Difference of blood’s oxygen between smokers and non-smokers patients with acute myocardial infarction and finding its cause in animal model

زمینه و هدف: در بیماران مبتلا به انفارکتوس حاد میوکارد، در اثر اختلالات قلبی-ریوی مقادیر گازهای خونی به خصوص اکسیژن غیر طبیعی می گردند، که می تواند موجب مرگ شود. ما در این تحقیق، اولاَ اختلاف اکسیژن خون در افراد سیگاری و غیر سیگاری مبتلا به انفارکتوس حاد میوکارد را نشان داده ایم. ثانیاَ مراحل مختلف تغییرات ناشی از مصرف سیگار و نیکوتین را بر هموگلوبین، هماتوکریت، تعداد گلبولهای قرمز و اکسیژن خون بطور تجربی در خرگوش مطالعه کرده ایم. همچنین روند تغییرات پس از ترک سیگار، و علت تفاوت اکسیژن خون بین افراد سیگاری و غیر سیگاری مبتلا به انفارکتوس حاد میوکارد مورد بررسی قرار گرفته است. روش مطالعه: ابتدا هموگلوبین، هماتوکریت و اکسیژن خون در تعداد 46 فرد سیگاری و غیر سیگاری مبتلا به انفارکتوس حاد میوکارد اندازه گیری شده است سپس 35 عدد خرگوش به سه گروه شاهد، سیگاری و نیکوتینی تقسیم شدند. گروه سیگاری به مدت 16 روز در معرض دود سیگار قرار گرفت و گروه نیکوتینی در همین مدت مورد تزریق نیکوتین واقع شد و میزان هموگلوبین، هماتوکریت و اکسیژن خون، قبل و بعد از 16 روز و یک هفته یا 20 روز پس از ترک سیگار مورد اندازه گیری قرار گرفت. آزمون t برای مقایسه استفاده شد. نتایج: مشاهده شد که هموگلوبین، هماتوکریت و اکسیژن خون در بیماران سیگاری، بیشتر بود. در آزمایشات حیوانی، در اثر مصرف سیگار، هموگلوبین، هماتوکریت و تعداد گلبول قرمز افزایش یافتند و نیکوتین در این افزایش نقش نداشت. پس از ترک سیگار، همه تغییرات حاصله، روند بازگشت بحالت نرمال را شروع کردند و فشار اکسیژن در روزهای اولیه ترک سیگار افزایش یافت. نتیجه گیری: اکسیژن خون در بیماران سیگاری مبتلا به انفارکتوس حاد میوکارد بیشتر از افراد غیر سیگاری است و علت آن بیشتر بودن هموگلوبین آزاد پس از ترک سیگار به دنبال انفارکتوس است

Re: Effect of Nigella sativa against cisplatin induced nephrotoxicity in rats

n.a

Early prevention by L-Arginine attenuates coronary atherosclerosis in a model of hypercholesterolemic animals; no positive results for treatment

<p>Abstract</p> <p>Background</p> <p>Endothelial dysfunction (ED) is an independent predictor of cardiovascular events. ED is also a reversible disorder, and nitric oxide donors like L-arginine may promote this process. Despite the positive results from several studies, there are some studies that have shown that L-arginine administration did not improve endothelium-dependent dilation or the inflammatory state of patients. In this study the early and the late effects of L-arginine on coronary fatty streak formation and ED biomarkers were considered in hypercholesterolemic rabbits.</p> <p>Methods</p> <p>36 white male rabbits randomly assigned in 3 groups. Rabbits were fed 1% high-cholesterol diet (LP group, n = 15), or high-cholesterol diet with oral L-arginine (3% in drinking water) (EP group, n = 15) or standard diet (control group, n = 6) for 4 weeks (phase I). Afterward, all animals were fed normal diet for 4 weeks (phase II). In the second phase, L-arginine was discontinued for EP group and was begun for LP group. The plasma levels of lipids, von Willebrand factor (vWF), and nitrite were compared before and after 4 and 8 weeks of experiment. Coronary fatty streak formation was measure after 4 and 8 weeks of experiment.</p> <p>Results</p> <p>The plasma levels of lipids were increased significantly in both groups of LP and EP after phase I. The hypercholesterolemia induced significant increased vWF release in LP group. The L-arginine supplementation led to significant plasma nitrite increment in EP group. The vWF in LP group was higher than other groups (p < 0.05). By the end of phase II, despite of start of L-arginine supplementation for LP group and L-arginine discontinuation in EP group, there were significantly more fatty streaks lesions in LP group coronary arteries than EP group. Furthermore, L-arginine supplementation did not result in significant nitrite increment in LP group.</p> <p>Conclusion</p> <p>Early prevention by L-arginine may be helpful to prevent the ED, but our study did not suggest the treatment. It seems reasonable to consider ED-aside from control the cardiovascular risk factors in primary prevention of atherosclerosis and its clinical outcomes before development of irreversible vascular damage.</p

