Petrov, Stojmir
Preferred name
Petrov, Stojmir
Official Name
Petrov, Stojmir
Main Affiliation
Email
stojmirpetrov@yahoo.com
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Item type:Publication, Улогата на ендоетелин-1 во развојот на дијабетична нефропатија индуцирана со стрептозоцин(Macedonian Pharmaceutical Association, Ss. Cyril and Methodius University in Skopje, Faculty of Pharmacy, 2006); ; ; ; Dijabeticnata nefropatija pretstavuva edna od hronicnite mikrovaskularni komplikacii na dijabetot, so multifaktorijalna i ne do kraj rasvetlena etiopatogeneza. So ogled na toa sto kaj pacientite so dijabet, osobeno kaj onie so dijabeticna nefropatija, se najdeni zgolemeni vrednosti na endotelin-1, se pretpostavuva deka istiot mozhe da ima znacajna uloga vo razvojot na dijabeticnata nefropatija. Osnovna cel na nashata studija beshe da se detektiraat promenite vo plazmatskoto nivo na endotelin-1 po eksperimentalno induciran dijabet, i dijabeticna nefropatija kaj staorci so streptozocin. So ogled na dobro poznatite efekti na AKE-inhibitorite, vo ovaa studija go ispituvavme i vlijanieto na enalapril (AKE inhibitor) na plazmatskite koncentracii na endotelin-1, kako i negovite efekti vo tretmanot na dijabeticna nefropatija. Ednokratnata i.p. administracija na streptozocin (STZ) predizvika signifikantno zgolemuvawe na plazmatskite koncentracii na endotelin-1, proprateni so jasno izrazeni simptomi i znaci na dijabeticna nefropatija (mikroalbuminurija, zgolemeni urinarni vrednosti na N-acetyl-fl-D-glucosamidase, zgolemeni serumski koncentracii na urea, poliurija). Cetiri nedelniot tretman so enalapril dovede do signifikantno namaluvawe na plazmatskite koncentracii na endotelin-1 i do podobruvawe na simtomite i znacite na dijabeticnata nefropatija. Dobienite rezultati potvrduvaat deka endotelin-1 mozhe da ima znacajna uloga vo razvojot i progresijata na dijabeticnata nefropatija, a AKE inhibitorite, odnosno enalapril, mozhat da ja ublazhat i usporat progresijata na dijabeticnata nefropatija. - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Effect of angiotensin II type 1 (AT1) receptor antagonist on the endothelial dysfunction in spontaneously hypertensive rats in correlation with the nitric oxide system(Comenius University, School of Medicine - AEPRESS SRO, 2003); ; ; Jovanoska, EHypertension is associated with impaired endothelial function, which can be explained by a decrease in nitric oxide (NO) generation or by an enhanced inactivation of NO after its release from endothelial cells. The aim of this study was to investigate the effect of long-term treatment with losartan, an angiotensin II (AT1) receptor antagonist, on endothelial dysfunction in an animal model of hypertension in relation to the nitric oxide system. Losartan was administered to 48 sixteen-week-old spontaneously hypertensive rats, in a dose of 10 mg/kg bw/daily in drinking water, for 12 weeks. Systolic blood pressure (SBP) was measured at the beginning, after 4, 8 and 12 weeks of treatment, by the tail-cuff plethysmographic method. At each mentioned time point, a group of 12 animals was sacrificed and blood was withdrawn from the abdominal aorta. Plasma samples were used for determination of total nitrate/nitirite levels, cyclic guanosine monophosphate (cGMP) and endothelin (ET) 1 levels. Statistical evaluation of the results was performed by the use of a computer statistical programme Statistica for Windows 5.0. Losartan produced a significant decrease of SBP at all time points. On the other hand, long-term treatment with this AT1 receptor antagonist produced a significant increase of nitrate/nitrite and cGMP plasma levels. When we compared the values of SBP with plasma nitrate/nitrite as well as with cGMP values, a statistically significant correlation was established. A statistically significant decrease in plasma endothelin 1 values was found during the whole study period. Also, a positive correlation between SBP and plasma endothelin 1 concentrations was observed. Long-term losartan (AT1 receptor antagonist) treatment, apart from its blood pressure lowering effect in hypertension, has beneficial effects on the endothelial dysfunction which is at least partially due to the activation of the nitric oxide system. (Tab. 1, Fig. 2, Ref. 33.) - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Erythropoietin reduces cumulative nephrotoxicity from cisplatin and enhances renal tubular cell proliferation(Macedonian Academy of Sciences and Arts, 2008-12); ; ; ; Cisplatin, a heavy metal complex, is one of the most active drugs used in the treatment of several human malignancies. However, high-dose therapy with cisplatin is limited by its cumulative nephrotoxicity. The main objectives of this study were to determine the role of recombinant human erythropoietin (Epoetin alfa) in the prevention of nephrotoxicity induced experimentally in Wistar rats by long-term administration of cisplatin (2 mg/kg/b.w./week) over eight weeks, and an evaluation of its effect on renal tubular cell proliferation. The animals were randomly assigned into three groups, each including 25 rats. Group 1 (CP) received only cisplatin (2 mg/kg/b.w./week), group 2 (CP+EPO) received cisplatin (2 mg/kg/b.w./week) and epoetin alfa (150 IE/kg/b.w./three times a week), and group 3 (control group) received only saline. During the study, the following tests for the assessment of the renal function and renal damages were performed: determination of concentration of serum creatinine and BUN and determination of total protein quantity in 24-hour urine samples. At the end of the study, the abdomen was opened and both kidneys of the rats were removed and sent for histological and morphometric analysis. Ki-67 was used as a tool to determine a proliferative index. The results obtained have shown that epoetin alfa significantly reduced the functional renal failures and renal damages, and increased toleration of high doses of cisplatin. At the same time, our results with regard to tubular proliferative index have confirmed that one of the possible mechanisms by which erythropoietin accomplishes its renoprotective effect is stimulation of tubular cell proliferation and regeneration.