Attenuation of Endothelium-mediated Vasodilation by Halothane

Muldoon, Sheila M.; Hart, Jayne L.; Bowen, Kimberly; Freas, William

doi:10.1097/00000542-198801000-00006

Cited by 130 publications

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“…Different studies have also postulated that volatile anesthetics such as halothane, isoflurane and even sevoflurane attenuated the endothelium-dependent relaxation. [24][25][26] The fact that sevoflurane reduced the NO-dependent relaxation may be explained by a possible binding activity of sevoflurane to NO, avoiding the action of NO on smooth muscle cells. However, a recent study has shown the inability of sevoflurane to interact chemically with NO and its ability to inhibit NO production directly in endothelial cells.…”

Section: Involvement Of Et-1 In the Endothelial Dysfunction Induced Bmentioning

confidence: 99%

Sevoflurane reduces endothelium-dependent vasorelaxation: role of Superoxide anion and endothelin

et al. 2002

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Section: Involvement Of Et-1 In the Endothelial Dysfunction Induced Bmentioning

confidence: 99%

Sevoflurane reduces endothelium-dependent vasorelaxation: role of Superoxide anion and endothelin

et al. 2002

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“…Both ROS and NO have been implicated in PAF shock, but whether their involvement is detrimental or beneficial is still a matter of debate (10)(11)(12). However, most studies were performed in animals under general anesthesia, which influences NO-mediated effects and blood pressure considerably (13)(14)(15). Also, conflicting results in anaphylactic shock models have been reported with regard to the possible involvement of NO (16)(17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

Anaphylactic shock depends on PI3K and eNOS-derived NO

Cauwels¹

2006

Journal of Clinical Investigation

123

117

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Anaphylactic shock is a sudden, life-threatening allergic reaction associated with severe hypotension. Platelet-activating factor (PAF) is implicated in the cardiovascular dysfunctions occurring in various shock syndromes, including anaphylaxis. Excessive production of the vasodilator NO causes inflammatory hypotension and shock, and it is generally accepted that transcriptionally regulated inducible iNOS is responsible for this. Nevertheless, the contribution of NO to PAF-induced shock or anaphylactic shock is still ambiguous. We studied PAF and anaphylactic shock in conscious mice. Surprisingly, hyperacute PAF shock depended entirely on NO, produced not by inducible iNOS, but by constitutive eNOS, rapidly activated via the PI3K pathway. Soluble guanylate cyclase (sGC) is generally regarded as the principal vasorelaxing mediator of NO. Nevertheless, although methylene blue partially prevented PAF shock, neither 1H-[1,2,4]oxadiazole[4,3-a]quinoxalin-1-one (ODQ) nor sGCα1 deficiency did. Also, in 2 different models of active systemic anaphylaxis, inhibition of NOS, PI3K, or Akt or eNOS deficiency provided complete protection. In contrast to the unsubstantiated paradigm that only excessive iNOS-derived NO underlies cardiovascular collapse in shock, our data strongly support the unexpected concept that eNOS-derived NO is the principal vasodilator in anaphylactic shock and define eNOS and/or PI3K or Akt as new potential targets for treating anaphylaxis.

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“…Halothane has been shown to inhibit sympathetic nervous transmission at several levels Larach et al, 1987;Rorie et al, 1990). Halothane was also found to alter endothelium-dependent vasodilatation (Muldoon et al, 1988;Blaise, 1991), and to abolish the pressor responses of other NO synthase inhibitors, namely N-nitro-L-arginine (L-NNA) and its methyl ester (L-NAME) (Wang et al, 1991a;Pang et al, 1992). The aim of this study was to (1) investigate the characteristics of the inhibitory effect of halothane on the pressor response to DPI; (2) to examine whether halothane suppresses the pressor response of DPI by inhibiting activities of the sympathetic nervous system; (3) to compare the effect of halothane with those of intravenous and inhalation anaesthetic agents on the pressor response of DPI.…”

Section: Introducdon Methodsmentioning

confidence: 99%

“…Halothane has been shown to potentiate (Blaise, 1991) or reduce (Muldoon et al, 1988) endothelium-dependent vasodilatation in different vascular preparations. We have also found that halothane (1.25%) abolishes the pressor effects of L-NNA and L-NAME but not those of noradrenaline or angiotensin II (Wang et al, 1991a;Pang et al, 1992).…”

Section: Effects Of Anaesthetics On Dpi-induced Map Responsementioning

confidence: 99%

Halothane inhibits the pressor effect of diphenyleneiodonium

Wang¹,

Pang²

1993

British J Pharmacology

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1 We have recently found that diphenyleneiodonium (DPI), a novel inhibitor of nitric oxide (NO) synthase, causes pressor and tachycardic responses in pentobarbitone-but not halothane-anaesthetized rats. The present study investigated the mechanism by which halothane suppresses the pressor response of DPI. The effects of halothane on the pressor response of DPI were also compared with those of other anaesthetic agents.2 In conscious rats, i.v. bolus injections of DPI (0.025 -1.6 mg kg-') caused dose-dependent increases in mean arterial pressure (MAP), with EDm of 0.07 ± 0.01 mg kg-' and maximal rise of MAP (Emax) of 59 ± 2 mmHg. While ketamine potentiated E,,, without altering the EDm and pentobarbitone increased the ED^, without changing Emax of the pressor response to DPI, chloralose, urethane and ethanol displaced the curve to the right and potentiated E,,.a. In contrast, halothane (0.5-1.25%) dosedependently and non-competitively reduced the pressor responses to DPI. 3 Intravenous bolus injection of a single dose of DPI (1.6 mg kg-') caused immediate and large increases in plasma noradrenaline and adrenaline, as well as MAP in conscious rats. Halothane (1.25%) almost completely inhibited these increases. 4 The results suggest that DPI causes a pressor response in conscious rats by activating the sympathetic nervous system and halothane abolishes this pressor response by inhibiting activities of the sympathetic nervous system. The results also show that influences of anaesthetics must be taken into consideration when evaluating pressor response of vasoactive agents.

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Attenuation of Endothelium-mediated Vasodilation by Halothane

Cited by 130 publications

References 0 publications

Sevoflurane reduces endothelium-dependent vasorelaxation: role of Superoxide anion and endothelin

Sevoflurane reduces endothelium-dependent vasorelaxation: role of Superoxide anion and endothelin

Anaphylactic shock depends on PI3K and eNOS-derived NO

Halothane inhibits the pressor effect of diphenyleneiodonium

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