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

Respiratory complications after major trauma in suez canal University Hospital: a prospective study

Trauma has become a major civilian problem, and is now a leading cause of mortality and morbidity. Unfortunately, most of the victims of trauma are young persons; however with proper treatment many injured patients can be saved. Aim of the Work: The objective of this study is to assess the incidence of post traumatic respiratory complications in emergency department Suez Canal University Hospital in the period from 1-9-2004 to 31-12-2004, to find out the recommendations needed to reduce the incidence of mortality and morbidity due to respiratory complications. One hundred and fifteen patients presented to emergency department Suez Canal University Hospital in the period from 1-9-2004 to 31-12-2004 with major trauma and follow up of these patient to find out the incidence of respiratory complications by chest X ray, ABG or CT chest. Data will be collected and results will be presented in tables, figures and graphs The mortality in our study was 14.8% although the mortality at emergency department was 2.6% due to severe head injury and excessive hemorrhage and within 24 hours in ICU which was 2.6% due to severe head injury and uncontrolled abdominal hemorrhage and within two weeks in ICU 9,6% due to severe chest infection. Chest infection is the,most common cause of death in post trauma patients

Role of serum neopterin level in unstable angina

Coronary artery disease is the most common form of heart disease and the important single cause of death. Unstable angina is a life threatening disorder and a major cause of emergency medical care. Disruption of vulnerable atheromatous plaque is the most common pathogenic mechanism in unstable angina. Macrophage and T cell lymphocytes are critical in the growth and changes of plaques through the secretion of growth factors, cytokines and extracellular matrix digesting enzymes, which weaken fibrous cap. Neopterin, which is a byproduct of guanosine triphosphate degradation in macrophages activated by interferon gamma being a marker of macrophage activation, is a more direct measurement of immune system activation. Immune system activation may play a pathogenic role in acute coronary syndrome. Neopterin can be used as a marker for activity of coronary disease. The purpose of this study to evaluate the neopterin level in patients had unstable angina and complex coronary artery disease lesions vs. patient with chronic stable angina. Prospective study was performed in 50 patients divided in three groups. Group1: [30 patients with unstable angina class IIIb according to Braunwald classification. Group2: 10 patients with chronic stable angina. Group3: 10 patients with normal coronary angiography. The neopterin level was high significantly in group 1 in compare to both other two groups. There was correlation between the neoperin level and the number of angiographically complex lesion. Neopterin level was not correlated vessel score or stenosis score

Early invasive strategy with facilitated PCI [GPIIBIIIa receptor blocker plus half dose fibrinolytic therapy plus PCI] versus primary PCI in acute ST segment slevation myocardial infarction

This study was done in El-Hussein and Bab Elsharia University Hospitals. From 2002 till 2004. Patients with ST-segment elevation acute myocardial infarction typically require reperfusion therapy either with fibrinolytic therapy or mechincal reperfusion with PTCA and stent implantation. Seventy patients presents within 12 hours of onset of chest pain with St-segment elevation myocardial infarction Half of the patients [group A] undergo aggressive management with facilitated PCI, half dose streptokinase 750000 IU, plus GP IIb/IIIa blocker Tirofiban in weight adjusted dose Coronary angiography done within 90 minutes of presentation with PCI for the infarct related artery [group A].The other half [group B] undergo coronary angiography within 90 minutes to asses TIMI flow with primary PCI to the infarct related artery. Low dose heparin 60 IU bolus then 7 IU/kg infusion for all patients. Aspirin 150 mg at presentation and then once daily. Clopidogrel 300 mg is given to all patients before the procedure and then 75 mg daily for at least one month. Twenty six patients out of thirty five in group A had an anterior wall MI [74.3%] and nine patients had an inferior wall MI [25.7%]. Twenty five patients out of thirty five in group B had an anterior wall MI [71.4%] and ten patients had an inferior wall MI [28.6%]. TIMI flow before PCI, In group A there was fifteen patients out of thirty five had TIMI three flow [42.9%], six patients had TIMI two flow [17.1%], three patients had TIMI one flow [8.6%], and eleven patients had TIMI O flow [3 1.4%]. In group B there was five patients out of thirty five patients had TIMI three flow [14.3%], nine patients had TIMI two flow [25.7%], four patients had TIMI one flow [11.4%], and seventeen patients had TIMI 0 flow [48.6%]. TIMI flow after PCI, in group A there were thirty one patients out of thirty five had TIMI three flow [88.6%], one patient had TIMI two flow [2.9%], and three patients had TIMI 0 flow [8.6%]. In group B there were twenty nine patients out of thirty five patients had TIMI three flow [82.9%], three patients had TIMI two flow [8.6%], one patient had TIMI one flow [2.9%], and two patients had TIMI 0 flow [5.7%]. During the period of follow up nine patients out of thirty five in group A developed chest pain and underwent coronary angiography total occlusion of the stent was present in four patients, significant [more than 50%] lesion was found in three patients, and insignificant [less than 50%] lesion was found in two patients. Nine patients out of thirty five in group B developed chest pain and underwent coronary angiography, total occlusion of the stent was present in one patient, significant [more than 50%] lesion was found in five patients, and insignificant [less than 50%] lesion was found in three patients. There was no statistically significant difference between the incidences of restenosis in both groups. Two patients out of thirty five in group A had a myocardial reinfarction during the period of follow up [5.7%].One patient out of thirty five in group B had a myocardial reinfarction during the period of follow up [2.9%]. In this study we conclude that facilitation of PCI did not affect the use of predilatation or the decrease the incidence of failed PCI. However it increased the incidence of TIMI 2 or 3 flow and decreased the incidence of TIMI 0 or 1 flow before PCI, as expected these incidences became nearly equal in both groups after PCI

NMDA Antagonist: ketamine for balanced analgesia in the perioperative period. What is the preferential route?

This study aimed to investigate whether intraoperative sub-anesthetic doses of ketamine could represent an efficient constituent of balanced analgesia and which is the preferential route of administration, either systemic [intravenous] or epidural. Fifty patients scheduled for upper abdominal operations under combined epidural/general anesthesia were included in the study. Before skin incision, all patients received an epidural bolus, followed by an infusion of continuous bupivacaine/fentanyl/clonidine mixture. They were randomly assigned to receive: No ketamine [group 1]; i.v. ketamine at a bolus dose of 0.25 mg/kg, followed by an infusion of 0.125 mg/kg/h [group 2]; i.v. ketamine 0.5 mg/kg and followed by an infusion of 0.25 mg/kg/h [group 3]; epidural ketamine 0.25 mg/kg and 0.125 mg/kg/h [group 4] or 0.5 mg/kg and 0.25 mg/kg/h [group 5]. All i.v. And epidural anesthesia stopped at the end of surgery and the patients were connected to i.v. Morphine patient-controlled analgesia [PCA] device. The study supported the theory that sub-anesthetic doses of i.v. ketamine [0.5 mg/kg bolus, followed by 0.25 mg/kg/h] given during anesthesia are useful adjuvant in perioperative-balanced analgesia. Moreover, they showed that the systemic route is the preferential route