Effects of ketamine and pentobarbital on noradrenaline release from the medial prefrontal cortex in rats

Kubota, Takeshi; Anzawa, Noriyuki; Hirota, Kazuyoshi; Yoshida, Hitoshi; Kushikata, Tetsuya; Matsuki, Akitomo

doi:10.1007/bf03013235

Cited by 54 publications

(37 citation statements)

References 25 publications

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“…It has been suggested that the doses of ketamine required to anesthetize the experiment animal such as guinea-pig range from 44 to 250 mg/kg (36). And according to previous reports, no anesthetic state was produced in rats received 10 mg/kg ketamine (37). So the doses of ketamine in our study may be sub-anesthetic to rats.…”

Section: Discussionmentioning

confidence: 74%

Effects of Ketamine on Pulmonary Inflammatory Responses and Survival in Rats Exposed to Polymicrobial Sepsis

Shao

Yang

et al. 2007

J Pharm Pharm Sci

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-PURPOSE.Ketamine is reported to suppress production of proinflammatory cytokines and activity of nuclear factor-kappa B (NF-κB) after lipopolysaccharide (LPS) stimulation. Our study was designed to investigate the effects of ketamine on pulmonary inflammatory responses and survival in a clinically relevant model of polymicrobial sepsis, induced by cecal ligation and puncture (CLP). METHODS. After the induction of sepsis or sham-operation, animals were treated with ketamine (0.5, 5 or 10 mg/kg) or saline (10 ml/kg) at 3h after operation. At 6 h post-operation, the levels of tumor necrosis factor alpha (TNF-α) and interleukin (IL)-6, activity of NF-κB, expression of Toll-like receptor 2 (TLR2) and Toll-like receptor 4 (TLR4) of the lungs were measured. And the mortality was recorded for 7 days. RESULTS. TNF-α and IL-6 production, NF-κB activity, TLR2 and TLR4 expression in rat lungs were increased after CLP. Ketamine at the doses of 5 mg/kg and 10 mg/kg suppressed CLP-induced elevation of TNF-α and IL-6 production, NF-κB activity and TLR2 expression. Ketamine 0.5, 5 and 10 mg/kg inhibited TLR4 expression in sepsis. Ketamine 5mg/kg and 10 mg/kg after CLP improved the survival of rats. CONCLUSIONS. Ketamine at sub-anesthetic doses could suppress the production of inflammatory cytokines such as TNF-α and IL-6, attenuate NF-κB activity, and inhibit TLR2 and TLR4 expression in polymicrobial sepsis. These anti-inflammatory effects of ketamine may correlate with improved survival in sepsis.

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Section: Discussionmentioning

confidence: 74%

Effects of Ketamine on Pulmonary Inflammatory Responses and Survival in Rats Exposed to Polymicrobial Sepsis

Shao

Yang

et al. 2007

J Pharm Pharm Sci

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“…Hirota et al (31) reported inhibition of NE (noradrenaline) and DA release after exposure of rat brain striatal slices to barbiturates, including pentobarbital. Other groups have similarly reported an inhibition of NE release (34,50,62) or no effect (41,56) by pentobarbital in their studies. Our laboratory has previously euthanized rats using isoflurane or pentobarbital, and we have not observed a difference in tissue catecholamine content with either of them, suggesting similar functions of uptake and release.…”

Section: Discussionmentioning

confidence: 82%

Organic cation transporter 3 contributes to norepinephrine uptake into perivascular adipose tissue

