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We are analyzing https://link.springer.com/article/10.1007/bf02919638.

Title:
The effect of insufficiency of tetrahydrobiopterin on endothelial function and vasoactivity | General Thoracic and Cardiovascular Surgery
Description:
Objective: It has recently been defined that levels of tetrahydrobiopterin, a cofactor of nitric oxide synthase, decreases under some disease conditions including atherosclerosis, hypercholesterolemia, diabetes, and ischemia-reperfusion. The present study was designed to investigate whether or not a deficiency in tetrahydrobiopterin affected vasoactivation in vivo and in vitro.Subjects and Methods: Male Sprague-Dawley rats were divided into two groups, and given either 2, 4-diamino-6-hydroxypyrimidine (DAHP), a selective inhibitor of tetrahydrobiopterin production, or a vehicle (10% polyethylene glycol 400 in 5% glucose, 20 ml/kg), intraperitoneally at 24 hr prior to examination. Responses to several vasodilating agents were examined in both pretreatment groups in vivo and in vitro. Furthermore, the isolated heart was perfused with a 37ยฐC Krebs-Henseleit solution for 30 min. The effects of insufficient tetrahydrobiopterin on the left ventricular function were examined. Moreover, nitrite plus nitrate (NOx) in the coronary effluent was examined in both groups.Results: Depressor and vasodilatation responses to an endothelium-dependent vasodilator were significantly attenuated in the DAHP Group in comparison with those in the vehicle Control Group, while the endothelium-independent vasodilator caused equivalent depressor and vasodilatation responses between the two groups. The NOx levels in the coronary effluent were lower in the DAHP Group than in the Control Group (p<0.05). The cardiovascular parameters were also lower in the DAHP Group than in the Control Group. Conclusions: We concluded from these findings that a deficiency in tetrahydrobiopterin aggravated endothelial dysfunction and the left ventricular dysfunction. These findings were consistent with the hypothesis that decreased levels of tetrahydrobiopterin may cause cardiac and vascular dysfunction.
Website Age:
28 years and 1 months (reg. 1997-05-29).

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๐ŸŒ  Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,734,772 visitors per month in the current month.

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How Does Link.springer.com Make Money? {๐Ÿ’ธ}

We're unsure how the site profits.

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Keywords {๐Ÿ”}

article, tetrahydrobiopterin, google, scholar, pubmed, cas, endothelial, nitric, function, oxide, dysfunction, content, effect, synthase, group, privacy, cookies, journal, cardiovascular, yamashiro, access, publish, search, miyagi, disease, dahp, vasodilator, injury, data, information, log, research, surgery, kuniyoshi, arakaki, levels, cofactor, ischemiareperfusion, vivo, groups, responses, examined, coronary, endotheliumdependent, control, vascular, discover, biochem, res, cosentino,

Topics {โœ’๏ธ}

month download article/chapter nitric oxide synthase male sprague-dawley rats endothelium-derived relaxing factor related subjects ischemia-reperfusion injury nitric oxide tetrahidrobiopterin synthasis reduces full article pdf privacy choices/manage cookies vascular endothelial function left ventricular dysfunction endothelium-dependent vasodilator aortic endothelial cells check access instant access spontaneously hypertensive rats guinea pig hearts conditions privacy policy european economic area krebs-henseleit solution dexamethasone suppression test functioning adrenal incidentaloma reactive hyperemia response experimental endotoxic shock left ventricular function tetrahydrobiopterin affected vasoactivation tetrahydrobiopterin-dependent formation ischemia-reperfusion article yamashiro vascular dysfunction accepting optional cookies coronary artery disease reperfusion injury lรผscher tf endothelial dysfunction cardiovascular surgery aims main content log tetrahydrobiopterin-dependent inhibition article log journal finder publish article cite vascular disease endothelial function vehicle control group critical cofactor subjects tetrahydrobiopterin production privacy policy personal data

Questions {โ“}

  • Tetrahydrobiopterin: A critical cofactor for eNOS and a strategy in the treatment of endothelial dysfunction?

Schema {๐Ÿ—บ๏ธ}

WebPage:
      mainEntity:
         headline:The effect of insufficiency of tetrahydrobiopterin on endothelial function and vasoactivity
         description:Objective: It has recently been defined that levels of tetrahydrobiopterin, a cofactor of nitric oxide synthase, decreases under some disease conditions including atherosclerosis, hypercholesterolemia, diabetes, and ischemia-reperfusion. The present study was designed to investigate whether or not a deficiency in tetrahydrobiopterin affected vasoactivation in vivo and in vitro.Subjects and Methods: Male Sprague-Dawley rats were divided into two groups, and given either 2, 4-diamino-6-hydroxypyrimidine (DAHP), a selective inhibitor of tetrahydrobiopterin production, or a vehicle (10% polyethylene glycol 400 in 5% glucose, 20 ml/kg), intraperitoneally at 24 hr prior to examination. Responses to several vasodilating agents were examined in both pretreatment groups in vivo and in vitro. Furthermore, the isolated heart was perfused with a 37ยฐC Krebs-Henseleit solution for 30 min. The effects of insufficient tetrahydrobiopterin on the left ventricular function were examined. Moreover, nitrite plus nitrate (NOx) in the coronary effluent was examined in both groups.Results: Depressor and vasodilatation responses to an endothelium-dependent vasodilator were significantly attenuated in the DAHP Group in comparison with those in the vehicle Control Group, while the endothelium-independent vasodilator caused equivalent depressor and vasodilatation responses between the two groups. The NOx levels in the coronary effluent were lower in the DAHP Group than in the Control Group (p<0.05). The cardiovascular parameters were also lower in the DAHP Group than in the Control Group. Conclusions: We concluded from these findings that a deficiency in tetrahydrobiopterin aggravated endothelial dysfunction and the left ventricular dysfunction. These findings were consistent with the hypothesis that decreased levels of tetrahydrobiopterin may cause cardiac and vascular dysfunction.
         datePublished:
         dateModified:
         pageStart:472
         pageEnd:477
         sameAs:https://doi.org/10.1007/BF02919638
         keywords:
            tetrahydrobiopterin
            nitric oxide synthase
            nitric oxide
            endothelial dysfunction
            Thoracic Surgery
            Cardiac Surgery
            Cardiology
            Surgical Oncology
         image:
         isPartOf:
            name:The Japanese Journal of Thoracic and Cardiovascular Surgery
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            volumeNumber:50
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         author:
               name:Satoshi Yamashiro
               affiliation:
                     name:University of the Ryukyus
                     address:
                        name:2nd Department of Surgery, School of Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Yukio Kuniyoshi
               affiliation:
                     name:University of the Ryukyus
                     address:
                        name:2nd Department of Surgery, School of Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan
                        type:PostalAddress
                     type:Organization
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               name:Katsuya Arakaki
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                     name:University of the Ryukyus
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                        name:2nd Department of Surgery, School of Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan
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      headline:The effect of insufficiency of tetrahydrobiopterin on endothelial function and vasoactivity
      description:Objective: It has recently been defined that levels of tetrahydrobiopterin, a cofactor of nitric oxide synthase, decreases under some disease conditions including atherosclerosis, hypercholesterolemia, diabetes, and ischemia-reperfusion. The present study was designed to investigate whether or not a deficiency in tetrahydrobiopterin affected vasoactivation in vivo and in vitro.Subjects and Methods: Male Sprague-Dawley rats were divided into two groups, and given either 2, 4-diamino-6-hydroxypyrimidine (DAHP), a selective inhibitor of tetrahydrobiopterin production, or a vehicle (10% polyethylene glycol 400 in 5% glucose, 20 ml/kg), intraperitoneally at 24 hr prior to examination. Responses to several vasodilating agents were examined in both pretreatment groups in vivo and in vitro. Furthermore, the isolated heart was perfused with a 37ยฐC Krebs-Henseleit solution for 30 min. The effects of insufficient tetrahydrobiopterin on the left ventricular function were examined. Moreover, nitrite plus nitrate (NOx) in the coronary effluent was examined in both groups.Results: Depressor and vasodilatation responses to an endothelium-dependent vasodilator were significantly attenuated in the DAHP Group in comparison with those in the vehicle Control Group, while the endothelium-independent vasodilator caused equivalent depressor and vasodilatation responses between the two groups. The NOx levels in the coronary effluent were lower in the DAHP Group than in the Control Group (p<0.05). The cardiovascular parameters were also lower in the DAHP Group than in the Control Group. Conclusions: We concluded from these findings that a deficiency in tetrahydrobiopterin aggravated endothelial dysfunction and the left ventricular dysfunction. These findings were consistent with the hypothesis that decreased levels of tetrahydrobiopterin may cause cardiac and vascular dysfunction.
      datePublished:
      dateModified:
      pageStart:472
      pageEnd:477
      sameAs:https://doi.org/10.1007/BF02919638
      keywords:
         tetrahydrobiopterin
         nitric oxide synthase
         nitric oxide
         endothelial dysfunction
         Thoracic Surgery
         Cardiac Surgery
         Cardiology
         Surgical Oncology
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      isPartOf:
         name:The Japanese Journal of Thoracic and Cardiovascular Surgery
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         volumeNumber:50
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            Periodical
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         name:Springer-Verlag
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            name:Satoshi Yamashiro
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                  name:University of the Ryukyus
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                     name:2nd Department of Surgery, School of Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan
                     type:PostalAddress
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            name:Yukio Kuniyoshi
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                  name:University of the Ryukyus
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                     name:2nd Department of Surgery, School of Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan
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            name:Katsuya Arakaki
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                  name:University of the Ryukyus
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                     name:2nd Department of Surgery, School of Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan
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            name:Kazufumi Miyagi
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                  name:University of the Ryukyus
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                     name:2nd Department of Surgery, School of Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan
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            name:Kageharu Koja
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                  name:University of the Ryukyus
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                     name:2nd Department of Surgery, School of Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan
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      name:Yukio Kuniyoshi
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            name:University of the Ryukyus
            address:
               name:2nd Department of Surgery, School of Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan
               type:PostalAddress
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      name:Katsuya Arakaki
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            name:University of the Ryukyus
            address:
               name:2nd Department of Surgery, School of Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan
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      name:Kazufumi Miyagi
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            name:University of the Ryukyus
            address:
               name:2nd Department of Surgery, School of Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan
               type:PostalAddress
            type:Organization
      name:Kageharu Koja
      affiliation:
            name:University of the Ryukyus
            address:
               name:2nd Department of Surgery, School of Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan
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      name:2nd Department of Surgery, School of Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan
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