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Biomedical subjects

Christos M Papamichael

Publications and source records attributed to Christos M Papamichael.

24 records · Page 2Linked to original sources
PubMed2004

Endothelial dysfunction and type of cigarette smoked: the impact of 'light' versus regular cigarette smoking.

Acute cigarette smoking leads to temporary endothelial dysfunction, which is an early event in atherogenesis. Sufficient data concerning the effect of cigarettes with low tar and nicotine yield are lacking. Seventeen healthy individuals (nine women, eight men, aged 27.8 +/- 3.6 years) were subjected to evaluation of endothelial function by means of endothelium-dependent, flow-mediated dilatation (FMD) of the brachial artery, before, immediately after and 30, 60 and 90 min after smoking a regular cigarette (nicotine 0.9 mg, tar 12 mg) orthe corresponding 'light' cigarette (nicotine 0.6 mg, tar 8 mg). The following day, measurements were repeated after smoking the opposite kind of cigarette. Baseline FMD was 6.1 +/- 1.6% and 7.2 +/- 2.0% in the light and regular cigarette groups, respectively (p = NS). The overall effect of the regular cigarette over time on FMD compared with the light cigarette was significantly different (F = 3.039, p = 0.023). FMD was significantly depressed after smoking both types (light: F = 8.192, p < 0.001; regular: F = 16.698, p < 0.001). Immediately after smoking, FMD declined in both groups (light: 3.0 +/- 2.4% and regular: 1.6 +/- 3.2%, p < 0.001 and p < 0.001, respectively), and it remained significantly depressed in the regular cigarette group at 30 min (0.75+/-1.5%, p < 0.001) and 60 min (3.5 +/- 3.1%, p = 0.024), while in the light cigarette group FMD differences were abolished at 30, 60 and 90 min after smoking. In conclusion, acute smoking of both regular and light cigarettes leads to temporary vasomotor dysfunction; its duration is shorter after smoking a 'light' cigarette.

Adult↗
PubMed2003

Ascorbic acid does not improve endothelium-dependent flow-mediated dilatation of the brachial artery in patients with Raynaud's phenomenon secondary to systemic sclerosis.

Previous studies have shown that patients with Raynaud's phenomenon secondary to systemic sclerosis present abnormal endothelial function; the mechanisms responsible for the endothelial dysfunction are unknown but increased vascular oxidative stress could be a possible cause. The hypothesis that a potent water-soluble antioxidant can reverse endothelial dysfunction in these patients was tested in the present study. We examined 11 female patients with Raynaud's phenomenon secondary to systemic sclerosis and ten healthy control women by ultrasound imaging of the brachial artery to assess flow-mediated (endothelium-dependent) and nitrate-induced (endothelium-independent) vasodilatation. Flow-mediated dilatation and nitrate-induced dilatation were significantly reduced in patients with Raynaud's phenomenon, indicating abnormal endothelial and smooth muscle cell function. Patients with Raynaud's phenomenon entered a double-blind, randomized, crossover placebo-controlled trial and received orally 2 g of ascorbic acid or placebo; vascular studies were repeated two hours after ascorbic acid or placebo administration. Flow-mediated dilatation did not improve after ascorbic acid (1.6 +/- 2.2% to 2.2 +/- 2.5%, ns) or placebo administration (1.2 +/- 1.9% to 1.7 +/- 1.4%, ns); also nitrate-induced dilatation was similar after ascorbic acid or placebo (16 +/- 7.4% vs 17 +/- 8%, ns), suggesting no effect of ascorbic acid on endothelial and vascular smooth muscle function. In conclusion, ascorbic acid does not reverse endothelial vasomotor dysfunction in the brachial circulation of patients with Raynaud's phenomenon secondary to systemic sclerosis. The use of different antioxidants or different dosing of ascorbic acid may be required to show a beneficial effect on endothelial vasodilator function.

Administration, Oral↗
PubMed2003

Oral administration of ascorbic acid attenuates endothelial dysfunction after short-term cigarette smoking.

Short-term cigarette smoking is associated with persistent endothelial dysfunction. Data on the reversibility of this effect with per os antioxidants after short-term smoking are lacking. This study examines the effect of orally administered ascorbic acid on cigarette smoking-induced endothelial dysfunction. In the present double-blind, randomized, crossover study, 19 healthy subjects (28.7 +/- 6.8 years, mean +/- SD) were examined by high-resolution ultrasonography of the brachial artery before and 0, 30, 60, 90, and 120 minutes after smoking a cigarette. Flow-mediated dilatation (FMD) was used as a method to examine endothelial function. Measurements were performed on two different days, 2 hours after oral administration of 2 g of ascorbic acid or placebo. FMD was similar for each subject between the two visits at baseline. FMD was significantly decreased after smoking with both placebo and ascorbic acid. However, there was a significant beneficial effect of ascorbic acid on the FMD change over time after smoking. After smoking, the FMD dropped to less than half of the baseline value. Thereafter in the placebo group, FMD increased to 70% of baseline value in 90 minutes, but in the ascorbic acid group the FMD increased to 70% of baseline value in 46 minutes. Oral administration of ascorbic acid attenuates endothelial dysfunction after short-term cigarette smoking by shortening its duration.

Administration, Oral↗
PubMed2002

Oral L-arginine improves endothelial dysfunction in patients with essential hypertension.

BACKGROUND: L-Arginine is a nitric oxide precursor, which augments endothelium-dependent vasodilatation in hypercholesterolemic humans and animals. Endothelium-dependent vasodilation is attenuated in patients with hypertension; however the effects of oral L-arginine on endothelial function of the conduit arteries in patients with essential hypertension have not previously been investigated. METHODS: In a prospective randomized double blind trial, 35 patients with essential hypertension received either 6 g L-arginine (18 subjects) or placebo (17 subjects). Patients were examined for flow-mediated endothelium-dependent dilatation of the brachial artery before and 1.5 h after administration of L-arginine or placebo. At the end of the protocol the nitrate-induced, endothelium-independent vasodilatation was evaluated. RESULTS: Two groups of L-arginine and placebo were similar regarding age, sex, blood lipids, smoking, diabetes, coronary artery disease, body mass index, intima-media thickness of the common carotid artery, clinics blood pressure and baseline brachial artery parameters. Administration of L-arginine or placebo did not change significantly heart rate, blood pressure, baseline diameter, blood flow or reactive hyperemia. L-Arginine resulted in a significant improvement of flow-mediated dilatation (1.7+/-3.4 vs. 5.9+/-5.4%, P=0.008) while placebo did not significantly change this parameter (3.0+/-2.7 vs. 3.1+/-2.2%, P=ns). The effect of L-arginine on flow-mediated dilatation was significantly different from the effect of placebo (P=0.05). L-Arginine did not significantly influence nitrate-induced dilatation (16+/-6.9 vs. 17.7+/-6.7%, P=ns). CONCLUSIONS: Oral administration of L-arginine acutely improves endothelium-dependent, flow-mediated dilatation of the brachial artery in patients with essential hypertension. The long-term effects of L-arginine in these patients require further investigation.

Administration, Oral↗