The prevention of endothelial dysfunction through endothelial cell apoptosis inhibition in a hypercholesterolemic rabbit model: the effect of L-arginine supplementation

<p>Abstract</p> <p>Background</p> <p>The impact of L-arginine on atherogenesis and its ability to prevent endothelial dysfunction have been studied extensively during the past years. L-arginine is a substance for nitric oxide synthesis which involves in apoptosis. Hypercholesterolemia promotes endothelial dysfunction, and it is hypothesized that L-arginine prevents endothelial dysfunction through endothelial cells apoptosis inhibition. To test this hypothesis, thirty rabbits were assigned into two groups. The control group received 1% cholesterol diet for 4 weeks, and the L-arginine group received same diets plus 3% L-arginine in drinking water.</p> <p>Results</p> <p>No significant differences were observed in cholesterol level between two groups, but the nitrite concentration in L-arginine group was significantly higher than other group (control group: 11.8 ± 1; L-arginine group: 14.7 ± 0.5 μmol/l); (<it>p </it>< 0.05). The aorta score of fatty streak in control group was 0.875 ± 0.35, but no fatty streak lesion was detected in L-arginine group (<it>p </it>< 0.05). The number of intimal apoptotic cells/500 cells of aorta in two groups of experiment were statistically different (control group: 39.3 ± 7.6; L-arginine group: 21.5 ± 5.3) (<it>p </it>< 0.05).</p> <p>Conclusion</p> <p>The inhibition of endothelial cells apoptosis by L-arginine restores endothelial function in a model of hypercholesterolemia.</p

LArginine supplementation influenced nitrite but not nitrate and total nitrite in rabbit model of hypercholesterolemia

ABSTRACT Background: The assessment of altered nitric oxide (NO) availability is of potentially important diagnostic and prognostic significance. The present study is aimed to investigate the effect of L-arginine (as a natural NO donor) supplementation on NO metabolite in a rabbit model of hypercholesterolemia to find a reliable marker for endothelial NO production. Methods: White male rabbits (n = 30) randomly assigned to 2 groups. Rabbits were fed 1% high-cholesterol diet (HC group, n = 15), or HC diet with oral L-arginine (3% in drinking water) (HC + L-arginine group, n = 15) for 4 weeks. The serum levels of lipids, L-arginine, total NO metabolites (NOx), nitrite and nitrate were measured before and after the study. Results: In this study, Larginine supplementation led to a significant increased plasma level of L-arginine. The serum level of nitrite was significantly higher in L-arginine treated group while serum level of nitrate and NOx was significantly lower than HC group. Conclusion: As the result of our study showed, nitrite is a useful marker of endogenous endothelial NO production and although frequently used, neither nitrate nor NOx are reliable markers of acute changes in endothelial NO synthase activity

Efficacy of Co-Administration of garlic extract and metformin for prevention of gentamicin-renal toxicity in wistar rats: A biochemical study