Ayala‐Lopez

Jackson

Burnett

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Watts SW. Organic cation transporter 3 contributes to norepinephrine uptake into perivascular adipose tissue. Am J Physiol Heart Circ Physiol 309: H1904 -H1914, 2015. First published October 2, 2015; doi:10.1152/ajpheart.00308.2015.-Perivascular adipose tissue (PVAT) reduces vasoconstriction to norepinephrine (NE). A mechanism by which PVAT could function to reduce vascular contraction is by decreasing the amount of NE to which the vessel is exposed. PVATs from male Sprague-Dawley rats were used to test the hypothesis that PVAT has a NE uptake mechanism. NE was detected by HPLC in mesenteric PVAT and isolated adipocytes. Uptake of NE (10 M) in mesenteric PVAT was reduced by the NE transporter (NET) inhibitor nisoxetine (1 M, 73.68 Ϯ 7.62%, all values reported as percentages of vehicle), the 5-hydroxytryptamine transporter (SERT) inhibitor citalopram (100 nM) with the organic cation transporter 3 (OCT3) inhibitor corticosterone (100 M, 56.18 Ϯ 5.21%), and the NET inhibitor desipramine (10 M) with corticosterone (100 M, 61.18 Ϯ 6.82%). Aortic PVAT NE uptake was reduced by corticosterone (100 M, 53.01 Ϯ 10.96%). Confocal imaging of mesenteric PVAT stained with 4-[4-(dimethylamino)-styrl]-N-methylpyridinium iodide (ASP ϩ ), a fluorescent substrate of cationic transporters, detected ASP ϩ uptake into adipocytes. ASP ϩ (2 M) uptake was reduced by citalopram (100 nM, 66.68 Ϯ 6.43%), corticosterone (100 M, 43.49 Ϯ 10.17%), nisoxetine (100 nM, 84.12 Ϯ 4.24%), citalopram with corticosterone (100 nM and 100 M, respectively, 35.75 Ϯ 4.21%), and desipramine with corticosterone (10 and 100 M, respectively, 50.47 Ϯ 5.78%). NET protein was not detected in mesenteric PVAT adipocytes. Expression of Slc22a3 (OCT3 gene) mRNA and protein in PVAT adipocytes was detected by RT-PCR and immunocytochemistry, respectively. These end points support the presence of a transporter-mediated NE uptake system within PVAT with a potential mediator being OCT3. PERIVASCULAR ADIPOSE TISSUE (PVAT) closely envelops many blood vessels of the body (65). This relationship between PVAT and the blood vessel has earned PVAT its place as the fourth layer of the blood vessel, the "tunica adiposa" (14). Beyond providing structural support, PVAT has many roles in modulating blood vessel function (68). The release of vasoactive molecules from PVAT influences vascular function by altering the proliferation, migration, inflammation, and contraction of vascular smooth muscle (9, 20 -22, 24, 46, 68, 72). Interestingly, a releasable pool of catecholamines is present in PVAT (5, 67). Although both contractile and anticontractile substances can be released from PVAT (9,22,24,25,72), the presence of PVAT on blood vessels generally reduces vessel contraction in response to various agonists, including norepinephrine (NE) (64). Knowledge on how these mechanisms interact to influence the anticontractile properties of PVAT in NE-induced contraction is not complete (36).The anticontractile effect of PVAT is lost in obesity and hypertension, implicating PVAT as an integral lin...

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“…8,9 Briefly, the 10 µL samples were injected into ODS-C18 reverse-phase column (CA-5ODS, EICOM, Kyoto, Japan) maintained at 25C. The mobile phase was 0.1 M phosphate buffer containing 5% methanol and its flow was 220 µL·min -1 .…”

Section: Methodsmentioning

confidence: 99%

Xenon inhalation increases norepinephrine release from the anterior and posterior hypothalamus in rats

Yoshida

Kushikata

Kubota

et al. 2001

Can J Anesth/J Can Anesth

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Purpose: To investigate the effect of xenon (Xe) and nitrous oxide (N 2 O) on norepinephrinergic neuronal activity in the rat medial preoptic area (mPOA) and posterior hypothalamus (PH) using microdialysis.Methods: Sixty male Wistar rats were equally allocated to two groups: mPOA and PH. A microdialysis probe was implanted into the mPOA or the PH. In both groups, each animal was exposed to one of the following inhalations: 25% oxygen (control, n=6), 30% Xe (n=6), 60% Xe (n=6), 30% N 2 O (n=6) or 60% N 2 O (n=6). Norepinephrine concentration in the perfused artificial cerebrospinal fluid was measured by high pressure liquid chromatography at ten-minute intervals. After plotting the time-norepinephrine concentration curve, the area under the curve (AUC) in each group was calculated.Results: In the mPOA, 30 and 60% Xe, but only 60% N 2 O significantly increased norepinephrine release. The AUC in the 30% Xe, 60% Xe or 60% N 2 O group was 160 ± 9 (P <0.05), 288 ± 42 (P <0.01) or 237 ± 46 pg·min/sample (P <0.01), respectively, compared to that in the control group: 77 ± 14 pg·min/sample. In the PH, only 60% Xe significantly increased norepinephrine release compared to control (AUC: 191 ± 38 vs 71 ± 1 pg·min/sample, P <0.01).Conclusion: The present data suggest that Xe stimulates norepinephrinergic neurons more potently than N 2 O; 1.2 times more in the mPOA and 2.5 times more in the PH. This stimulant effect may contribute to the hypnotic and sympathotonic effects of Xe in rats.

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Effects of ketamine and pentobarbital on noradrenaline release from the medial prefrontal cortex in rats

Cited by 54 publications

References 25 publications

Effects of Ketamine on Pulmonary Inflammatory Responses and Survival in Rats Exposed to Polymicrobial Sepsis

Effects of Ketamine on Pulmonary Inflammatory Responses and Survival in Rats Exposed to Polymicrobial Sepsis

Organic cation transporter 3 contributes to norepinephrine uptake into perivascular adipose tissue

Xenon inhalation increases norepinephrine release from the anterior and posterior hypothalamus in rats

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