Biomedical subjects

P Boor

Publications and source records attributed to P Boor.

4 recordsLinked to original sources

PubMed2005

Rooibos tea (Aspalathus linearis) partially prevents oxidative stress in streptozotocin-induced diabetic rats.

The aim of this study was to investigate the effects of rooibos tea as a natural source of a wide scale of antioxidants on the prevention and treatment of oxidative stress in streptozotocin-induced diabetic rats. Expected significant changes of biochemical parameters characteristic for experimental diabetic state were found in plasma and tissues eight weeks after single dose streptozotocin application. Administration of aqueous and alkaline extracts of rooibos tea (or N-acetyl-L-cysteine for comparison) to diabetic rats did not affect markers of the diabetic status (glucose, glycated hemoglobin and fructosamine). Besides the parameters characterizing hepatotoxic effect of streptozotocin, rooibos tea significantly lowered advanced glycation end-products (AGEs) and malondialdehyde (MDA) in the plasma and in different tissues of diabetic rats, particularly MDA concentration in the lens. From these results we can conclude that antioxidant compounds in rooibos tea partially prevent oxidative stress and they are effective in both hydrophobic and hydrophilic biological systems. Therefore, rooibos tea as a commonly used beverage can be recommended as an excellent adjuvant support for the prevention and therapy of diabetic vascular complications, particularly for protecting ocular membrane systems against their peroxidation by reactive oxygen species.

Acetylcysteine↗

PubMed2001

[Increased levels of circulating advanced glycation end products in a model of acute renal insufficiency in rats].

BACKGROUND: Advanced glycation end products (AGEs) are formed from proteins and peptides by non-enzymatic glycation or glycooxidation. AGEs are formed slowly during aging, and they accumulate in circulation and tissues in diabetes and chronic renal failure. Kidney plays a key role in the disposal of AGEs. Aim of this study was to verify the hypothesis that, acute loss of renal function with enhanced oxidative and carbonyl stress should result in a rise of circulating AGEs levels. METHOD AND RESULTS: Acute renal failure (ARI) was induced in rats by bilateral nephrectomy (24-72 hours). The data on AGEs levels, oxidative status and antioxidative defense was compared to those of sham operated animals. 48 hours after the induction of ARI concentrations of AGEs, determined fluorimetrically or as carboxymethyllysine, rose 2-fold, and they correlated with concentrations of creatinine (r = 0.938, p < 0.001 and r = 0.815, p < 0.001, respectively). Malondialdehyde (MDA) and lipofuscine (LF) concentrations rose in a time dependent manner, suggesting an enhanced oxidative and carbonyl stress. Enhanced lipid peroxidation did not result from the suppressed antioxidant defense: activity of superoxide dismutase rose by 50%, while that of glutathione peroxidase was not compromised. Total antioxidant status increased, probably due to the accumulation of uremic toxins with scavenging capacity, such as hyppurate. CONCLUSIONS: According to our knowledge our data was first to show a rapid increase in circulating AGEs concentrations in the model of acute renal failure in rats. If AGEs accumulate in acute renal failure in humans, their contribution to acute toxicity, and/or to the development of later complications, might be of a great importance.

Acute Kidney Injury↗

PubMed2000

Ventricular arrhythmias following thermal damage of epicardial tissue: possible causes and clinical implications.

Epicardial heating may be used for ventricular tachycardia (VT) ablation and transmyocardial revascularization. However, the potential risks of thermal epicardial injury, including arrhythmia, have not been fully explored. This study relates the pathologic and arrhythmic sequellae of epicardial heating when applied with a diode laser at varying doses. Acute pathology and dosimetry were determined in a group of normal dogs using 2-3 W over 30-90 seconds. Another group received a similar dose range before undergoing 24-hour monitoring, and electrophysiological testing was done at 4 weeks. In this group, four dogs each received 12 lesions (90-180 J) according to a randomized block design. Another dog received nine lower dose lesions (30-120 J). Acute lesions measured 2.5-8.0-mm wide by 4-8.5-mm deep. Charring and vaporization were common when 3 W were applied over 45 seconds. Within 24 hours, VT with features of abnormal automaticity occurred in all dogs receiving this dose. The dog in whom lower doses induced coagulation only had no VT. Four weeks later, electrophysiological study induced no VT. At this time fibrosis and granulation tissue were organizing the contraction band necrosis seen acutely, and some lesion borders were becoming calcified. No major vessels had been damaged. Abnormal automaticity and VT may occur if thermal damage of the epicardium exceeds coagulation. This could be related to tissue injury caused by sudden water vaporization, and may have clinical relevance given the growing indications for myocardial heating.

Acute Disease↗

PubMed1999

Slow intramural heating with diffused laser light: A unique method for deep myocardial coagulation.

BACKGROUND: Catheter ablation of postinfarction ventricular tachycardia (VT) may be limited by insufficient myocardial coagulation or excessive endocardial or epicardial damage. We propose that volumetric heating restricted to intramural sites may improve the outcome and safety of this procedure, especially if delivered at rates that enhance heat conduction and forestall adverse tissue changes. METHODS AND RESULTS: A novel optical fiber with a diffusing tip for direct intramural, volumetric laser heating was tested via thoracotomy and percutaneously in normal dogs. Low-power (2.0- to 4.5-W) diode laser light (805 nm) diffused within tissue induced large lesions but no visible surface damage, mural thrombi, or transmural perforation. Mean lesion depth approximated tip length (10 mm). Mean lesion widths in the thoracotomy and percutaneous groups were 5.8+/-0.5 to 9.1+/-0.84 mm and 5.2+/-0.85 to 7.9+/-1.1 mm, respectively, depending on the light dose. Mean volumes in the percutaneous group were 1006+/-245 to 2471+/-934 mm. ST-segment depression, appearing in unfiltered bipolar electrograms recorded from the guiding catheter, was specific for lesion induction. All dogs survived the protocol, which included a 1-hour observation period. In cross section, lesions were elliptical to spherical and characterized by extensive contraction-band necrosis abruptly bordering viable tissue. No platelets or fibrin adhered to the endocardium. CONCLUSIONS: Slow, volumetric, and direct intramyocardial heating induces large, deep lesions without hazardous tissue damage. Such heating might cure postinfarction VT more successfully and safely than present techniques. Further testing and development of this method seem warranted.

Animals↗