Deterioration of cardiac autonomic function over a period of one year in relation to cardiovascular and somatic neuropathy complications in type 2 diabetes mellitus.

AIMS: Progression of cardiac autonomic dysfunction (CADF) in relation to severity of diabetic autonomic neuropathy is well documented. But its progression while coexisting with somatic neuropathy (PNP) and cardiovascular disease (CVD) is less described. We monitored CADF over a period of one year in relation to PNP and CVD in patients with type 2 diabetes mellitus. METHODS: Cardiac autonomic function was assessed in 104 type 2 diabetics. Based on complications study subjects were divided into four subgroups: Group A (No complications); Group B (with CVD); Group C (with PNP); Group D (with CVD and PNP). The parameters measured were: Expiratory:Inspiratory ratio (E:I ratio) and standard deviation of all the N-N intervals (SDNN). These parameters were measured at the baseline and at follow-up. Data analysis was done by employing suitable statistical tests. RESULTS: In Group B: SDNN declined (p<0.001); E:I ratio did not change. In Group C: E:I ratio declined (p<0.01); SDNN did not change. In Group D: SDNN and E:I ratio declined significantly (p<0.001). CONCLUSION: CADF coexisting with PNP and CVD deteriorates with time. E:I ratio and SDNN are suitable markers in monitoring CADF coexisting with PNP and CVD respectively in type 2 diabetes mellitus.

An experimental study of the anticonvulsant effect of amlodipine in mice.

INTRODUCTION: The need for the rational development of newer and adjuvant drugs to treat epilepsy has prompted this study of the potential anticonvulsant effect of amlodipine. METHODS: The acute effect was studied in mice in single doses of 1 mg/kg, 2 mg/kg and 4 mg/kg of amlodipine and the chronic effect was studied in doses of 1 mg/kg and 4 mg/kg (administered daily for 21 days) using the maximal electroshock seizure and pentylenetetrazole-induced seizure models of epilepsy. Sodium valproate and normal saline were used as the standard and control, respectively. RESULTS: For the acute study, in the maximal electroshock seizure model, the administration of 1 mg/kg of amlodipine resulted in the complete abolition of seizures in 33 percent of the mice, and this was increased to 67 percent with the administration of 4 mg/kg. In the pentylenetetrazole-induced seizure model, the administration of 1 mg/kg and 2 mg/kg amlodipine protected 33 percent of the animals from mortality, and 67 percent were protected with the administration of 4 mg/kg. For the chronic study, in the maximal electroshock seizure model, the administration of 1 mg/kg amlodipine resulted in the complete abolition of seizures in 40 percent of the mice and in 60 percent, with the administration of 4 mg/kg. In the pentylenetetrazole-induced seizure model, 50 percent of the mice were protected from mortality with 1 mg/kg amlodipine and 60 percent, with 4 mg/kg amlodipine. CONCLUSION: These findings indicate that amlodipine may be a good candidate as an add-on therapy for epilepsy.

Influencing factors of QTc among the clinical characteristics in type 2 diabetes mellitus.

AIMS: Although the clinical implications of prolonged Q-T interval have been described, the clinical determinants of Q-T interval in type 2 diabetes mellitus are not clear. We examined the influencing factors of QTc in type 2 diabetes mellitus. METHODS: This study involved 207 patients with type 2 diabetes mellitus and 141 healthy controls. QTc was estimated from resting lead II electrocardiogram. Data analysis was done using unpaired Student's 't' and Pearson correlation tests. RESULTS: Only female diabetics with somatic neuropathy had longer QTc compared to controls (p<0.01). Only in male diabetics negative correlation was found between QTc and heart rate response to deep breathing (p<0.01). Male and female study subjects with diabetic retinopathy had longer QTc compared to controls (p<0.01, 0.05). Only male diabetics with hypertension had longer QTc compared to controls (p<0.05). CONCLUSION: QTc prolongation is associated with diabetic neuropathy with sex difference in its manifestation. It is influenced by diabetic retinopathy in male and female diabetics. It is influenced by hypertension in male type 2 diabetics.