An opioid basis for early-phase isoflurane-induced hypotension in rats

Ellenberger, Elizabeth A.; Lucas, Heather L.; Russo, John; Mueller, Janet L.; Barrington, Peggy L.; Tseng, Leon F.; Quock, Raymond M.

doi:10.1016/s0024-3205(03)00667-2

Cited by 7 publications

(9 citation statements)

References 33 publications

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“…In the opioid antagonist studies, either naloxone (3.0 mg/kg), naltrindole (5.0 mg/kg), nor-BNI (0.3 mg/kg), or CTOP (0.1 mg/kg) was administered at doses previously used in our laboratory alone or 10 min before EET administration. The antisera (25 mg/kg iv) to the various endogenous opioid peptides were administered 50 min before EET administration (8,24). In all groups, hemodynamic measurements and blood gas analyses were performed at baseline and at 15 min into the 30-min occlusion period and at the end of 2 h of reperfusion.…”

Section: Methodsmentioning

confidence: 99%

Evidence for a role of opioids in epoxyeicosatrienoic acid-induced cardioprotection in rat hearts

Gross

Baker

Hsu

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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We previously demonstrated that several epoxyeicosatrienoic acids (EETs) produce reductions in myocardial infarct size in rats and dogs. Since a recent study demonstrated the release of opioids in mediating the antinociceptive effect of 14,15-EET, we hypothesized that endogenous opioids may also be involved in mediating the cardioprotective effect of the EETs. To test this hypothesis, we used an in vivo rat model of infarction and a rat Langendorff model. In the infarct model, hearts were subjected to 30 min occlusion of the left coronary artery and 2 h reperfusion. Animals were treated with 11,12-EET or 14,15-EET (2.5 mg/kg) alone 15 min before occlusion or with opioid antagonists [naloxone, naltrindole, nor-binaltorphimine (nor-BNI), and d-Phe-Cys-Tyr-d-Trp-Om-Thr-Pen-Thr-NH(2) (CTOP), a nonselective, a selective delta, a selective kappa, and a selective mu receptor antagonist, respectively] 10 min before EET administration. In four separate groups, antiserum to Met- and Leu-enkephalin and dynorphin-A-(1-17) was administered 50 min before the 11,12-EET administration. Infarct size expressed as a percent of the area at risk (IS/AAR) was 63.5 + or - 1.2, 45.3 + or - 1.0, and 40.9 + or - 1.2% for control, 11,12-EET, and 14,15-EET, respectively. The protective effects of 11,12-EET were abolished by pretreatment with either naloxone (60.5 + or - 1.8%), naltrindole (60.8 + or - 1.0%), nor-BNI (62.3 + or - 2.8%), or Met-enkephalin antiserum (63.2 + or - 1.7%) but not CTOP (42.0 + or - 3.0%). In isolated heart experiments, 11,12-EET was administered to the perfusate 15 min before 20 min global ischemia followed by 45 min reperfusion in control hearts or in those pretreated with pertussis toxin (48 h). 11,12-EET increased the recovery of left ventricular developed pressure from 33 + or - 1 to 45 + or - 6% (P < 0.05) and reduced IS/AAR from 37 + or - 4 to 20 + or - 3% (P < 0.05). Both pertussis toxin and naloxone abolished these beneficial effects of 11,12-EET. Taken together, these results suggest that the major cardioprotective effects of the EETs depend on activation of a G(i/o) protein-coupled delta- and/or kappa-opioid receptor.

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Section: Methodsmentioning

confidence: 99%

Evidence for a role of opioids in epoxyeicosatrienoic acid-induced cardioprotection in rat hearts

Gross

Baker

Hsu

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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“…We earlier reported that early-phase isoflurane-induced hypotension was attenuated by opioid antagonists and was also blocked by rabbit antisera against the opioid peptide met-enkephalin (Ellenberger et al, 2003). We postulated that this early hypotensive response to isoflurane might involve release of either met-enkephalin or a met-enkephalin-like peptide which presumably activates A opioid receptors.…”

Section: Discussionmentioning

confidence: 97%

“…Recently we reported that inhalation of isoflurane by rats under basal urethane anesthesia caused a triphasic change in the mean arterial pressure (MAP) (Ellenberger et al, 2003). There was an initial sharp reduction in MAP that was followed by a transient recovery toward basal pressure then a prolonged and more gradual reduction in MAP.…”

Section: Introductionmentioning

confidence: 99%

“…This early-phase isoflurane-induced hypotension was antagonized by pretreatment with peripherally active opioid antagonists as well as rabbit antisera against rat met-enkephalin. We suggested that this early hypotensive response might be due to isoflurane-stimulated release of met-enkephalin or a metenkephalin-like opioid peptide (Ellenberger et al, 2003). It is widely thought that relaxation of peripheral vascular smooth muscle may be dependent on endothelium-derived nitric oxide (NO) (Furchgott, 1983;Ignarro et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

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Possible involvement of neuronal nitric oxide synthase enzyme in early-phase isoflurane-induced hypotension in rats

et al. 2004

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“…More recently, it was found that the methylnaloxone-sensitive, early-phase hypotension produced in rats by isoflurane was attenuated by pretreatment with rabbit antisera against methionine-enkephalin but not h-endorphin (Ellenberger et al, 2003). Such reports of functional antagonism of anesthetic effects by antisera against endogenous opioid peptides is further evidence that at least some effects caused by anesthetic drugs involve a stimulated release of opioid peptides.…”

Section: An Opioid Component To General Anesthesia?mentioning

confidence: 98%

Do inhalation general anesthetic drugs induce the neuronal release of endogenous opioid peptides?

Quock

Vaughn

2005

Life Sciences

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The antagonism of some effects of inhalation general anesthetic agents by naloxone suggests that there may be an opioid component to anesthetic action. There is evidence that this opioid action component is due to neuronal release of endogenous opioid peptides. The strongest evidence is provided by studies that monitor changes in the concentration of opioid peptides in the perfused brain following inhalation of the anesthetic. Indirect or circumstantial evidence also comes from studies of anesthetic effects on regional brain levels of opioid peptides, antagonism of selected anesthetic effects by antisera to opioid peptides and anesthetic-induced changes radioligand binding to opioid receptors. It is likely that some inhalation general anesthetics (e.g., nitrous oxide) can induce neuronal release of opioid peptides and that this may contribute to certain components of general anesthesia (e.g., analgesia). More definitive studies utilizing in vivo microdialysis or autoradiography in selected areas of the brain during induction and successive states of general anesthesia have yet to be conducted.

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An opioid basis for early-phase isoflurane-induced hypotension in rats

Cited by 7 publications

References 33 publications

Evidence for a role of opioids in epoxyeicosatrienoic acid-induced cardioprotection in rat hearts

Evidence for a role of opioids in epoxyeicosatrienoic acid-induced cardioprotection in rat hearts

Possible involvement of neuronal nitric oxide synthase enzyme in early-phase isoflurane-induced hypotension in rats

Do inhalation general anesthetic drugs induce the neuronal release of endogenous opioid peptides?

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