Browsing by Author "Djuric, Dragan (36016317400)"

In this study the authors evaluated correlation between aging and brachial endothelial and vascular smooth muscle dysfunction, changes in carotid geometry, and left ventricular remodeling. Vasomotor influences of brachial endothelium and brachial smooth muscle function to reactive hyperemia and nitroglycerin (400μg, sublingual spray) were assessed by noninvasive ultrasound in 66 healthy subjects of different ages (20-82 years). Carotid intima-media thickness and left ventricular mass index were also assessed by ultrasound and compared with brachial hemodynamic parameters. All results were analyzed by linear regression analysis. The response of brachial artery diastolic diameter to reactive hyperemia decreased with aging (p < 0.0001). Also, the response of brachial artery diastolic diameter to nitroglycerin increased relative to aging (p < 0.004). Age-related correlations between increased carotid intima-media thickness and brachial artery diastolic diameter response to reactive hyperemia (p < 0.01) as well as between increased carotid intima-media thickness and increased left ventricular mass index (p < 0.001) were found. However, there was no correlation between brachial artery diastolic diameter response to reactive hyperemia and increased left ventricular mass index (p > 0.05). The study showed that aging influences not only brachial endothelial vasomotor properties but also vascular and cardiac geometry. The authors believe that modern therapeutic approach should take these results into consideration to establish new vasculoprotective and cardioprotective strategies.

The aim of this study was to examine the effects of a methionine-enriched diet on anxiety-related behavior in rats and to determine the role of the brain oxidative status in these alterations. Adult male Wistar rats were fed from the 30th to 60th postnatal day with standard or methionine-enriched diet (double content comparing with standard diet: 7.7 g/kg). Rats were tested in open field and light-dark tests and afterwards oxidative status in the different brain regions were determined. Hyperhomocysteinemia induced by methionine-enriched diet in this study decreased the number of rearings, as well as the time that these animals spent in the center of the open field, but increased index of thigmotaxy. Oxidative status was selectively altered in the examined regions. Lipid peroxidation was significantly increased in the cortex and nc. caudatus of rats developing hyperhomocysteinemia, but unaltered in the hippocampus and thalamus. Based on the results of this research, it could be concluded that hyperhomocysteinemia induced by methionine nutritional overload increased anxiety-related behavior in rats. These proanxiogenic effects could be, at least in part, a consequence of oxidative stress in the rat brain. © 2016, Canadian Science Publishing. All rights reserved.

The aim of this study was to examine the effects of a methionine-enriched diet on anxiety-related behavior in rats and to determine the role of the brain oxidative status in these alterations. Adult male Wistar rats were fed from the 30th to 60th postnatal day with standard or methionine-enriched diet (double content comparing with standard diet: 7.7 g/kg). Rats were tested in open field and light-dark tests and afterwards oxidative status in the different brain regions were determined. Hyperhomocysteinemia induced by methionine-enriched diet in this study decreased the number of rearings, as well as the time that these animals spent in the center of the open field, but increased index of thigmotaxy. Oxidative status was selectively altered in the examined regions. Lipid peroxidation was significantly increased in the cortex and nc. caudatus of rats developing hyperhomocysteinemia, but unaltered in the hippocampus and thalamus. Based on the results of this research, it could be concluded that hyperhomocysteinemia induced by methionine nutritional overload increased anxiety-related behavior in rats. These proanxiogenic effects could be, at least in part, a consequence of oxidative stress in the rat brain. © 2016, Canadian Science Publishing. All rights reserved.

Extensive experimental evidence confirms the role of oxidative stress as a major contributor to the pathogenesis of acute kidney injury (AKI). However, less information is available on the evolution of prooxidant-antioxidant parameters from early to end-phase renal function decline in humans. This study aimed to determine the oxidative status in dynamic throughout the evolutionary phases of the disease. The study included patients with cardiovascular pathology and AKI hospitalized in the intensive care unit (n = 69) and age-matched healthy controls (n = 30). They were followed through three phases of AKI; first phase was the phase of diagnosis, which is characterized by oliguria/anuria, second phase was established diuresis, and third phase was the polyuric phase. In these phases of the disease, blood samples were taken from the patients for biochemical analysis. From the collected whole blood, we measured spectrophotometrically prooxidants: index of lipid peroxidation, measured as Thiobarbituric acid reactive substances (TBARS), nitrite (NO 2 – ), superoxide anion radical (O 2 – ) and hydrogen peroxide (H 2 O 2 ), and antioxidants: activity of superoxide dismutase (SOD), catalase (CAT) and reduced glutathione (GSH) from erythrocyte lysate. Comparing the results of the three measurements, a significant difference was found in the levels of NO 2 – and GSH, both of which increased in the second phase (P < 0.05) and then decreased in the third phase, and a significant increase in TBARS, which was elevated in the second phase (P < 0.05) and did not change significantly until the third phase. Our results showed phase-dependent modification in 3 parameters of the oxidative status (TBARS, NO 2 – and GSH). Whether these changes contribute to the deterioration of renal function in AKI remains to be established. © 2015 by The Chinese Physiological Society and Airiti Press Inc.

