Volatile anaesthetics reduce adhesion of blood platelets under low‐flow conditions in the coronary system of isolated guinea pig hearts

Heindl, B.; Becker, B.F.; Zahler, Stefan; Conzen, P.

doi:10.1111/j.1399-6576.1998.tb05361.x

Cited by 41 publications

(15 citation statements)

References 34 publications

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“…32,37 A similar effect was also shown for platelets. 45,47 Reduced neutrophil/platelet entrapment by anesthetics was accompanied by enhancement of postischemic mechanical function. 37,47 However, the effects of halogenated anesthetics on neutrophil/platelet sequestration have been studied by a limited number of research groups.…”

Section: Different Approaches To Assess Myocardial Injurymentioning

confidence: 99%

“…57 These studies imply that halogenated anesthetics can act directly on neutrophils at the time of reperfusion. Volatile anesthetics also reduced platelet adhesion to the vascular wall after ischemia, 45,47 but sevoflurane failed to reduce the expression of glycoprotein IIb/IIIa, a platelet adhesion molecule involved in the platelet-endothelium interaction. 47 Another possibility of coronary protection by halogenated anesthetics is via an ischemic preconditioning-like effect.…”

Section: Coronary Vasculaturementioning

confidence: 99%

“…This anesthetic improves postischemic mechanical and coronary function, and reduces infarct size. 32,34,37,[45][46][47][48][49][50] A beneficial effect of desflurane was suggested by a few groups. 34,49,51 Further investigations are needed to determine the effect of desflurane in other experimental settings.…”

Section: Sevoflurane and Desfluranementioning

confidence: 99%

“…37,47 However, the effects of halogenated anesthetics on neutrophil/platelet sequestration have been studied by a limited number of research groups. 32,37,45,47 Novalija and coworkers measured coronary flow changes in response to endothelial-dependent and independent vasodilators. Sevoflurane preserved the reaction provoked by both types of vasodilators during the reperfusion period better than no treatment.…”

Section: Different Approaches To Assess Myocardial Injurymentioning

confidence: 99%

“…[29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45] A new agent whose protection was demonstrated recently is sevoflurane. This anesthetic improves postischemic mechanical and coronary function, and reduces infarct size.…”

Section: Sevoflurane and Desfluranementioning

confidence: 99%

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Myocardial protection by anesthetic agents against ischemia-reperfusion injury: An update for anesthesiologists

Kato

Foëx

2002

Can J Anesth/J Can Anesth

196

126

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P Pu ur rp po os se e: : The aim of this review of the literature was to evaluate the effectiveness of anesthetics in protecting the heart against myocardial ischemia-reperfusion injury.S So ou ur rc ce e: : Articles were obtained from the Medline database (1980-, search terms included heart, myocardium, coronary, ischemia, reperfusion injury, infarction, stunning, halothane, enflurane, desflurane, isoflurane, sevoflurane, opioid, morphine, fentanyl, alfentanil sufentanil, pentazocine, buprenorphine, barbiturate, thiopental, ketamine, propofol, preconditioning, neutrophil adhesion, free radical, antioxidant and calcium).P Pr ri in nc ci ip pa al l f fi in nd di in ng gs s: : Protection by volatile anesthetics, morphine and propofol is relatively well investigated. It is generally agreed that these agents reduce the myocardial damage caused by ischemia and reperfusion. Other anesthetics which are often used in clinical practice, such as fentanyl, ketamine, barbiturates and benzodiazepines have been much less studied, and their potential as cardioprotectors is currently unknown. There are some proposed mechanisms for protection by anesthetic agents: ischemic preconditioning-like effect, interference in the neutrophil/platelet-endothelium interaction, blockade of Ca 2+ overload to the cytosolic space and antioxidant-like effect. Different anesthetics appear to have different mechanisms by which protection is exerted. Clinical applicability of anesthetic agent-induced protection has yet to be explored. C Co on nc cl lu us si io on n: : There is increasing evidence of anesthetic agentinduced protection. At present, isoflurane, sevoflurane and morphine appear to be most promising as preconditioning-inducing agents. After the onset of ischemia, propofol could be selected to reduce ischemia-reperfusion injury. Future clinical application depends on the full elucidation of the underlying mechanisms and on clinical outcome trials. Objectif

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Section: Different Approaches To Assess Myocardial Injurymentioning

confidence: 99%

Section: Coronary Vasculaturementioning

confidence: 99%

Section: Sevoflurane and Desfluranementioning

confidence: 99%

Section: Different Approaches To Assess Myocardial Injurymentioning

confidence: 99%

Section: Sevoflurane and Desfluranementioning

confidence: 99%

See 3 more Smart Citations

Myocardial protection by anesthetic agents against ischemia-reperfusion injury: An update for anesthesiologists

Kato

Foëx

2002

Can J Anesth/J Can Anesth

196

126

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Halothane affects focal adhesion proteins in the A 549 cells

et al. 2006

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Halothane is a volatile anaesthetic, which is known to induce alterations in cellular plasma membranes, modulating the physical state of the membrane lipids and/or interacting directly with membrane-bound proteins, such as integrin receptors. Integrin-mediated cell adhesion is a general property of eukaryotic cells, which is closely related to cell viability. Our previous investigations showed that halothane is toxic for A 549 lung carcinoma cells when applied at physiologically relevant concentrations and causes inhibition of adhesion to collagen IV. The present study is focused on the mechanisms underlying halothane toxicity. Our results imply that physiologically relevant concentrations of halothane disrupt focal adhesion contacts in A 549 cells, which is accompanied with suppression of focal adhesion kinase activity and paxillin phosphorylation, and not with proteolytic changes or inhibition of vinculin and paxillin expression.We suggest that at least one of the toxic effects of halothane is due to a decreased phosphorylation of the focal contact proteins.

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Anesthesia for Myocardial Revascularization

London¹,

Mittnacht²,

Kaplan³

2011

Kaplan's Cardiac Anesthesia: The Echo Era

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Volatile anaesthetics reduce adhesion of blood platelets under low‐flow conditions in the coronary system of isolated guinea pig hearts

Abstract: Volatile anaesthetics in a concentration of 1 MAC can reduce the adhesion of platelets in the coronary system under reduced flow conditions. This action does not arise from vasodilation or inhibition of ischaemic stress.

Cited by 41 publications

References 34 publications

Myocardial protection by anesthetic agents against ischemia-reperfusion injury: An update for anesthesiologists

Myocardial protection by anesthetic agents against ischemia-reperfusion injury: An update for anesthesiologists

Halothane affects focal adhesion proteins in the A 549 cells

Anesthesia for Myocardial Revascularization

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