesthetic for TIVA due to its role as a vasodilator [1]. The advantages for ESS of a lower patient blood pressure, however, may be negated by reports that propofol has an adverse effect on blood coagulation [1][2][3][4][5][6]. The choice of anesthesia regimen is further complicated by research indicating inhalational anesthetics also inhibit platelet aggregation [5,6].The purpose of this study was to investigate the potential differences in effects of two anesthesia regimens by measuring blood loss and platelet function. It was our hypothesis that, for the purposes of ESS, TIVA with propofol/remifentanyl would result in reduced blood loss than inhalational anesthesia with sevoflurane/remifentanyl. MethodsThis study was registered with the National Institutes of Health and can be found at http://clinicaltrials.gov/ct2/show/NCT01214057. After obtaining approval from the Committee for the Protection of Human Subjects, 23 patients aged 18-80, American Society of Anesthesia (ASA) grade I or II, scheduled to undergo endoscopic sinus surgery (ESS) for chronic rhinosinusitis were screened, consented and enrolled. Exclusion criteria included known coagulopathy or use of any drug that could affect thrombocyte function (e.g., aspirin, clopidogrel). Anesthetic ProtocolPatients were randomly assigned using a blocked randomization method to receive either propofol/remifentanil (PR, n=12) or sevoflurane/remifentanil (SR, n=11) general anesthesia. Both patients and surgeons were blinded to the type of anesthetic used. Patients were premedicated in the holding area with dexamethasone and midazolam. The patients were monitored by American Society of Anesthesia (ASA) standards with ECG, non-invasive blood pressure, pulse oximetry and temperature probe. Their blood pressure was recorded every 2 minutes for the first 10 minutes, then every 5 minutes.In order to reduce the visual bias of a propofol infusion, anesthesia was induced in both SR and PR groups with lidocaine 0.5 mg/kg, propofol infusion at 250 mcg/kg/min and total volume infused was adjusted for an induction dose of 2-3 mg/kg before bolus of muscle relaxant, rocuronium 0.5 mg/kg. Remifentanil infusion was started at a rate of 0.4 mcg/kg/min one to two minutes before the propofol infu- AbstractBackground: Few studies have attempted to demonstrate a benefit of a total intraveneous anesthesia (TIVA) as the sole technique to optimize and reduce bleeding. Also few reports have linked the use of propofol to platelet dysfunction, and while Thromboelastography (TEG ® ) has been used previously, its complement platelet mapping (PM™) has not. The aim of the study was to exclude different causes for blood loss during surgery, including drug effects on platelet function. Methods:After IRB approval, we studied 23 patients scheduled to undergo endoscopic sinus surgery. Using a double-blind experimental method, we randomly assigned patients to receive either TIVA with propofol/remifentanil (PR) or inhalational anesthesia with sevoflurane/remi...

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“…Several anesthetic agents, including volatile and intravenous anesthetics, are reported to affect human platelets through different mechanisms [1,8,15]. The principal objective of this study was to describe the detailed mechanisms involved in the inhibition of agonist-induced human platelet aggregation by ketamine.…”

Section: Discussionmentioning

confidence: 99%

“…For example, triazolam and alprazolam inhibit platelet-activating factor (PAF)-induced aggregation [16], and the inhibition of PAF binding to platelets has been proposed to explain this anti-aggregatory effect [5]. Furthermore, the inhibitory effects of halothane and sevoflurane on human platelet aggregation have been shown in in vitro and in vivo studies [8,15]. On the other hand, studies of ketamine in platelets have relatively rarely been com-pared with other sedative-hypnotic drugs or anesthetics.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms Involved in the Antiplatelet Activity of Ketamine in Human Platelets

Chen¹,

Chen²,

Wu³

et al. 2004

J Biomed Sci

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The aim of this study was to systematically examine the inhibitory mechanisms of ketamine in platelet aggregation. In this study, ketamine concentration-dependently (100–350 µM) inhibited platelet aggregation both in washed human platelet suspensions and platelet-rich plasma stimulated by agonists. Ketamine inhibited phosphoinositide breakdown and intracellular Ca²⁺ mobilization in human platelets stimulated by collagen. Ketamine (200 and 350 µM) significantly inhibited thromboxane (Tx) A₂formation stimulated by collagen. Moreover, ketamine (200 and 350 µM) increased the fluorescence of platelet membranes tagged with diphenylhexatriene. Rapid phosphorylation of a platelet protein of Mr 47,000 (P47), a marker of protein kinase C activation, was triggered by phorbol-12,13-dibutyrate (100 nM). This phosphorylation was markedly inhibited by ketamine (350 µM). These results indicate that the antiplatelet activity of ketamine may be involved in the following pathways. Ketamine may change platelet membrane fluidity, with a resultant influence on activation of phospholipase C, and subsequent inhibition of phosphoinositide breakdown and phosphorylation of P47, thereby leading to inhibition of intracellular Ca²⁺ mobilization and TxA₂ formation, ultimately resulting in inhibition of platelet aggregation.

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Platelet aggregation is impaired during anaesthesia with sevoflurane but not with isoflurane

Cited by 36 publications

References 20 publications

La technique anesthésique n’affecte pas la performance d’un modèle de réductions cycliques de flot chez le lapin : une étude pilote

La technique anesthésique n’affecte pas la performance d’un modèle de réductions cycliques de flot chez le lapin : une étude pilote

Platelet Function as Affected by Total Intravenous and Inhalational Anesthesia

Mechanisms Involved in the Antiplatelet Activity of Ketamine in Human Platelets

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