Extensive experimental evidence confirms the role of oxidative stress as a major contributor to the pathogenesis of acute kidney injury (AKI). However, less information is available on the evolution of prooxidant-antioxidant parameters from early to end-phase renal function decline in humans. This study aimed to determine the oxidative status in dynamic throughout the evolutionary phases of the disease. The study included patients with cardiovascular pathology and AKI hospitalized in the intensive care unit (n = 69) and age-matched healthy controls (n = 30). They were followed through three phases of AKI; first phase was the phase of diagnosis, which is characterized by oliguria/anuria, second phase was established diuresis, and third phase was the polyuric phase. In these phases of the disease, blood samples were taken from the patients for biochemical analysis. From the collected whole blood, we measured spectrophotometrically prooxidants: index of lipid peroxidation, measured as Thiobarbituric acid reactive substances (TBARS), nitrite (NO 2 – ), superoxide anion radical (O 2 – ) and hydrogen peroxide (H 2 O 2 ), and antioxidants: activity of superoxide dismutase (SOD), catalase (CAT) and reduced glutathione (GSH) from erythrocyte lysate. Comparing the results of the three measurements, a significant difference was found in the levels of NO 2 – and GSH, both of which increased in the second phase (P < 0.05) and then decreased in the third phase, and a significant increase in TBARS, which was elevated in the second phase (P < 0.05) and did not change significantly until the third phase. Our results showed phase-dependent modification in 3 parameters of the oxidative status (TBARS, NO 2 – and GSH). Whether these changes contribute to the deterioration of renal function in AKI remains to be established. © 2015 by The Chinese Physiological Society and Airiti Press Inc.

The aim of our study was to investigate the behavioral and electroencephalographic manifestations of thioaceta-mide-induced encephalopathy in rats. Male Wistar rats were divided among (i) control, saline-treated, and (ii) thioaceta-mide-treated groups (TAA300 (300 mg/kg body mass); TAA600 (600 mg/kg); and TAA900 (900 mg/kg)). The daily dose of thioacetamide (300 mg/kg) was administered intraperitoneally once (TAA300), twice (TAA600), or 3 times (TAA900), on subsequent days. Behavioral manifestations were determined at 0, 2, 4, 6, and 24 h, while electroencephalographic changes were recorded 22-24 h after the last dose. General motor activity and exploratory behavior, as well as head shake, auditory startle reflex, placement, and equlibrium tests were diminished in the TAA600 and TAA900 groups compared with the control, and were absent in the TAA900 group 24 h after treatment. Corneal, withdrawal, grasping, and righting reflexes were significantly diminished in the TAA900 group compared with the control. Mean electroencephalographic power spectra density was significantly higher in TAA300 and TAA600 and lower in the TAA900 group by comparison with the control. Only a score of 3 (mean dominant frequency ≤ 7.3 Hz and d relative power ≥ 45%) was observed in the TAA900 group. Thioacetamide induces encephalopathy in rats in a dose-dependent manner. A dose of 900 mg/kg TAA may be used as a suitable model of all stages of hepatic encephalopathy.

