Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the coverage of the most important and influential journals to meet the needs of the global scientific community.  
ASCI Database
308-Lasani Town,
Sargodha Road,
Faisalabad, Pakistan
Fax: +92-41-8815544
Contact Via Web
Suggest a Journal
 
Articles by P.L. Sharma
Total Records ( 3 ) for P.L. Sharma
  R. Taliyan , M. Singh and P.L. Sharma
  The present study was designed to investigate the effect of cyclosporine on hyperglycemia induced decrease antinociceptive effect of morphine in rats. Streptozotocin (STZ) (50 mg kg-1, i.p., once) was administered to induce experimental diabetes in the rats. Pain sensitivity was measured using tail-flick and paw withdrawal test. Urinary and serum nitrite concentration was estimated using Greiss reagent. Spleen Homogenate Supernatant (SHS) was prepared from spleen of 28th day diabetic rats and administered to normal rats (400 μL. i.v.) for 28 days. Experimental diabetes significantly decreased paw withdrawal latency to thermal stimuli on day 28 as compared to age matched control rats, indicating that diabetic rats exhibit thermal hyperalgesia. Moreover, analgesic effect of morphine (4 and 8 mg kg-1 s.c.), was progressively decreased in diabetic and SHS treated non diabetic rats. Further, the levels of nitric oxide were also elevated in 28th day diabetic and SHS treated non diabetic rats. However, administration of Cyclosporine (12.5 and 25 mg kg-1 i.p.), an IL-2 inhibitor and splenectomy attenuated diabetes and SHS induced decrease in nociceptive threshold and increase in serum and urinary nitrite levels. It is concluded that cyclosporine have beneficial effect in diabetic neuropathy and also improved the analgesic effect of morphine.
  R. Taliyan and P.L. Sharma
  Diabetic neuropathy is one of the most painful complications of diabetes mellitus, involving progressive neuronal damage and dysfunction and up to 30% of patients with diabetes mellitus developed diabetic neuropathy. Pain caused by diabetic neuropathy is debilitating and often is refractory to classical analgesic, including morphine. The mechanisms underlying cause of diabetic neuropathic pain are complex and both peripheral and central components of the sensory systems are reported to be involved in progression and maintenance of neuropathy. This study summarises data on pathogenesis and on existing and new analgesics such as NSAIDS, opioids, anti-epileptic, membrane stabilising and anti-depressant drugs, that are the mainstay of treatment for alleviating diabetic neuropathic pain. In addition, novel pharmacological approaches and strategies for analgesics such as use of drug combination and their implications will be discussed.
  Harlokesh Narayan Yadav , Manjeet Singh , P.L. Sharma , Dhiraj Mittal , Tapan Behl and Atinder Pal Kaur
  Background: Recently it has been noted that Cyclooxygenase-2 (COX-2) is involved in early phase of ischemic preconditioning (IPC) induced cardioprotection. The present study was designed to investigate the role of COX-2 in the cardioprotective effect of remote aortic preconditioning (RAPC) in rat. RAPC was given by 4 times of 5’ occlusion of abdominal aorta. Materials and Methods: Isolated perfused rat heart was subjected to global ischemia of 30 min., followed by reperfusion for 120 min. Coronary effluent was analyzed for LDH and CK release to access the degree of cardiac injury. Myocardial infarct size was estimated macroscopically using TTC staining. Results: RAPC produced a significant decrease in LDH and CK release and decrease in the myocardial infarct size, as compared to ischemia/reperfusion (I/R) control group. Pretreatment with celecoxib, a selective COX-2 inhibitor and glibenclamide, a blocker of KATP channels, given separately significantly attenuated the RAPC-induced cardioprotection. The cardioprotective effect of celecoxib and glibenclamide, administered in combination was almost equal to the sum total of the effect produced by these drugs when administered singly. Conclusion: On the basis of these results it was concluded that the cardioprotective effect of RAPC may be mediated through upregulation of COX-2 and subsequent activation of KATP channels.
 
 
 
Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility