The effect of adenosine triphosphate on propofol-induced myopathy in rats: a biochemical and histopathological evaluation

Propofol infusion syndrome characterized by rhabdomyolysis, metabolic acidosis, kidney, and heart failure has been reported in long-term propofol use for sedation. It has been reported that intracellular adenosine triphosphate (ATP) is reduced in rhabdomyolysis. The study aims to investigate the protective effect of ATP against possible skeletal muscle damage of propofol in albino Wistar male rats biochemically and histopathologically. PA-50 (n = 6) and PA-100 (n = 6) groups of animals was injected intraperitoneally to 4 mg/kg ATP. An equal volume (0.5 ml) of distilled water was administered intraperitoneally to the P-50, P-100, and HG groups.One hour after the administration of ATP and distilled water, 50 mg/kg propofol was injected intraperitoneally to the P-50 and PA-50 groups. This procedure was repeated once a day for 30 days. The dose of 100 mg/kg propofol was injected intraperitoneally to the P-100 and PA-100 groups. This procedure was performed three times with an interval of 1 days. Our experimental results showed that propofol increased serum CK, CK-MB, creatinine, BUN, TP I, ALT, AST levels, and muscle tissue MDA levels at 100 mg/kg compared to 50 mg/kg and decreased tGSH levels. At a dose of 100 mg/ kg, propofol caused more severe histopathological damage compared to 50 mg/ kg. It was found that ATP prevented propofol-induced muscle damage and organ dysfunction at a dose of 50 mg/kg at a higher level compared to 100 mg/kg. ATP may be useful in the treatment of propofol-induced rhabdomyolysis and multiple organ damage.

The effect of adenosine triphosphate on propofol-induced myopathy in rats: a biochemical and histopathological evaluation

Propofol infusion syndrome characterized by rhabdomyolysis, metabolic acidosis, kidney, and heart failure has been reported in long-term propofol use for sedation. It has been reported that intracellular adenosine triphosphate (ATP) is reduced in rhabdomyolysis. The study aims to investigate the protective effect of ATP against possible skeletal muscle damage of propofol in albino Wistar male rats biochemically and histopathologically. PA-50 (n = 6) and PA-100 (n = 6) groups of animals was injected intraperitoneally to 4 mg/kg ATP. An equal volume (0.5 ml) of distilled water was administered intraperitoneally to the P-50, P-100, and HG groups.One hour after the administration of ATP and distilled water, 50 mg/kg propofol was injected intraperitoneally to the P-50 and PA-50 groups. This procedure was repeated once a day for 30 days. The dose of 100 mg/kg propofol was injected intraperitoneally to the P-100 and PA-100 groups. This procedure was performed three times with an interval of 1 days. Our experimental results showed that propofol increased serum CK, CK-MB, creatinine, BUN, TP I, ALT, AST levels, and muscle tissue MDA levels at 100 mg/kg compared to 50 mg/kg and decreased tGSH levels. At a dose of 100 mg/ kg, propofol caused more severe histopathological damage compared to 50 mg/ kg. It was found that ATP prevented propofol-induced muscle damage and organ dysfunction at a dose of 50 mg/kg at a higher level compared to 100 mg/kg. ATP may be useful in the treatment of propofol-induced rhabdomyolysis and multiple organ damage.

Relation between proepileptic activity of indomethacin and adrenal gland hormones

The role of inflammation has been shown in the pathogenesis of epilepsy, while glucocorticoids and adrenaline have anti-inflammatory effects. The aim of the present study was to investigate the effects of adrenaline, prednisolone, and indomethacin on caffeine-induced epilepsy [epileptiform activity] in rats and to examine the mechanism of the pro-epileptic effect of indomethacin. The adrenalectomized rats that had been given only adrenaline [the control group] did not die; however, adrenaline did not prevent the adrenalectomized rats which were given prazosin, phenoxybenzamine, yohimbine, metoprolol, and propranolol from dying. In the rats given propranolol + adrenaline, the rate of death was 100%, while this rate was 50% in the groups receiving prazosin + adrenaline, phenoxybenzamine + adrenaline, and metoprolol + adrenaline. The rate was 75% in the group given yohimbine + adrenaline. Prednisolone increased the degree of convulsion in adrenalectomized rats. Over-reduction in the blood catecholamine level made epileptogenesis more severe. It was observed that adrenaline pressed epileptogenesis via its own receptors [alpha -1, alpha - 2, beta - 1, beta - 2]. It was also revealed that all of the adrenergic receptors were responsible due to antiepileptic activity; beta - 2 receptors played the most important role. It was observed that both acute and chronic indomethacin administration reduced the catecholamine levels. The situation in which acute administration of indomethacin did not affect epileptogenesis might originate from the fact that the structure of indomethacin did not significantly increase the corticosterone level