The aim of our study was to investigate the behavioral and electroencephalographic manifestations of thioaceta-mide-induced encephalopathy in rats. Male Wistar rats were divided among (i) control, saline-treated, and (ii) thioaceta-mide-treated groups (TAA300 (300 mg/kg body mass); TAA600 (600 mg/kg); and TAA900 (900 mg/kg)). The daily dose of thioacetamide (300 mg/kg) was administered intraperitoneally once (TAA300), twice (TAA600), or 3 times (TAA900), on subsequent days. Behavioral manifestations were determined at 0, 2, 4, 6, and 24 h, while electroencephalographic changes were recorded 22-24 h after the last dose. General motor activity and exploratory behavior, as well as head shake, auditory startle reflex, placement, and equlibrium tests were diminished in the TAA600 and TAA900 groups compared with the control, and were absent in the TAA900 group 24 h after treatment. Corneal, withdrawal, grasping, and righting reflexes were significantly diminished in the TAA900 group compared with the control. Mean electroencephalographic power spectra density was significantly higher in TAA300 and TAA600 and lower in the TAA900 group by comparison with the control. Only a score of 3 (mean dominant frequency ≤ 7.3 Hz and d relative power ≥ 45%) was observed in the TAA900 group. Thioacetamide induces encephalopathy in rats in a dose-dependent manner. A dose of 900 mg/kg TAA may be used as a suitable model of all stages of hepatic encephalopathy.

Objectives: The present study examined the association between carotid atherosclerosis, coronary atherosclerosis and common carotid artery intima-media thickness (CCA-IMT) in patients with incident ischemic stroke and its subtypes (75 cases and 21 controls). Methods: Cases with ischemic brain infarctions (IBIs) were consecutively recruited and classified into subtypes by computed tomography and Bamford's classification (the size and site of the infarct) as one of the following: total anterior circulation infarcts (TACIs); partial anterior circulation infarcts (PACIs); posterior circulation infarcts (POCIs); and lacunar infarcts. Controls were recruited among individuals hospitalized for a reason other than cerebrovascular disease at the same institutions and matched for age and sex. Patients and controls underwent B-mode ultrasonographic measurements of CCA-IMT, and were evaluated by a qualified internist and neurologist for the presence of ischemic coronary disease and a history of previous stroke or transient ischemic attack. Results: Of the 75 patients with an acute ischemic stroke, 10 (14%) were classified as TACIs, 34 (45%) as PACIs, 12 (16%) as POCIs and 19 (25%) as lacunar infarcts. Mean CCA-IMT was higher in patients (1.03±0.18 mm) than in controls (0.85±0.18 mm; P<0.0001). The history of cerebrovascular disease was much lower in the patients with POCI and TACI, and the prevalence of ischemic cardiac disease was in the range of 20% in patients with TACIs to more than 40% in patients with PACIs. Conclusions: An increased CCA-IMT as a marker of general atherosclerosis was associated with IBI and reflects cardiovascular risk. Carotid and coronary atherosclerosis were positively correlated with IBIs, with significant differences across the subtypes. © 2006 Pulsus Group Inc. All rights reserved.

Objectives: The present study examined the association between carotid atherosclerosis, coronary atherosclerosis and common carotid artery intima-media thickness (CCA-IMT) in patients with incident ischemic stroke and its subtypes (75 cases and 21 controls). Methods: Cases with ischemic brain infarctions (IBIs) were consecutively recruited and classified into subtypes by computed tomography and Bamford's classification (the size and site of the infarct) as one of the following: total anterior circulation infarcts (TACIs); partial anterior circulation infarcts (PACIs); posterior circulation infarcts (POCIs); and lacunar infarcts. Controls were recruited among individuals hospitalized for a reason other than cerebrovascular disease at the same institutions and matched for age and sex. Patients and controls underwent B-mode ultrasonographic measurements of CCA-IMT, and were evaluated by a qualified internist and neurologist for the presence of ischemic coronary disease and a history of previous stroke or transient ischemic attack. Results: Of the 75 patients with an acute ischemic stroke, 10 (14%) were classified as TACIs, 34 (45%) as PACIs, 12 (16%) as POCIs and 19 (25%) as lacunar infarcts. Mean CCA-IMT was higher in patients (1.03±0.18 mm) than in controls (0.85±0.18 mm; P<0.0001). The history of cerebrovascular disease was much lower in the patients with POCI and TACI, and the prevalence of ischemic cardiac disease was in the range of 20% in patients with TACIs to more than 40% in patients with PACIs. Conclusions: An increased CCA-IMT as a marker of general atherosclerosis was associated with IBI and reflects cardiovascular risk. Carotid and coronary atherosclerosis were positively correlated with IBIs, with significant differences across the subtypes. © 2006 Pulsus Group Inc. All rights reserved.

