Lack of effect of oral vitamin C on blood pressure, oxidative stress and endothelial function in Type II diabetes

2002 ◽  
Vol 103 (4) ◽  
pp. 339-344 ◽  
Author(s):  
D. DARKO ◽  
A. DORNHORST ◽  
F.J. KELLY ◽  
J.M. RITTER ◽  
P.J. CHOWIENCZYK
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Blood Flow ◽  
Vitamin C ◽  
Endothelial Function ◽  
Type Ii Diabetes ◽  
Forearm Blood Flow ◽  
Plasma Concentrations ◽  
Type Ii ◽  
Oral Vitamin

Type II diabetes is characterized by increased oxidative stress, endothelial dysfunction and hypertension. We investigated whether short-term treatment with oral vitamin C reduces oxidative stress and improves endothelial function and blood pressure in subjects with Type II diabetes. Subjects (n = 35) received vitamin C (1.5g daily in three doses) or matching placebo for 3 weeks in a randomized, double-blind, parallel-group design. Plasma concentrations of 8-epi-prostaglandin F2α (8-epi-PGF2α), a non-enzymically derived oxidation product of arachidonic acid, were used as a marker of oxidative stress. Endothelial function was assessed by measuring forearm blood flow responses to brachial artery infusion of the endothelium-dependent vasodilator acetylcholine (with nitroprusside as an endothelium-independent control) and by the pulse wave responses to systemic albuterol (endothelium-dependent vasodilator) and glyceryl trinitrate (endothelium-independent vasodilator). Plasma concentrations of vitamin C increased from 58±6 to 122±10μmol/l after vitamin C, but 8-epi-PGF2α levels (baseline, 95±4pg/l; after treatment, 99±5pg/l), blood pressure (baseline, 141±5/80±2mmHg; after treatment, 141±5/81±3mmHg) and endothelial function, as assessed by the systemic vasodilator response to albuterol and by the forearm blood flow response to acetylcholine, were not significantly different from baseline or placebo. Thus treatment with vitamin C (1.5 g daily) for 3 weeks does not significantly improve oxidative stress, blood pressure or endothelial function in patients with Type II diabetes.

Vascular KATP channel blockade by glibenclamide, but not by acarbose, in patients with Type II diabetes

2002 ◽  
Vol 102 (3) ◽  
pp. 307-314
Author(s):  
E.J. ABBINK ◽  
P. PICKKERS ◽  
A. Jansen VAN ROSENDAAL ◽  
J.A. LUTTERMAN ◽  
C.J. TACK ◽  
...  
Keyword(s):  
Blood Flow ◽  
Type Ii Diabetes ◽  
Katp Channel ◽  
Forearm Blood Flow ◽  
Cardiovascular Effects ◽  
Venous Occlusion ◽  
Type Ii Diabetes Mellitus ◽  
Protective Mechanism ◽  
Type Ii ◽  
Double Blind

Glibenclamide inhibits the opening of vascular ATP-sensitive potassium (KATP) channels, which represents a protective mechanism during ischaemia. This effect may imply harmful cardiovascular effects of glibenclamide when used under conditions of ischaemia in patients with Type II diabetes. Acarbose is not associated with effects on the cardiovascular system, because the drug is not absorbed from the bowel. Therefore we hypothesized that treatment of Type II diabetes patients with glibenclamide will impair the vasodilator function of KATP opening, unlike treatment with acarbose. A double-blind randomized cross-over study in 12 patients with Type II diabetes was performed to compare the effects of glibenclamide with those of acarbose on the vasodilator responses to KATP channel opening in the forearm vascular bed. The study consisted of two periods: 8 weeks of treatment with orally administered glibenclamide (10mgċday-1) followed by 8 weeks of treatment with acarbose (300mgċday-1), or vice versa. At the end of each treatment period, forearm blood flow (venous occlusion plethysmography) in response to intra-arterially administered diazoxide, acetylcholine and dipyridamole and to forearm ischaemia was measured. The diazoxide-mediated increase in the forearm blood flow ratio (infused/control arm) was significantly less pronounced after glibenclamide than after acarbose (290±58% and 561±101% respectively; P < 0.0005). Forearm blood flow responses to acetylcholine, dipyridamole and forearm ischaemia were similar during glibenclamide and acarbose treatment. Thus, in patients with Type II diabetes mellitus, treatment with glibenclamide is associated with an attenuated response to KATP opening as compared with treatment with acarbose. This implies that glibenclamide may affect defensive mechanisms under conditions of KATP channel activation.

scholarly journals Oral treatment with an antioxidant (raxofelast) reduces oxidative stress and improves endothelial function in men with Type II diabetes

Diabetologia ◽  
2000 ◽  
Vol 43 (8) ◽  
pp. 974-977 ◽  
Author(s):  
P. J. Chowienczyk ◽  
S. E. Brett ◽  
N. K. Gopaul ◽  
D. Meeking ◽  
M. Marchetti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Function ◽  
Type Ii Diabetes ◽  
Oral Treatment ◽  
Type Ii

Impact Of Caffeine On Exercising Forearm Blood Flow And VO2 In Type II Diabetes

2010 ◽  
Vol 42 ◽  
pp. 242
Author(s):  
Veronica Poitras ◽  
Michael Bravo ◽  
Melissa Pak ◽  
Michael E. Tschakovsky
Keyword(s):  
Blood Flow ◽  
Type Ii Diabetes ◽  
Forearm Blood Flow ◽  
Type Ii

