Isoflurane and Sevoflurane Induce Vasodilation of Cerebral Vessels via ATP-sensitive K+Channel Activation

Iida, Hiroki; Ohata, Hiroto; Iida, Mami; Watanabe, Yukinaga; Dohi, Shuji

doi:10.1097/00000542-199810000-00020

Cited by 129 publications

(100 citation statements)

References 30 publications

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“…We compared eIOS responses in awake and isoflurane anaesthetized mice (figure 1). Consistent with previous studies showing that isoflurane has vasodilatory properties [43,53], we observed strong dilation of pial arterioles when isoflurane was administered at 1.8% (v/v) in oxygen (figure 1b). Although we observed that isoflurane anaesthesia suppressed the amplitude of the eIOS ( figure 1a,c), isoflurane improved the signal-to-noise of the eIOS deoxygenation signal by suppressing vasodynamic responses (figures 1a,c and 2).…”

Section: Discussionsupporting

confidence: 92%

Precision mapping of the vibrissa representation within murine primary somatosensory cortex

Knutsen

Matéo

Kleinfeld

2016

Phil. Trans. R. Soc. B

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The ability to form an accurate map of sensory input to the brain is an essential aspect of interpreting functional brain signals. Here, we consider the somatotopic map of vibrissa-based touch in the primary somatosensory (vS1) cortex of mice. The vibrissae are represented by a Manhattan-like grid of columnar structures that are separated by inter-digitating septa. The development, dynamics and plasticity of this organization is widely used as a model system. Yet, the exact anatomical position of this organization within the vS1 cortex varies between individual mice. Targeting of a particular column in vivo therefore requires prior mapping of the activated cortical region, for instance by imaging the evoked intrinsic optical signal (eIOS) during vibrissa stimulation. Here, we describe a procedure for constructing a complete somatotopic map of the vibrissa representation in the vS1 cortex using eIOS. This enables precise targeting of individual cortical columns . We found, using C57BL/6 mice, that although the precise location of the columnar field varies between animals, the relative spatial arrangement of the columns is highly preserved. This finding enables us to construct a canonical somatotopic map of the vibrissae in the vS1 cortex. In particular, the position of any column, in absolute anatomical coordinates, can be established with near certainty when the functional representations in the vS1 cortex for as few as two vibrissae have been mapped with eIOS. This article is part of the themed issue ‘Interpreting BOLD: a dialogue between cognitive and cellular neuroscience’.

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Section: Discussionsupporting

confidence: 92%

Precision mapping of the vibrissa representation within murine primary somatosensory cortex

Knutsen

Matéo

Kleinfeld

2016

Phil. Trans. R. Soc. B

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“…This is consistent with several studies that suggest that activation of K ATP channels could play a prominent role in volatile anaesthesia-induced relaxation of peripheral airways [24], coronary vessels [25], and cerebral vessels [28]. In contrast, FUKUSHIMA et al [14] found that glibenclamide pretreatment did not modify the concentrationdependent relaxation produced by halothane on canine tracheal strips incubated with indomethacin and precontracted with acetylcholine.…”

Section: Discussionsupporting

confidence: 91%

“…The anaesthetic concentrations, as well as the O 2 and CO 2 concentrations, were controlled just before entering the organ baths by the infrared absorption technique (Capnomac Datex; Ohmeda) and adjusted as needed. The bubbling was set at a relatively high rate (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30) …”

Section: Volatile Anaesthetic Delivery To the Tissue Preparationmentioning

confidence: 99%

Relaxation of proximal and distal isolated human bronchi by halothane, isoflurane and desflurane