Rheumatoid arthritis is a chronic inflammatory disease. Reactive oxygen species have been considered as aggravating factors for autoimmune diseases. Fatty acids had been linked in reduction of various diseases by augment of their antioxidant potential and antiinflammatory mechanisms. The aim of this study was to assess the oxidative status in patients with rheumatoid arthritis who used concentrated fish oil only or concentrated fish oil in combination with evening primrose oil in a period of 3 months. Subjects were divided into three groups. The group I consists of patients who had been taking only their regular rheumatologic therapy; group II, patients who had been taking concentrated fish oil; and group III, patients who had been taking concentrated fish oil and evening primrose oil. Peripheral blood samples were used for all the assays. We assessed the following oxidative stress markers: index of lipid peroxidation (thiobarbituric acid-reactive substances (TBARS)), hydrogen peroxide (H2O2), superoxide anion radical (O2 −), nitric oxide (NO), superoxide dismutase activity (SOD), catalase activity (CAT), and glutathione levels (GSH) in erythrocytes. There were no statistically significant changes for any of the oxidative stress parameters in group I. In group II, levels of TBARS, NO2 −, and GSH were increased, while levels of H2O2 decreased. Increased values of TBARS, NO2 −, and SOD were found in group III. Our findings indicate that intakes of fish oil and evening primrose oil may be of importance in mitigation of inflammation, disease activity, and oxidative stress biomarkers, through increased activities of antioxidant enzymes. © 2016, International League of Associations for Rheumatology (ILAR).

Regular training has been claimed to increase the activity of antioxidant enzymes and, consequently, augments the resistance to oxidative stress; however, large volumes of training performed by elite sportsmen could lead to a chronic oxidative stress state. The aim of our study was to assess the oxidative status of elite athletes at the beginning of the preparatory and the beginning of the competition training phases, so that the influence of three months of programmed physical activity on redox status could be determined. The chronic effects of exercise on the redox state of the athletes were compared to the effects of a single bout of karate training. Thirty elite karate athletes, 16-30 years old, were subjected to maximal graded exercise test to estimate their aerobic capacity; blood sampling was also performed to measure levels of superoxide anion radical (O2-), hydrogen peroxide (H2O2), superoxide dismutase activity (SOD) and catalase activity (CAT). The only significant change after the three-month training process was found in the significantly decreased CAT activity (X ± SE: 7.95 ± 0.13 U/g Hb × 103 in the preparatory period, 6.65 ± 0.28 U/g Hb × 103 in the competition stage; P < 0.01). After a single karate training session, there was statistically significant decrease of O2- (X ± SE: 32.7 ± 4.9 nmol/ml in the preparatory period, 24.5 ± 2.5 nmol/ml in the competition stage; P < 0.05) and increase of H2O2 (X ± SE: 11.8 ± 1.0 nmol/ml in the preparatory period, 14.2 ± 0.9 nmol/ml in the competition stage; P < 0.01), as well as significant CAT increase (X ± SE: 6.6 ± 0.6 U/g Hb × 103 in the preparatory period, 8.5 ± 0.5 U/g Hb × 103 in the competition stage; P < 0.05). Although the three-month training process induced, at the first sight, negative changes in the redox state, expressed through the decrease in CAT activity, adequate response of the antioxidant system of our athletes to acute exercise was preserved. © 2012 by The Chinese Physiological Society and Airiti Press Inc.

Regular training has been claimed to increase the activity of antioxidant enzymes and, consequently, augments the resistance to oxidative stress; however, large volumes of training performed by elite sportsmen could lead to a chronic oxidative stress state. The aim of our study was to assess the oxidative status of elite athletes at the beginning of the preparatory and the beginning of the competition training phases, so that the influence of three months of programmed physical activity on redox status could be determined. The chronic effects of exercise on the redox state of the athletes were compared to the effects of a single bout of karate training. Thirty elite karate athletes, 16-30 years old, were subjected to maximal graded exercise test to estimate their aerobic capacity; blood sampling was also performed to measure levels of superoxide anion radical (O2-), hydrogen peroxide (H2O2), superoxide dismutase activity (SOD) and catalase activity (CAT). The only significant change after the three-month training process was found in the significantly decreased CAT activity (X ± SE: 7.95 ± 0.13 U/g Hb × 103 in the preparatory period, 6.65 ± 0.28 U/g Hb × 103 in the competition stage; P < 0.01). After a single karate training session, there was statistically significant decrease of O2- (X ± SE: 32.7 ± 4.9 nmol/ml in the preparatory period, 24.5 ± 2.5 nmol/ml in the competition stage; P < 0.05) and increase of H2O2 (X ± SE: 11.8 ± 1.0 nmol/ml in the preparatory period, 14.2 ± 0.9 nmol/ml in the competition stage; P < 0.01), as well as significant CAT increase (X ± SE: 6.6 ± 0.6 U/g Hb × 103 in the preparatory period, 8.5 ± 0.5 U/g Hb × 103 in the competition stage; P < 0.05). Although the three-month training process induced, at the first sight, negative changes in the redox state, expressed through the decrease in CAT activity, adequate response of the antioxidant system of our athletes to acute exercise was preserved. © 2012 by The Chinese Physiological Society and Airiti Press Inc.

