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  • 1
    Online Resource
    Online Resource
    Nicotine Does Not Influence Arterial Lipid Deposits in Rabbits Exposed to Second-Hand Smoke
    Ovid Technologies (Wolters Kluwer Health) ; 2001
    In:  Circulation Vol. 104, No. 7 ( 2001-08-14), p. 810-814
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 104, No. 7 ( 2001-08-14), p. 810-814
    Abstract: Background Second-hand smoke (SHS) accelerates atherogenesis and impairs vascular function. The role of nicotine in this process has not been defined. Methods and Results To examine the potential effects of nicotine on atherogenesis and vascular function, 48 rabbits receiving a 0.5% cholesterol diet were randomized to control (cholesterol diet only), SHS from nicotine-standard research cigarettes (SHS-ST), and SHS from nicotine-free research cigarettes (SHS-NF). The SHS rabbits were exposed to 48 nicotine-standard (12 animals) or nicotine-free (12 animals) cigarettes/d, 5 d/wk for 10 weeks. Air carbon monoxide and particulates and plasma carboxyhemoglobin were significantly higher in the 2 SHS groups than the control group ( P 〈 0.001). The SHS-ST group had significant increases in plasma nicotine and cotinine compared with the other groups ( P 〈 0.001). There was no difference in serum lipids. Lipid lesions were increased in both SHS groups (54±5% [SEM] aorta and 66±4% pulmonary artery, 53±7% and 69±4%, and 39±4% and 43±3% in the SHS-ST, SHS-NF, and control groups, respectively; P =0.049 aorta and P 〈 0.001 pulmonary artery). Conclusions SHS exposure increased arterial lipid lesions, but nicotine did not contribute significantly to this effect. This effect is presumably due to other combustion products in the smoke.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/hc3301.092788
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2001
    detail.hit.zdb_id: 1466401-X
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  • 2
    Online Resource
    Online Resource
    Lactate Accumulation in Ischemic- and Anoxic-Isolated Rat Hearts Assessed by H-l Spectroscopy
    Ovid Technologies (Wolters Kluwer Health) ; 1987
    In:  Investigative Radiology Vol. 22, No. 8 ( 1987-08), p. 638-641
    Details
    In: Investigative Radiology, Ovid Technologies (Wolters Kluwer Health), Vol. 22, No. 8 ( 1987-08), p. 638-641
    Type of Medium: Online Resource
    ISSN: 0020-9996
    URL: Article
    DOI: 10.1097/00004424-198708000-00004
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1987
    detail.hit.zdb_id: 2041543-6
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  • 3
    Online Resource
    Online Resource
    Effects of l -Arginine on Atherogenesis and Endothelial Dysfunction due to Secondhand Smoke
    Ovid Technologies (Wolters Kluwer Health) ; 1999
    In:  Hypertension Vol. 34, No. 1 ( 1999-07), p. 44-50
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 34, No. 1 ( 1999-07), p. 44-50
    Abstract: Abstract —Secondhand smoke (SHS) and hypercholesterolemia increase cardiovascular risk. We hypothesized that l -arginine, the precursor of nitric oxide (NO), might protect against atherogenesis and endothelial dysfunction caused by SHS. The effects of l -arginine supplementation (2.25% solution ad libitum) and SHS (smoking chambers for 10 weeks) were examined in 32 hypercholesterolemic rabbits. Eight normal rabbits served as controls. Acetylcholine- and nitroglycerin-induced vasorelaxation was assessed in aortic rings precontracted with norepinephrine. Hypercholesterolemia increased intimal lesion area ( P =0.012), reduced endothelium-dependent relaxation ( P =0.009), and reduced basal ( P =0.005) and stimulated ( P 〈 0.0005) production of NOs. SHS increased intimal lesion area ( P =0.01) norepinephrine-induced contraction ( P =0.001) and reduced endothelium-dependent relaxation ( P =0.02). SHS-induced increase in norepinephrine contraction was abolished by the inhibition of NO synthase and removal of endothelium. l -Arginine improved endothelium-dependent relaxation ( P =0.001) and attenuated SHS-induced endothelial dysfunction ( P =0.007) and atherogenesis ( P =0.001). Basal production of nitrogen oxides correlated inversely with intimal lesion area ( r =−0.66; P 〈 0.0005) and stimulated production of NOs correlated with endothelium-dependent relaxation ( r =−0.66; P 〈 0.001). SHS causes endothelial dysfunction and increased adrenergic responsiveness and atherogenesis in hypercholesterolemic rabbits. Chronic dietary supplementation with the NO precursor l -arginine mitigates these effects. The adverse vascular consequences of SHS appear to be mediated via deleterious effects on endothelial function.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.34.1.44
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1999
    detail.hit.zdb_id: 2094210-2
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  • 4
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    Online Resource
    Reduction of Infarct Size During Myocardial Ischemia and Reperfusion by Lazaroid U-74500A, a Nonglucocorticoid 21 -Aminosteroid
    Ovid Technologies (Wolters Kluwer Health) ; 1994
    In:  Journal of Cardiovascular Pharmacology Vol. 23, No. 1 ( 1994-01), p. 136-140
    Details
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 23, No. 1 ( 1994-01), p. 136-140
    Type of Medium: Online Resource
    ISSN: 0160-2446
    URL: Article
    DOI: 10.1097/00005344-199401000-00019