Biological and histopathological investigations of moclobemide on injured ovarian tissue following induction of ischemia-reperfusion in rats

The effects of moclobemide on damaged ovarian tissue induced by is-chemia-reperfusion and damaged contralateral ovarian tissue were investigated in rats, biochemically and histologically. In this experimental study, 40 rats were equally divided into four groups: 10 mg/kg moclobemide, 20 mg/kg moclobemide, ischemia/reperfusion control, and intact control groups. A 2-2.5-cm-long vertical incision was made in the lower abdomen of each rat in order to reach the ovaries, after which a vascular clip was placed on the lower side of the right ovary of each animal in the two treatment groups and the ischemia-reperfusion control group, but not in the healthy [intact control] animal group. The purpose of this procedure was to create ischemia over the course of three hours, then the clips were unclamped to provide reperfusion for the next two hours. At the end of the two hours of reperfusion, all the animals were killed by high-dose anaesthesia and their ovaries were taken and subjected to histological and biochemical [malondialdehyde, nitric oxide, glutathione] studies. The obtained results showed that moclobemide suppressed nitric oxide and malondialdehyde production in the ischemia - reperfusion damage area, and prevented the decrease in endogenous antioxidant levels [glutathione] in the rat ovarian tissue. Moclobemide also prevented infiltration of leukocytes to the ovarian tissue. These results showed that moclobemide protected ovarian tissue against ischemia-reperfusion injury. This study shows that moclobemide represses malondialdehyde and nitric oxide production in the rat ovarian tissue subjected to ischemia-reperfusion injury and keeps the endogenous antioxidant glutathione level from decreasing. Moclobemide also inhibits leukocytic migration into ovarian tissue following ischemia-reperfusion injury. From these results, it is suggested that moclobemide can be used in the treatment of ovarian ischemia-reperfusion injury

effect of metyrosine/prednisolone combination to oophorectomy-induced osteoporosis

Osteoporosis is a chronic disease characterized by a decrease in bone mineral density [BMD] and corruption of the microarchitectural structure of bone tissue. It was investigated whether methylprednisolone had a favorable effect on osteoporotic bone tissue in Oophorectomy induced osteoporotic rats whose endogenous adrenaline levels are suppressed with metyrosine. Bone Mineral Density, number of osteoblast-osteoclast, bone osteocalcin levels and alkaline phosphatase [ALP] measurements were performed. Obtained results were compared with that of alendronate. Oophorectomy induced osteoporosis was exacerbated by methylprednisolone. Alentronate prevented ovariectomised induced osteoporosis, but it couldn't prevent methylprednisolone +ovariectomised induced osteoporosis in rats. Combined treatment with methylprednisolon and metyrosine was the best treatment for preventing osteoporosis but metyrosine alone couldn't prevent osteoporosis in ovariectomised rats

Investigation of the relationship of some antihypertensive drugs with oxidant/antioxidant parameters and dna damage on rat uterus tissue

In this study, we investigated the effects of treatment with chronic antihypertensive drugs [clonidine, methyldopa, amlodipine, ramipril and rilmenidine] on oxidant-antioxidant parameters and toxic effects on DNA in rat uterus tissue. In addition, uterus tissues were examined histopathologically. A total of 36 albino Wistar rats were divided into the following six groups: 0.075 mg/kg clonidine group; 100 mg/kg methyldopa group; 2 mg/kg amlodipine group; 2.5 mg/kg ramipril group; 0.5 mg/kg rilmenidine group; and the healthy group. Rats underwent chronic drug administration for 30 days and at the end, biochemical and histopathological examinations were performed. All data were subjected to one-way ANOVA test. We divided these drugs into the following three groups according to their effects on rat uteri: [I] mild negative effects [clonidine], [II] moderate negative effects [rilmenidine, methyldopa] and [III] drugs which had severe negative effects [amlodipine, ramipril]. These data may help with selection of antihypertensive drugs, in order to determine which drugs have the lowest toxicity in pregnant and non-pregnant [pre-pregnancy] women