Heart failure (HF) is one of the major cardiovascular causes of death worldwide. In this study, we explored the Effects of folic acid (FA) on cardiometabolic, oxidative stress biomarker changes, and the activity of proliferation marker Ki67 in monocrotaline-induced HF. The research was conducted during a 4 week period using five experimental groups (eight animals per group): Blank solution exposed controls (C1: 1 mL/kg physiological saline, 1 day; C2: 1 mL/kg physiological saline, 28 days), monocrotaline (MCT) induced HF (50 mg/kg MCT), FA (5 mg·kg−1·day−1 FA), and MCT+FA (50 mg/kg MCT, 5 mg·kg−1·day−1 FA). Superoxide dismutase and glutathione peroxidase activities together with total glutathione and parameters of oxidative damage of proteins were determined in cardiac tissue as well as cardiometabolic parameters in plasma or serum. The total glutathionylation was determined by Western blot and proliferation marker Ki67 was assessed by immunohistochemistry. The right ventricular (RV) wall hypertrophy and Ki67 positivity, accompanied by a significant increase of troponin T, has been shown in MCT-induced HF. The antioxidant effect of FA was reflected through superoxide dismutase activity, reduced Ki67 positivity in the RV wall, and a slightly decreased total glutathionylation level. © 2020, Canadian Science Publishing. All rights reserved.

Heart failure (HF) is one of the major cardiovascular causes of death worldwide. In this study, we explored the Effects of folic acid (FA) on cardiometabolic, oxidative stress biomarker changes, and the activity of proliferation marker Ki67 in monocrotaline-induced HF. The research was conducted during a 4 week period using five experimental groups (eight animals per group): Blank solution exposed controls (C1: 1 mL/kg physiological saline, 1 day; C2: 1 mL/kg physiological saline, 28 days), monocrotaline (MCT) induced HF (50 mg/kg MCT), FA (5 mg·kg−1·day−1 FA), and MCT+FA (50 mg/kg MCT, 5 mg·kg−1·day−1 FA). Superoxide dismutase and glutathione peroxidase activities together with total glutathione and parameters of oxidative damage of proteins were determined in cardiac tissue as well as cardiometabolic parameters in plasma or serum. The total glutathionylation was determined by Western blot and proliferation marker Ki67 was assessed by immunohistochemistry. The right ventricular (RV) wall hypertrophy and Ki67 positivity, accompanied by a significant increase of troponin T, has been shown in MCT-induced HF. The antioxidant effect of FA was reflected through superoxide dismutase activity, reduced Ki67 positivity in the RV wall, and a slightly decreased total glutathionylation level. © 2020, Canadian Science Publishing. All rights reserved.

Various studies have shown that the serum concentration of folic acid is inversely related to the serum homocysteine concentration. In addition, data suggest that increases in serum homocysteine levels decrease the activity of acetyl cholinesterase (AChE). The aim of this study was to investigate the effects of acute folic acid treatment on AChE activity in the brain, heart and the blood of a rat. We used male Wistar rats, with a body mass of 250-300 g divided into two categories: a control group given placebo (1 ml 0.9% NaCl, i.p. n1=6) and an experimental group treated with folic acid (1 ml 0.011 μmol/g per body mass, pH 7.4, i.p., n2=6). Sixty minutes after the treatment, the rats were decapitated. The brain and the heart were removed, and blood was taken. The brain and heart were homogenised in phosphate buffer pH 8 (1 ml buff er/20 mg tissue). Th e homogenised tissues and blood were used as a substrate for the spectrophotometric analysis, and enzyme activity was measured in vitro by the Ellman method. Rats treated with folic acid showed significantly reduced AChE activity in the brain and blood compared to the control group (38% and 82%, respectively). We did not observe a significant difference between the enzyme activity in the blood of treated versus untreated rats. In conclusion, this study shows that acute treatment with folic acid decreases the AChE activity in the brain and heart of rats without affecting the AChE activity in the blood.

