Background: Carvedilol is a commonly used drug in hypertension, congestive heart failure in diabetics. It has moderate calcium channel blocking property in addition to α1 and non selective β antagonistic activity. Though some studies bring forth the beneficial effects of Carvedilol in cardiovascular comorbidities in diabetes, there is no consensus on its effects on glycaemic levels.
Aims:To evaluate the effect of oral Carvedilol administration for 5 days on blood glucose levels in normal albino rats through Oral Glucose Tolerance Test.
Material and Methods:Twelve adult albino rats of either sex weighing between 150 -200 g were selected from central animal facility and randomly divided into 2 groups -Control [Distilled water (1ml/rat orally)] and Test (0.8mg/kg body weight orally) and the respective drugs were administered over 5 days. Following overnight fasting, on the fifth day 1 hour after the last dose of the respective drug, OGTT was performed. The CBG (Capillary Blood Glucose) levels were measured at 0 min, glucose (2g/ kg body weight) dissolved in water was administered to all the rats orally. The blood sample from tail vein (obtained by tail snipping) at 60 and 150 minutes were analysed for CBG levels using a standardized glucometer.Statistical Analysis: Data was presented as Mean ± SEM. One way ANOVA, independent samples t-test, non-parametric tests, percentages and cross tabs were used in the analysis of data within the same group and between different groups when required.Results: Carvedilol group showed higher CBG levels at all time intervals of OGTT as compared to the Control group i.e., 0, 60 and 150 minutes, the highest being (103.8±5.029 )mg/dl at 60 minutes and was statistically significant. Carvedilol group however showed lesser inter-interval variation compared to the Control group at the same time intervals respectively but was statistically insignificant.
Conclusions:Carvedilol has hyperglycaemic potential when given orally for 5 days in normal albino rats. Though it may be beneficial in diabetics for various comorbid conditions, the glycaemic control may worsen during its use in subjects with prediabetes, diabetes, high risk diabetes.
Acorus calamus, commonly known as sweet flag, has a long history of use in the treatment of a variety of ailments including inflammation, chest pain, digestive disorders and some mental illnesses. Its effects on the neurological conditions have been well documented for axinolytic and antidepressant activities. With this background, the aim of the present study is evaluate the anticonvulsant activity of methanolic extract of Acorus calamus leaves in albino mice. The study included albino mice divided into 8 groups of 6 mice each. Maximum electroshock induced seizures (MES) and Pentylenetetrazole (PTZ) tests were performed on the animal models to evaluate the antiepileptic activity (4 groups were allocated to MES and 4 to PTZ). The methanolic extract of Acorus calamus leaves exhibited a significant reduction in the duration of hind limb extensor phase in MES model (7.116±0.501 seconds for control and 9.116± 0.527 seconds for extract) and delayed the latency of seizures induced by PTZ (485.500±14.941 seconds) when compared with that of the control group (297.000±21.918 seconds). In addition, the groups administered with the extract and sodium valproate in combination exhibited significant results in both MES and PTZ models (T2-92.61% and T4-21.95 %, respectively). Preliminary phytochemical screening performed in several studies has shown the presence of triterpenoids, flavonoids, saponins and tannins. The anticonvulsant activity of Acorus calamus may be mediated by its GABA potentiating activity. It can thus be concluded that the observed anticonvulsant effects could be the resultant of a synergistic action of these phytochemicals. Further studies should be undertaken to substantiate these results on various animal models along with a thorough phytochemical analysis and in silico studies to understand the mode of action of these phytochemicals on various GABA receptor-mediated signaling.
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