Mercier¹,

Naline²,

Bardou³

et al. 2002

Eur Respir J

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Volatile anaesthetics relax airway smooth muscle in vitro. The amount of relaxation might depend on the type and concentration of volatile anaesthetics, the calibre and precontraction level of the bronchi, and also on the species considered. These effects were investigated on isolated human bronchi.Isometric relaxations produced by halothane, isoflurane and desflurane bubbled on human bronchial rings precontracted with carbachol were recorded and compared with time controls.Volatile anaesthetics induced a concentration-dependent relaxation at 0.66, 1.33 and 2 minimum alveolar concentration (MAC). The relaxation was greater in mildly (carbachol 3610 -7 M) than in highly (carbachol 2610 -6 M) precontracted bronchi. Halothane was more potent in relaxing distal as compared to proximal bronchi; this differential effect was less pronounced with isoflurane and not observed with desflurane. While the three volatile anaesthetics induced similar relaxation on proximal bronchi, halothane was significantly more potent than desflurane on distal bronchi, with isoflurane being intermediate. The relaxation induced by 1.33 MAC of halothane, isoflurane and desflurane on moderately precontracted distal bronchi (carbachol 1610 -6 M) was attenuated by pretreatment with glibenclamide 1610 -5 M. In conclusion, halothane, isoflurane and desflurane exert direct but differential relaxant effects on human isolated bronchial smooth muscle. This may provide supplemental bronchodilation during anaesthesia. Although adenosine triphosphatesensitive K z channels are involved in these relaxant effects, they are unlikely to explain the observed differences between the three volatile anaesthetics. Eur Respir J 2002; 20: 286-292. Halothane and isoflurane are well-established bronchodilators in vivo both in animals [1][2][3][4][5] and humans [6,7]. Part of this bronchodilation is due to a direct effect on airway smooth muscle. For example, in dogs in vivo, the direct relaxant effect of halothane on airway smooth muscle contributed as much as the indirect effect on the vagal pathway [4]. These direct relaxant effects in vivo have been reproduced in vitro in many animal studies [8][9][10][11][12][13][14][15][16][17][18][19]. However, the intensity of the relaxation in vitro varies widely among studies. Factors that may explain these variations include: 1) anaesthetic concentration; 2) level of precontraction and contractile agonist used [11]; 3) airway calibre [13,19,20]; 4) differences in efficacy between volatile anaesthetics [7,13,17,20]; and 5) animal species. This latter factor might be particularly important, and so far, no in vitro studies involving volatile anaesthetics appear to be available on human airway smooth muscle.Desflurane, a more recent volatile anaesthetic, has some interesting properties including rapid onset/ offset of action. However, breath-holding, partial laryngospasm and coughing have been reported during induction of anaesthesia with desflurane in humans [21]. Such irritant effects on the upper airways do not seem...

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“…But, glibenclamide reduced the sevoflurane induced relaxations, implying that K ATP channels may play an important role in the relaxant effects of sevoflurane. This is consistent with the findings of Iida et al, who reported K ATP channels are involved in the vasorelaxant effects of sevoflurane and isoflurane in dog cerebral arteries (13). However, a previous study has shown that sevoflurane exerts a cardioprotective effect that is mediate via activation of K ATP channels in ischemic canine hearts (14).…”

Section: Discussionsupporting

confidence: 92%

The Mechanisms of the Direct Vascular Effects of Sevoflurane on Saphenous Veins in Vitro

et al. 2009

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Aim:The purpose of this study was to determine the mechanism of the directs effects of sevoflurane on human veins in vitro.Methods: Dose-response curves were obtained for cumulative doses of sevoflurane (0.5, 1, 1.5 and 2 MAC) on saphenous vein strips precontracted with 5-hydroxytryptamine ( 5-HT 10 -6 mol/L) incubated with either Nω-nitroL-arginine-methyl ester (L-NAME) (10 -4 mol/L), indomethacine (10 -5 mol/L), glibenclamide (10 -6 mol/L) or tetraethylammonium (10 -4 mol/L) Results: Preincubation of vein strips with tetraethylammonium (TEA, Ca ++ -activated K + channel blocker) did not influence the relaxant responses to sevoflurane (p>0.05). L-NAME, indomethacine and glibenclamide reduced the relaxation response to sevoflurane (p<0.05).Conclusion: Our results demonstrated that sevoflurane produces concentration dependent relaxation in human saphenous vein. The relaxant effects of sevoflurane are probably related with activation of nitric oxide synthase, cyclooxygenase and K ATP channels pathways.

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Isoflurane and Sevoflurane Induce Vasodilation of Cerebral Vessels via ATP-sensitive K+Channel Activation

Abstract: The vasodilation of cerebral pial vessels induced by isoflurane and sevoflurane appears to be mediated, at least in part, via activation of adenosine triphosphate-sensitive K+ channels.

Cited by 129 publications

References 30 publications

Precision mapping of the vibrissa representation within murine primary somatosensory cortex

Precision mapping of the vibrissa representation within murine primary somatosensory cortex

Relaxation of proximal and distal isolated human bronchi by halothane, isoflurane and desflurane

The Mechanisms of the Direct Vascular Effects of Sevoflurane on Saphenous Veins in Vitro

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