Homocysteine, an amino acid containing a sulfhydryl group, is an intermediate product during metabolism of the amino acids methionine and cysteine. Hyperhomocysteinemia is used as a predictive risk factor for cardiovascular disorders, the stroke progression, screening for inborn errors of methionine metabolism, and as a supplementary test for vitamin B12 deficiency. Two organic systems in which homocysteine has the most harmful effects are the cardiovascular and nervous system. The adverse effects of homocysteine are achieved by the action of several different mechanisms, such as overactivation of N-methyl-D-aspartate receptors, activation of Toll-like receptor 4, disturbance in Ca2+ handling, increased activity of nicotinamide adenine dinucleotide phosphate-oxidase and subsequent increase of production of reactive oxygen species, increased activity of nitric oxide synthase and nitric oxide synthase uncoupling and consequent impairment in nitric oxide and reactive oxygen species synthesis. Increased production of reactive species during hyperhomocysteinemia is related with increased expression of several proinflammatory cytokines, including IL-1α, IL-6, TNF-α, MCP-1, and intracellular adhesion molecule-1. All these mechanisms contribute to the emergence of diseases like atherosclerosis and related complications such as myocardial infarction, stroke, aortic aneurysm, as well as Alzheimer disease and epilepsy. This review provides evidence that supports the causal role for hyperhomocysteinemia in the development of cardiovascular disease and nervous system disorders. © 2018, Canadian Science Publishing. All rights reserved.

Homocysteine, an amino acid containing a sulfhydryl group, is an intermediate product during metabolism of the amino acids methionine and cysteine. Hyperhomocysteinemia is used as a predictive risk factor for cardiovascular disorders, the stroke progression, screening for inborn errors of methionine metabolism, and as a supplementary test for vitamin B12 deficiency. Two organic systems in which homocysteine has the most harmful effects are the cardiovascular and nervous system. The adverse effects of homocysteine are achieved by the action of several different mechanisms, such as overactivation of N-methyl-D-aspartate receptors, activation of Toll-like receptor 4, disturbance in Ca2+ handling, increased activity of nicotinamide adenine dinucleotide phosphate-oxidase and subsequent increase of production of reactive oxygen species, increased activity of nitric oxide synthase and nitric oxide synthase uncoupling and consequent impairment in nitric oxide and reactive oxygen species synthesis. Increased production of reactive species during hyperhomocysteinemia is related with increased expression of several proinflammatory cytokines, including IL-1α, IL-6, TNF-α, MCP-1, and intracellular adhesion molecule-1. All these mechanisms contribute to the emergence of diseases like atherosclerosis and related complications such as myocardial infarction, stroke, aortic aneurysm, as well as Alzheimer disease and epilepsy. This review provides evidence that supports the causal role for hyperhomocysteinemia in the development of cardiovascular disease and nervous system disorders. © 2018, Canadian Science Publishing. All rights reserved.

[No abstract available]

[No abstract available]

It has been assumed that the cardioprotective effects of propofol are due to its non-anesthetic pleiotropic cardiac and vasodilator effects, in which gasotransmitters (NO, H2S, and CO) as well as calcium influx could be involved. The study on isolated rat heart was performed using 4 experimental groups (n = 7 in each): (1) bolus injection of propofol (100 mg/kg body mass, i.p.); (2) L-NAME (NO synthase inhibitor, 60 mg/kg body mass, i.p.) + propofol; (3) DL-PAG (H2S synthase inhibitor, 50 mg/kg body mass, i.p.) + propofol; (4) ZnPPIX (CO synthase inhibitor, 50 μmol/kg body mass, i.p.) + propofol. Before and after the verapamil (3 μmol/L) administration, cardiodynamic parameters were recorded (dp/dtmax, dp/dtmin, systolic left ventricular pressure, diastolic left ventricular pressure, heart rate, coronary flow), as well as coronary and cardiac oxidative stress parameters. The results showed significant increases of diastolic left ventricular pressure following NO and CO inhibition, but also increases of coronary flow following H2S and CO inhibition. Following verapamil administration, significant decreases of dp/dtmax were noted after NO and CO inhibition, then increase of diastolic left ventricular pressure following CO inhibition, and increase of coronary flow following NO, H2S, or CO inhibition. Oxidative stress markers were increased but catalase activity was significantly decreased in cardiac tissue. Gasotransmitters and calcium influx are involved in pleiotropic cardiovascular effects of propofol in male Wistar rats. © 2019, Canadian Science Publishing. All rights reserved.