Acute Hyperglycemia and Hyperinsulinemia Enhance Adrenergic Vasoconstriction and Decrease Calcitonin Gene-Related Peptide-Containing Nerve-Mediated Vasodilation in Pithed Rats

Zamami, Yoshito; Takatori, Shingo; Yamawaki, Kousuke; Miyashita, Satoko; Mio, Mitsunobu; Kitamura, Yoshihisa; Kawasaki, Hiromu

doi:10.1291/hypres.31.1033

Cited by 35 publications

(19 citation statements)

References 31 publications

(30 reference statements)

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“…45 Studies on glucose effects on neuropeptides are limited thus far, but there are indications that either dextrose elevations or a related reduction in insulin levels downregulate the activity of the transient receptor potential vanilloid type 1 (TRPV1) receptor which reduces production of pain producing (substance P) and degenerative (calcitonin gene-related peptide [CGRP]) neuropeptides. [46][47][48] …”

Section: Consideration Of Possible Mechanisms and Explanationsmentioning

confidence: 99%

Hyperosmolar Dextrose Injection for Recalcitrant Osgood-Schlatter Disease

Topol¹,

Podestá

Reeves

et al. 2011

Pediatrics

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WHAT'S KNOWN ON THIS SUBJECT:Osgood-Schlatter disease symptoms may wax and wane until maturity and affect sport confidence and participation periodically. Chronic sequelae may include anterior knee pain, kneeling discomfort, or sports limitation. Symptom reduction parallels resolution of patellar tendinopathy by MRI/ultrasound, although ossicles may persist radiographically. WHAT THIS STUDY ADDS:Small-needle injection of the patellar tendon enthesis/tibial apophysis with 12.5% dextrose was safe and well tolerated in adolescents with recalcitrant OsgoodSchlatter disease. Dextrose injection resulted in more rapid and frequent achievement of unaltered sport and asymptomatic sport than did usual care. abstract OBJECTIVE: To examine the potential of dextrose injection versus lidocaine injection versus supervised usual care to reduce sport alteration and sport-related symptoms in adolescent athletes with OsgoodSchlatter disease. PATIENTS AND METHODS: Girls aged 9 to 15 and boys aged 10 to 17 were randomly assigned to either therapist-supervised usual care or double-blind injection of 1% lidocaine solution with or without 12.5% dextrose. Injections were administered monthly for 3 months. All subjects were then offered dextrose injections monthly as needed. Unaltered sport (Nirschl Pain Phase Scale Ͻ 4) and asymptomatic sport (Nirschl Pain Phase Scale ϭ 0) were the threshold goals. RESULTS: Sixty-five knees in 54 athletes were treated. Compared with usual care at 3 months, unaltered sport was more common in both dextrose-treated (21 of 21 vs 13 of 22; P ϭ .001) and lidocaine-treated (20 of 22 vs 13 of 22; P ϭ .034) knees, and asymptomatic sport was more frequent in dextrose-treated knees than either lidocaine-treated (14 of 21 vs 5 of 22; P ϭ .006) or usual-care-treated (14 of 21 vs 3 of 22; P Ͻ .001) knees. At 1 year, asymptomatic sport was more common in dextrose-treated knees than knees treated with only lidocaine (32 of 38 vs 6 of 13; P ϭ .024) or only usual care (32 of 38 vs 2 of 14; P Ͻ .0001). CONCLUSIONS: Our results suggest superior symptom-reduction efficacy of injection therapy over usual care in the treatment of OsgoodSchlatter disease in adolescents. A significant component of the effect seems to be associated with the dextrose component of a dextrose/ lidocaine solution. Dextrose injection over the apophysis and patellar tendon origin was safe and well tolerated and resulted in more rapid and frequent achievement of unaltered sport and asymptomatic sport than usual care. Pediatrics 2011;128:e1121-e1128

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Section: Consideration Of Possible Mechanisms and Explanationsmentioning

confidence: 99%

Hyperosmolar Dextrose Injection for Recalcitrant Osgood-Schlatter Disease

Topol¹,

Podestá

Reeves

et al. 2011

Pediatrics

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“…Therefore, both adrenergic and CGRPergic nerves regulate the tone of resistance arteries by reciprocal interaction (Kawasaki et al, 1988(Kawasaki et al, , 1990. Previous reports demonstrated that an acute (insulin infusion) or chronic hyperinsulinemic state (FDR) caused increased adrenergic nerve-mediated vasoconstriction and decreased CGRPergic nervemediated vasodilatation, suggesting that hyperinsulinemia in FDR results in dysfunction of the neuronal vascular control system, leading to the development of hypertension (Takatori et al, 2006;Zamami et al, 2008). Therefore, the previous findings are supported by the present immunohistochemistry findings that hyperinsulinemia caused abnormal perivascular innervation in mesenteric resistance arteries of FDR resulting in increased adrenergic (TH-LI) nerve density and decreased CGRPergic (CGRP-LI) nerve density.…”

Section: Discussionmentioning

confidence: 99%

Ameliorative effect of Eucommia ulmoides Oliv. leaves extract (ELE) on insulin resistance and abnormal perivascular innervation in fructose-drinking rats

Jin

Amitani

Zamami

et al. 2010

Journal of Ethnopharmacology

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“…Taking all together, considering the observed reduction of the ischemic threshold (time to 1 mm ST-segment depression) associated to an increment of the ischemic burden (greater WMSI at stress echocardiography), it is likely that the mechanism by which HCM induced a greater ischemic impairment could be mainly related to an increase of vascular tone, confirming that acute hyperglycemia and hyperinsulinemia may increase adrenergic nerve-mediated vasoconstriction [29] and, consequentely, reduced coronary supply.…”

Section: Mechanisms Of Reduced Ischemic Threshold After Hcmmentioning

confidence: 92%