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1994
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
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  • 5
    Online Resource
    Online Resource
    Measurement of Regional : Myocardial Blood Flow in Dogs by Ultrafast CT
    Ovid Technologies (Wolters Kluwer Health) ; 1988
    In:  Investigative Radiology Vol. 23, No. 5 ( 1988-05), p. 348-353
    Details
    In: Investigative Radiology, Ovid Technologies (Wolters Kluwer Health), Vol. 23, No. 5 ( 1988-05), p. 348-353
    Type of Medium: Online Resource
    ISSN: 0020-9996
    URL: Article
    DOI: 10.1097/00004424-198805000-00003
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1988
    detail.hit.zdb_id: 2041543-6
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  • 6
    Online Resource
    Online Resource
    Effect of Lovastatin on Suppression and Regression of Atherosclerosis in Lipid-Fed Rabbits
    Ovid Technologies (Wolters Kluwer Health) ; 1992
    In:  Journal of Cardiovascular Pharmacology Vol. 19, No. 2 ( 1992-02), p. 246-255
    Details
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 19, No. 2 ( 1992-02), p. 246-255
    Type of Medium: Online Resource
    ISSN: 0160-2446
    URL: Article
    DOI: 10.1097/00005344-199202000-00013
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1992
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
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  • 7
    Online Resource
    Online Resource
    Catalase Inhibition With 3-Amino-1,2,4-Triazole Does Not Abolish Infarct Size Reduction in Heat-Shocked Rats
    Ovid Technologies (Wolters Kluwer Health) ; 1995
    In:  Circulation Vol. 92, No. 11 ( 1995-12), p. 3318-3322
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 92, No. 11 ( 1995-12), p. 3318-3322
    Abstract: Background Recent studies have shown that improved myocardial salvage after heat-shock pretreatment correlates with the amount of induced cardiac heat-shock protein (HSP)72. However, heat shock also induces myocardial catalase activity, potentially reducing free radical–mediated ischemic injury. The aim of the present study was to determine whether catalase inhibition with 3-amino-1,2,4-triazole (3-AT) abolishes the reduction of infarct size conferred by heat-shock treatment in rats. Methods and Results Myocardial catalase activity was measured in both heat-shocked and control rats 60 minutes after either 3-AT (1000 mg/kg IV) or saline infusion. In separate experiments, heat-shocked and control rats were treated with 3-AT or saline 60 minutes before being subjected to 35 minutes of left coronary artery occlusion and 120 minutes of reperfusion. Infarct size was determined by dual perfusion with triphenyltetrazolium chloride and phthalocyanine blue dye. Heat-shock treatment significantly increased myocardial catalase compared with control animals (180.5±4.8, n=6, versus 86.2±14.7, n=5, units/g wet wt; P 〈 .05). Treatment with 3-AT significantly reduced myocardial catalase activity in both heat-shocked and control animals (29.6±5.7, n=5, and 36.4±15.3, n=6, respectively). Heat-shock treatment significantly reduced infarct size in rats that were both treated and untreated with 3-AT compared with respective control groups (22.5±3.7%, n=26, 28.2±4.0%, n=22, 52.0±3.0%, n=23, and 48.6±3.2%, n=26, respectively; P 〈 .0001 for both heat-shocked groups versus both control groups; infarct mass/risk area mass×100). Conclusions Catalase inhibition with 3-AT does not abolish the reduction of infarct size in heat-shocked rats.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.92.11.3318
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1995
    detail.hit.zdb_id: 1466401-X
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  • 8
    Online Resource
    Online Resource
    Chronic Dietary l -Arginine Prevents Endothelial Dysfunction Secondary to Environmental Tobacco Smoke in Normocholesterolemic Rabbits
    Ovid Technologies (Wolters Kluwer Health) ; 1997
    In:  Hypertension Vol. 29, No. 5 ( 1997-05), p. 1186-1191
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 29, No. 5 ( 1997-05), p. 1186-1191
    Abstract: Abstract Our goal was to determine whether environmental tobacco smoke causes endothelial dysfunction in the absence of hypercholesterolemia and whether such an effect can be prevented by supplementation with l -arginine. Environmental tobacco smoke exposure is associated with an increase in coronary artery disease events and mortality. We have previously demonstrated that environmental tobacco smoke causes endothelial dysfunction and atherosclerosis in rabbits with diet-induced hypercholesterolemia and atherosclerosis and that chronic dietary l -arginine supplementation prevents this. The effects of l -arginine supplementation (2.25% solution ad libitum) and environmental tobacco smoke (smoking chambers for 10 weeks) were examined with a 2×2 design in 32 rabbits fed a normal diet. Acetylcholine, calcium ionophore A23187, and nitroglycerin-induced vasorelaxation were assessed in aortic rings precontracted with phenylephrine. Endothelial l -arginine levels were measured by chromatography. Chronic l -arginine supplementation increased serum ( P 〈 .001) and endothelial ( P =.003) l -arginine levels. Environmental tobacco smoke reduced endothelium-dependent acetylcholine-induced relaxation, and l -arginine blocked this adverse effect ( P =.04). Environmental tobacco smoke tended to increase phenylephrine-induced contraction ( P =.06). Neither environmental tobacco smoke nor l -arginine influenced A23187-induced relaxation nor endothelium-independent nitroglycerin-induced relaxation. Endothelial dysfunction secondary to environmental tobacco smoke may occur in the absence of diet-induced hypercholesterolemia and atherosclerosis. Chronic dietary supplementation with a nitric oxide donor such as l -arginine offsets the endothelial dysfunction associated with environmental tobacco smoke in normocholesterolemic rabbits, possibly through substrate loading of the nitric oxide pathway.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.29.5.1186
