Vasomotor effects of dimethyl sulfoxide on cat cerebral arteries in vitro and in vivo.

Pitts, Lawrence H.; Young, Alan R.; McCulloch, James; MacKenzie, Eric T.

doi:10.1161/01.str.17.3.483

Cited by 18 publications

(13 citation statements)

References 25 publications

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“…Pitts et al [13] showed that DMSO (>10 mmol/l) inhibited high K + -, 5-hydroxytryptamine-, or prostaglandin F 2α -induced contractions in isolated cat cerebral arteries, and DMSO (>1%) increased the cat pial arteriolar caliber in artificial cerebrospinal fluid. Because a high concentration of DMSO increased the osmolality of the Krebs' solution, the authors concluded that this was the mechanism through which DMSO induced vasorelaxation.…”

Section: Discussionmentioning

confidence: 99%

Endothelium-Dependent and -Independent Vasodilator Effects of Dimethyl Sulfoxide in Rat Aorta

Kaneda

Sasaki²,

Urakawa³

et al. 2016

Pharmacology

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This study examined the mechanism of vasorelaxation induced by dimethyl sulfoxide (DMSO) in endothelium-intact and -denuded rat aorta. DMSO (0.1-3%) inhibited phenylephrine (PE, 1 μmol/l)-induced contraction in a dose-dependent manner. However, this relaxation was lower in the absence of the endothelium. Increase in DMSO-induced relaxation in the presence of the endothelium was attenuated by preincubation in L-N^G-nitroarginine methyl ester (L-NAME, 100 μmol/l) and by the removal of the endothelium. In the aorta with endothelium, DMSO (3%) and CCh (3 μmol/l) increased cGMP contents, significantly and L-NAME (100 μmol/l) inhibited the DMSO-induced increases of cGMP. In fura 2-loaded endothelium-denuded aorta, cumulative application of DMSO (1-3%) inhibited PE-induced muscle tension; however, this application did not affect the [Ca²⁺]_i level. In PE-precontracted endothelium-denuded aorta, relaxation responses to fasudil were significantly less in the presence of DMSO compared to the control. These results suggest that DMSO causes relaxation by increasing the cGMP content in correlation with the release of NO from endothelial cells and by decreasing the Ca²⁺ sensitivity of contractile elements partly via inhibiting Rho-kinase in rat aorta.

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Section: Discussionmentioning

confidence: 99%

Endothelium-Dependent and -Independent Vasodilator Effects of Dimethyl Sulfoxide in Rat Aorta

Kaneda

Sasaki²,

Urakawa³

et al. 2016

Pharmacology

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“…DMSO has a wide spectrum of biological activities, including high penetrating activity and significant vasoactive effects on blood vessels [138,139] . It is used for local treatment of trauma, arthrosis, and rheumatoid a r t h r i t i s [ 1 4 0 , 1 4 1 ] .…”

Section: Pharmacological Effects Of Dimethyl Sulfoxide (Dmso)mentioning

confidence: 99%

Advances in small animal mesentery models for in vivo flow cytometry, dynamic microscopy, and drug screening

Galanzha¹

2007

WJG

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Using animal mesentery with intravital optical microscopy is a well-established experimental model for studying blood and lymph microcirculation in vivo . Recent advances in cell biology and optical techniques provide the basis for extending this model for new applications, which should generate significantly improved experimental data. This review summarizes the achievements in this specific area, including in vivo label-free blood and lymph photothermal flow cytometry, super-sensitive fluorescence image cytometry, light scattering and speckle flow cytometry, microvessel dynamic microscopy, infrared (IR) angiography, and high-speed imaging of individual cells in fast flow. The capabilities of these techniques, using the rat mesentery model, were demonstrated in various studies; e.g., real-time quantitative detection of circulating and migrating individual blood and cancer cells, studies on vascular dynamics with a focus on lymphatics under normal conditions and under different interventions (e.g. lasers, drugs, nicotine), assessment of lymphatic disturbances from experimental lymphedema, monitoring cell traffic between blood and lymph systems, and high-speed imaging of cell transient deformability in flow. In particular, the obtained results demonstrated that individual cell transportation in living organisms depends on cell type (e.g., normal blood or leukemic cells), the cell's functional state (e.g., live, apoptotic, or necrotic), and the functional status of the organism. Possible future applications, including in vivo early diagnosis and prevention of disease, monitoring immune response and apoptosis, chemo-and radio-sensitivity tests, and drug screening, are also discussed. TOPIC HIGHLIGHT

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“…XA was dissolved into saline solution and the pH was adjusted to 7.4 with 1N NaOH. We did not use DMSO to avoid influences on vasocontraction (Pitts et al, 1986). …”

Section: Methodsmentioning

confidence: 99%

Vasorelaxing Action of the Kynurenine Metabolite, Xanthurenic Acid: The Missing Link in Endotoxin-Induced Hypotension?

et al. 2017

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The kynurenine pathway of tryptophan metabolism is activated by pro-inflammatory cytokines. L-kynurenine, an upstream metabolite of the pathway, acts as a putative endothelium-derived relaxing factor, and has been hypothesized to play a causative role in the pathophysiology of inflammation-induced hypotension. Here, we show that xanthurenic acid (XA), the transamination product of 3-hydroxykynurenine, is more efficacious than L-kynurenine in causing relaxation of a resistance artery, but fails to relax pre-contracted aortic rings. In the mesenteric artery, XA enhanced activating phosphorylation of endothelial nitric oxide synthase (NOS), and the relaxing action of XA was abrogated by pharmacological inhibition of NOS and endothelial-derived hyperpolarizing factor. Systemic injection of XA reduced blood pressure in mice, and serum levels of XA increased by several fold in response to a pulse with the endotoxin, lipopolysaccharide (LPS). LPS-induced hypotension in mice was prevented by pre-treatment with the kynurenine monooxygenase (KMO) inhibitor, Ro-618048, which lowered serum levels of XA but enhanced serum levels of L-kynurenine. UPF 648, another KMO inhibitor, could also abrogate LPS-induced hypotension. Our data identify XA as a novel vasoactive compound and suggest that formation of XA is a key event in the pathophysiology of inflammation-induced hypotension.

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Vasomotor effects of dimethyl sulfoxide on cat cerebral arteries in vitro and in vivo.

Cited by 18 publications

References 25 publications

Endothelium-Dependent and -Independent Vasodilator Effects of Dimethyl Sulfoxide in Rat Aorta

Endothelium-Dependent and -Independent Vasodilator Effects of Dimethyl Sulfoxide in Rat Aorta

Advances in small animal mesentery models for in vivo flow cytometry, dynamic microscopy, and drug screening

Vasorelaxing Action of the Kynurenine Metabolite, Xanthurenic Acid: The Missing Link in Endotoxin-Induced Hypotension?

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