Impaired cerebral CO2 vasoreactivity: association with endothelial dysfunction

2006 ◽  
Vol 291 (4) ◽  
pp. H1856-H1861 ◽  
Author(s):  
Shahar Lavi ◽  
Diana Gaitini ◽  
Victor Milloul ◽  
Giris Jacob
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Sodium Nitroprusside ◽  
Forearm Blood Flow ◽  
Reactive Hyperemia ◽  
Area Under The Curve ◽  
Healthy Controls ◽  
No Donor

Conflicting data exist on the role of nitric oxide (NO) in cerebral blood flow (CBF) autoregulation. Previous studies involving human and animal subjects seem to indicate that NO involvement is limited to the CO2-dependent mechanism (chemoregulation) and not to the pressure-dependent autoregulation (mechanoregulation). We tested this hypothesis in patients with impaired endothelial function compared with healthy controls. Blood pressure, heart rate, end-tidal Pco2, CBF velocities (CBFV), forearm blood flow, and reactive hyperemia were assessed in 16 patients with diabetes mellitus and/or hypertension and compared with 12 age- and sex-matched healthy controls. Pressure-dependent autoregulation was determined by escalating doses of phenylephrine. CO2 vasoreactivity index was extrapolated from individual slopes of mean CBFV during normocapnia, hyperventilation, and CO2 inhalation. Measurements were repeated after sodium nitroprusside infusion. Indexes of endothelial function, maximal and area under the curve (AUC) of forearm blood flow (FBF) changes, were significantly impaired in patients (maximal flow: 488 ± 75 vs. 297 ± 31%; P = 0.01, AUC ΔFBF: 173 ± 17 vs. 127 ± 11; P = 0.03). Patients and controls showed similar changes in cerebrovascular resistance during blood pressure challenges (identical slopes). CO2 vasoreactivity was impaired in patients compared with controls: 1.19 ± 0.1 vs. 1.54 ± 0.1 cm·s−1·mmHg−1; P = 0.04. NO donor (sodium nitroprusside) offsets this disparity. These results suggest that patients with endothelial dysfunction have impaired CO2 vasoreactivity and preserved pressure-dependent autoregulation. This supports our hypothesis that NO is involved in CO2-dependent CBF regulation alone. CBFV chemoregulation could therefore be a surrogate of local cerebral endothelial function.

Individuals with cystic fibrosis do not display impaired endothelial function or evidence of oxidative damage in endothelial cells exposed to serum

2001 ◽  
Vol 101 (5) ◽  
pp. 507-513 ◽  
Author(s):  
Lawrence T. McGRATH ◽  
Damien McCALL ◽  
Colm G. HANRATTY ◽  
Siobhan BRENNAN ◽  
Adrian DEVINE ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cystic Fibrosis ◽  
Endothelial Cells ◽  
Blood Flow ◽  
Lactate Dehydrogenase ◽  
Endothelial Function ◽  
Forearm Blood Flow ◽  
Lipid Hydroperoxides ◽  
Human Endothelial Cells ◽  
Systemic Oxidative Stress

Heightened systemic oxidative stress is increasingly recognized as a feature of cystic fibrosis (CF). The consequences of long-term exposure to free radical attack include a predisposition to diseases such as cancer and atherosclerosis. An increased incidence of malignancy among adult patients with CF has been reported, but the absence of atherosclerotic disease is well described. The aim of the present study was to assess endothelial function in vivo and relate this to the potential of serum from patients with CF to induce oxidative-mediated damage in cultured human endothelial cells. A group of 11 CF patients was matched with a group of healthy volunteers with regard to age and sex. Endothelial function was assessed as endothelium-dependent and -independent vasodilation by measuring forearm blood flow in response to infused acetylcholine and sodium nitroprusside respectively. Confluent monolayers of cultured human endothelial cells were exposed to serum from CF patients and control subjects. Following exposure, cell death was assessed by lactate dehydrogenase release, and the degree of lipid peroxidation in the membrane was assessed by measuring the content of lipid hydroperoxides, malondialdehyde and 4-hydroxynonenal. Endothelial monolayers exposed to serum from CF patients released significantly less lactate dehydrogenase following exposure than those exposed to serum from healthy controls (1.8% and 3.0% respectively; mean difference -1.2%; 95% confidence intervals -1.9% to -0.1%; P < 0.05) and contained significantly less 4-hydroxynonenal (0.75 and 3.41μmol/g of protein respectively; mean difference -2.66μmol/g; 95% confidence intervals -5.10 to -0.22μmol/g; P < 0.05). There was no significant difference between patients and controls in the extent of serum-induced membrane peroxidation, as assessed by malondialdehyde or lipid hydroperoxides, or in endothelial function, as assessed by forearm blood flow. In conclusion, despite evidence for heightened systemic oxidative stress in CF, patients displayed no impairment of endothelial function, and their serum caused significantly less damage to human endothelial cells than that from matched controls.

scholarly journals Novel Soy Germ Pasta Improves Endothelial Function, Blood Pressure, and Oxidative Stress in Patients With Type 2 Diabetes: Figure 1

Diabetes Care ◽  
2011 ◽  
Vol 34 (9) ◽  
pp. 1946-1948 ◽  
Author(s):  
Carlo Clerici ◽  
Elisabetta Nardi ◽  
Pier Maria Battezzati ◽  
Stefania Asciutti ◽  
Danilo Castellani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Type 2 Diabetes ◽  
Endothelial Function ◽  
And Oxidative Stress
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