effects of variations in sleep deprivation on muscle performance, body weight, and body temperature in rats

The objective of this study is to investigate the effect of sleep deprivation [SD] at different duration for one week and two weeks on the muscle performance in the form force of peak contraction, contraction time, and half relaxation time. The study also demonstrates the effect of sleep deprivation on body weight, and level of body temperature in young and old rats. 60 male albino rats are divided into 30 young [30 days old] with mean weight 143 +/- 26.2 grams. 10 control group and rest were subjected to one week and two weeks of sleep deprivation each group 10 rats. The other 30 old rats [70 days old] with mean weight 243 +/- 37.7 grams. 10 control group and rest were subjected to one week and two weeks sleep deprivation each group 10 rats. The results demonstrated that sleep deprivation for one week and two weeks in young and old rats groups caused significant decrease in force of peak contraction, and significant increase in contraction time and in half relaxation time compared with the corresponding values in normal control group. There were significant decreases in body weight in young rats and old rats groups in one week and two weeks sleep deprivation compared with the corresponding values in normal control group. Also there were significant decreases in body temperture in young rats groups in one week and two weeks sleep deprivation in relation to control group. This experiment highlights that muscle performance, body weight, and body temperature are impaired during sleep deprivation either with one or two weeks sleep lack. The impairment increased with the prolonged time of sleep deprivation and with old aged groups than young ones

Comparative effect of antioxidants and l-arginine treatment on nerve conduction velocity and regeneration in streptozotocin-induced diabetic rats

Diabetic polyneuropathy [DPN] is the most common chronic complication of diabetes. In the last two decades it has become increasingly evident that underlying vascular and metabolic mechanisms emerged as a prominent pathogenetic factors for DPN. Oxidative stress is increased in both human and experimental diabetes and has been related to the development of diabetic neuropathy. Vascular factors include increased peripheral resistance also have been implicated in the pathogenesis of experimental diabetic neuropathy [EDN]. It seems still controversial, whether EDN is primarily of vascular or metabolic origin and the aim of the present study was to evaluate the possible contribution of two pathways to the development of such neural complications in type II diabetic animals. Ninety male albino rats were included. The animals groups were as follows: Group I: Control rats which were injected by intraperitoneal [i.p.] by vehicle solution alone, Group II: Diabetic rats not receiving any form of treatment [with fasting blood glucose level above 300mg/kg], Group III: Diabetic rats received daily subcutaneous insulin injection in a dose IIU/day, Group IV: Diabetic rats received intramuscular injection of Vitamin E in a dose 300mg/kg BW, three times/week, Group V: Diabetic rats received intramuscular injection of Vitamin E in a dose 600mg/kg BW, three times/week, Group VI: Diabetic rats received subcutaneous insulin [IIU/day], and intramuscular injection of Vitamin E [300mg/kg BW, three times/week], Group VII: Diabetic rats received subcutaneous insulin [IIU/day], and intramuscular injection of Vitamin E [600mg/kg BW, three times/week], Group VIII: Diabetic rats received daily intragastric L-arginine in a dose of 50mg/kg BW, Group IX: Diabetic rats received daily intragastric L-arginine in a dose of 50mg/kg BW, and subcutaneous insulin [IIU/day]. After 4 weeks, nerve conduction velocity studies were performed, serum glucose was measured, and sciatic nerves malondialdehyde [MDA], glutathione peroxidase [GTPx], endothelial nitric oxide synthase [eNOS] were measured. Diabetic rats had significant higher serum glucose levels, oxidative stress markers, lower eNOS, with delayed nerve conduction velocity [NCV] and lower amplitude of muscle contraction [AMC] as compared with the control group. Treating rats with insulin corrected serum glucose to control values. Treating rats with vitamin E significantly reduced oxidative stress markers, and corrected NCV and improved AC. L-arginine treatment had no effect on serum glucose, oxidative stress markers, but significantly improved NCV and AMC. It can be concluded that EDN is a multifactorial disease, caused by hyperglycemia, oxidative stress and vascular impairment. Conjugate treatment with vitamin E especially in higher doses [600mg/kg B. W.] with insulin could be of great value. Moreover correction of impaired nerve blood flow by drugs that induce NO has proved to be efficient in the protection against, and correction of EDN