Background: Gentamicin (GM) nephrotoxicity has been related to oxidative stress. Garlic and metformin (MF) have anti-oxadant activity and therefore, this study was aimed to evaluate the preventive and curative effects of garlic, MF and their combination on GM indeced tubular toxicity in Wistar rats. Methods: In a pre-clinical study, 70 male Wistar rats were randomly designated into 7 groups of 10 and treated as follows: Group 1: Received saline for 20 days. Group 2: Were injected 100 mg/kg/d of GM intraperitoneally (ip), for 10 days and saline for 10 more days. Group 3: Received GM for 10 days then 20 mg/kg garlic ip for the next 10 days. Group 4: Received GM for 10 days and MF (100 mg/kg) orally for the next 10 days. Group 5: Received GM for 10 days and a combination of MF and garlic for the next 10 days (100 and 20 mg/kg, respectively). Group 6: The same as group 5but with half-doses of MF and Garlic. Group 7: Received GM for 10 days together with a combination ofMF and garlic. On 20th day of the experiment the serum blood urea nitrogen (BUN) and creatinine (Cr) were measured and compared in different groups. Results: GM injection significantly increased the serum BUN and Cr (P &lt; 0.05). Administration of MF, garlic or their combination with or after injection of GM (high doses) could atenuate BUN and Cr. Conclusions: The results indicate that MF and garlic or their combination have curative and protective activity against GM nephrotoxicity

Ameliorative effect of melatonin against contrast media induced renal tubular cell injury

Background and Objective: Reactive oxygen species (ROS) is a mediator of renal damage. Melatonin is a potent-free radical scavenger. Our objective was to test whether melatonin would protect against the nephrotoxicity of contrast media. Methods: In an experimental study 40 adult male Wistar rats were randomly divided into four equal groups including: 1) Control group (No drug), 2) Contrast media group (10 ml/kg iodixanol i.v. single dose), 3) Contrast media and melatonin (first 10 ml/kg iodixanol then 10 ml/kg/day melatonin by i.p. injection on days 3,4 and 5) and 4) Contrast media and melatonin pretreatment group (melatonin 10 ml/kg/day by i.p. injection on 1, 2 and 3 days, then 10 ml/kg iodixanol by i.v. injection on third day. The blood creatinine and BUN as well as the histological changes were evaluated for severity of renal injury (degeneration, vacuolization of tubular renal cells, dilatation of tubular lumen and presence of debris in the lumens), by scoring from one to four. Results: Contrast media significantly increased the creatinine and BUN and renal injury (p < 0.05). Melatonin prevented and reversed the injury induced by contrast media (P < 0.05). Pretreatment with melatonin reduced the renal injury induced by contrast media (P < 0.05). Conclusion: Melatonin is an effective drug to prevent contrast-induced renal injury. Therefore its usage (especially pretreatment) might be beneficial in patients who are planning to use contrast media agents

Paradoxical Effects of Atorvastatin on Renal Tubular Cells An Experimental Investigation

Introduction. Atorvastatin has antioxidant activity and has been reported to increase blood antioxidant capacity. This study aimed to evaluate the effect of different doses of atorvastatin on gentamicin-induced kidney injury. Materials and Methods. In this experimental study, 30 male Wistar rats were designated into 6 equal groups for a 7-day period of intraperitoneal injections of gentamicin and atorvastatin. Group 1 received gentamicin, 80 mg/kg. Group 2 received phosphate buffer as the vehicle of atorvastatin. All rats in groups 3, 4, and 5 received gentamicin, 80 mg/kg/d, and then, after a 1-hour interval, atorvastatin was injected for 7 days as follow: group 3, 10 mg/kg/d; group 4, 50 mg/kg/d; and group 5, 150 mg/kg/d. Rats in group 6 received only 150 mg of atorvastatin. On the 8th day, blood samples were collected for evaluation of creatinine and blood urea nitrogen levels, and the animals' kidneys were dissected out for histopathological examinations. Results. Morphological damages to the tubular cells in groups 3 and 4 were less than the those in groups 1 and 5. Injuries to the renal tubular cells in the rats of group 5 (gentamicin and atorvastatin, 150 mg/kg/d) and in group 6 (atorvastatin 150 mg/kg/d alone) were more extensive than those in group 1. Conclusions. The none-dose-dependent effect of atorvastatin in inducing renal tubular cell protection and renal tubular toxicity of atorvastatin in higher dose suggest administration of low-dose atorvastatin in critical conditions associated with renal tubular cell protection

The hepatic response following infection with Listeria monocytogenes

In the present study, we investigated the liver specific response upon infection with L. monocytogenes, a model pathogen for Gram-positive infections over a period of 5days. We used whole genome microarray chips to determine the temporal transcriptome at five observation points. Relative mRNA levels were validated for a representative subset of genes by quantitative Real-Time PCR. In the analysis of these data we followed a strict methodology. The quality of microarray data was ensured by several measures, including quality control tools developed and optimized at our institution. The biological effects of differentially expressed genes were investigated and interpretation of these results was followed by confirmatory experiments. In conclusion, this work allows a unique insight into regulatory networks of several biological processes and interconnections following an infection with L. monocytogenes. Based on our results and by integration of known literature, LXR-&#945; and related transcription factors are proposed to be fundamental for the regulation of hepatic and subsequently systemic response to pathogens.In der vorliegenden Studie untersuchten wir die Leber-spezifische Antwort nach Infektion mit L. monocytogenes, ein Gram-positives Modell-Bakterium über einen Zeitraum von 5 Tagen hinweg. Dabei machten wir Gebrauch von whole genome microarrays, mit dessen Hilfe das transiente Transkriptom zu fünf verschiedenen Zeitpunkten bestimmt wurde. Relative mRNA-Veränderungen wurden anhand einer repräsentativen Auswahl von Genen mittels quantitativer Echtzeit-PCR validiert. Die Analyse gewonnener Daten folgte einer strikten Methodologie. Die Qualität der microarray Daten wurde durch bioinformatische Programme, die an unserem Institut enwickelt und optimiert wurden, gesichert. Basierend auf dem Expressionsmuster differenziell regulierter Gene wurden biologische Rückschlüsse gezogen, die in subsequenten Experimenten untersucht und validiert wurden. Zusammenfassend bietet diese Arbeit einen einzigartigen Einblick in regulatorische Netzwerke verschiedenster biologischer Funktionen und Interaktionen nach Infektion mit L. monocytogenes. Basierend auf diesen Resultaten und eingebettet in bekannte Literatur, stellt sich eine herausragende Rolle für LXR und verwandte Transkriptionsfaktoren bei der hepatischen und subsequent auch systemischen Immunantwort dar

Nephrotoxicity of hydroalcoholic extract of Teucrium polium in Wistar rats

Background and Objectives: Teucrium polium L. (Calpoureh) is a wild-growing flowering plant, found abundantly in South-West of Asia, Europe and North Africa. Traditionally, Teucrium polium L. (Calpoureh) has been used for different pathological conditions. In traditional Iranian medicine, the tea of Teucrium polium L. is used for treating many diseases such as type 2 diabetes. It is believed that this plant has beneficial therapeutic properties. However, further studies are necessary to identify its toxic effects. The aim of this study was to evaluate the nephrototoxicity of hydroalcoholic extract of T. polium in male Wistar rats. Methodology: In this experimental study, 100 rats were divided into 10 groups of ten each. Five groups were injected intraperitoneally (ip), 50, 100, 150, 200 mg/kg extracts or normal saline for 28 days and sacrificed to study the probable kidney damage. Five other groups were injected the same drug regimen, but they were sacrificed 28 days after cessation of drug injections to investigate the effect of possible complication or regeneration during recovery. Results: Following 28 days of T. Polium consumption (phase I), kidney damages were not increased in comparison with control group (P > 0.05). However, following 28 days of drug cessation, kidney damages including degeneration, destruction and vacuolization, appeared in comparison with control group and with increasing the doses of TP. Conclusion: Due to nephrotoxicity, T. polium should not be used or should be consumed with great caution