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1997
    detail.hit.zdb_id: 2094210-2
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  • 9
    Online Resource
    Online Resource
    One Minute of Marijuana Secondhand Smoke Exposure Substantially Impairs Vascular Endothelial Function
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Journal of the American Heart Association Vol. 5, No. 8 ( 2016-08-08)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 5, No. 8 ( 2016-08-08)
    Abstract: Despite public awareness that tobacco secondhand smoke (SHS) is harmful, many people still assume that marijuana SHS is benign. Debates about whether smoke‐free laws should include marijuana are becoming increasingly widespread as marijuana is legalized and the cannabis industry grows. Lack of evidence for marijuana SHS causing acute cardiovascular harm is frequently mistaken for evidence that it is harmless, despite chemical and physical similarity between marijuana and tobacco smoke. We investigated whether brief exposure to marijuana SHS causes acute vascular endothelial dysfunction. Methods and Results We measured endothelial function as femoral artery flow‐mediated dilation (FMD) in rats before and after exposure to marijuana SHS at levels similar to real‐world tobacco SHS conditions. One minute of exposure to marijuana SHS impaired FMD to a comparable extent as impairment from equal concentrations of tobacco SHS, but recovery was considerably slower for marijuana. Exposure to marijuana SHS directly caused cannabinoid‐independent vasodilation that subsided within 25 minutes, whereas FMD remained impaired for at least 90 minutes. Impairment occurred even when marijuana lacked cannabinoids and rolling paper was omitted. Endothelium‐independent vasodilation by nitroglycerin administration was not impaired. FMD was not impaired by exposure to chamber air. Conclusions One minute of exposure to marijuana SHS substantially impairs endothelial function in rats for at least 90 minutes, considerably longer than comparable impairment by tobacco SHS. Impairment of FMD does not require cannabinoids, nicotine, or rolling paper smoke. Our findings in rats suggest that SHS can exert similar adverse cardiovascular effects regardless of whether it is from tobacco or marijuana.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.116.003858
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 2653953-6
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  • 10
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    Online Resource
    Abstract 1421: In Vivo Measurement of Flow-Mediated Vasodilation in Living Rats using High Resolution Ultrasound: Age-Dependent Endothelial Dysfunction
    Ovid Technologies (Wolters Kluwer Health) ; 2007
    In:  Circulation Vol. 116, No. suppl_16 ( 2007-10-16)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 116, No. suppl_16 ( 2007-10-16)
    Abstract: In humans, endothelial function serves as a surrogate marker for cardiovascular health and is measured as changes in arterial diameter after temporary ischemia (flow-mediated dilation; FMD). We developed an FMD-related approach to study conduit artery vasodilation in living rats, and demonstrate a reduction in FMD in older versus younger animals consistent with age-related endothelial dysfunction. Diameter and Doppler-flow measurements were obtained from the femoral artery using high-resolution ultrasound (35 MHz). We observed dose-dependent vasodilation using both endothelium-dependent and endothelium-independent pharmacologic vasodilators (acetylcholine and nitroglycerine). Flow-dependent vasodilation was observed in response to flow increase induced both by adenosine and local saline infusion. Transient hindlimb ischemia led to reactive hyperemia with sequential flow velocity increase and femoral artery dilation, the latter of which was completely abolished by NO-synthase (NOS) inhibition with L-NMMA. To demonstrate its applicability in a model of endothelial dysfunction, we show that FMD is significantly reduced in older versus younger animals. While FMD was completely NOS-dependent in younger animals, NOS-dependent mechanisms accounted for only half of the FMD in older animals, with the remainder being blocked by charybdotoxin (CTx) and apamin suggesting contribution of endothelium-derived-hyperpolarizing-factor. Using this new integrative physiologic model to reproducibly study FMD in living rats, we show that age-dependent endothelial dysfunction is accompanied by a shift in mechanisms underlying vasodilatory endothelial function.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.116.suppl_16.II_292-b
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2007
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