Subclinical autonomic neuropathy in Saudi type 2 diabetic patients

To compare the results of autonomic function tests obtained from diabetic patients who had no symptoms or signs of somatic or autonomic neuropathy with those obtained from control subjects. We studied 32 diabetic Saudi patients [17 males, 15 females] and 34 control subjects [17 of either gender] at King Khalid University Hospital, Riyadh, in the period 2004-2005. The mean age of patients was 50.3 +/- 5.04, and of controls was 49.9 +/- 5.86 years. In diabetics, the mean duration of the disease was 8.7 +/- 3.1 years [range 5-15 years], and the mean glycated hemoglobin was 7.76 +/- 1.14. The same observer performed the autonomic function tests. In diabetics, the resting heart rate [beats/min] was 80.5 +/- 4.13, mean orthostasis ratio was 1.06 +/- 0.035, mean Valsalva ratio was 1.19 +/- 0.036, mean forced sinus arrhythmia was 12.66 +/- 0.8 beats/min, mean diastolic blood pressure increase in response to isometric exercise was 13.03 +/- 1.36 mm Hg, and sympathetic skin response was present in only 18 [56.3%] out of 32 patients. These results were significantly different from the control group [p<0.001]. Diabetic patients, with no symptoms or signs of neuropathy, can have impaired autonomic function. We consider this subclinical autonomic neuropathy

effect of vitamine E, L-arginine, N-nitro L-arginine methyle ester and forskolin on endocrine and metabolic changes of rats exposed to acute cold stress

It is a well documented fact that under stress conditions the hypothalamic-pituitary-adrenal axis [HPA] and the sympathetic nervous system [SNS] are stimulated. This results in a series of neural and endocrine adaptations known as the stress response. The current study assessed the effects of acute cold stress on adrenomedullin [ADM] levels in plasma and peripheral tissues [kidneys and heart] of rats, as well as on blood glucose, cholesterol, triglycerides [TG], total proteins both before and after intraperitoneal administration of each of the following: vitamin-E, L-arginine, forskolin and L-NAME. Methods:The current study was conducted in the Department of Physiology, Faculty of Medicine, King Saud University, Saudi Arabia, between September 2003 and March 2004. We observed 6 groups of Wistar rats for their plasma ADM, tissue plasminogen activator [t-PA], total protein, glucose and cholesterol levels. Following exposure to cold stress [-10 degree celcius for 3 hours].Results:Acute cold stress produced a significant increase in ADM levels in plasma, heart and kidney tissues of rats. Furthermore, acute cold stress produced a reduction in cholesterol and plasma protein levels. On the other hand, acute cold stress caused an increase in TG, glucose plasma levels and tissue plasminogen activator [t-PA]. We found hormonal and metabolic changes caused by cold exposure to be decreased or even prevented after vitamin E treatment or after changing nitric oxide [NO] level by L-arginine or L-NAME treatment.Conclusion:The results suggest a regulatory or protective role for ADM in counteracting HPA activation following a variety of physiological and psychological stressors. Oxidative stress or changes in intracellular signals as NO, cyclic-AMP may play a role in explaining some of the metabolic and hormonal changes occurring during acute cold stress

Effect of diclofenac alone or in combination with alpha-tocopherol on the oxidative activity of polymorphonuclear leukocytes in healthy and osteoarthritic individuals

To investigate the effects of diclofenac alone or when combined with alpha-tocopherol on the oxidative activity of polymorphonuclear leukocytes [PMNs] in healthy and osteoarthritic [OA] patients. The study was carried out at the College of Medicine, King Saud University, Riyadh, Kingdom of Saudi Arabia, over the period 1999 to 2000. Twelve healthy controls and 12 osteoarthritic patients were recruited to the study. Twelve healthy controls and osteoarthritic patients were given diclofenac 50 mg thrice daily orally, initially for 5 days then alpha-tocopherol at 200 mg thrice daily orally, was added for another 5 days. Blood samples were drawn before the start of the study [pre-treatment] and at 5 days following treatment with diclofenac alone and 10 days following treatment with diclofenac and alpha-tocopherol. Chemiluminescence [CL] response was measured for whole blood and isolated polymorphonuclear leukocytes [PMNs] on all samples. Diclofenac enhanced CL response of whole blood and of PMNs of healthy controls when stimulated with phorbol myristate acetate [PMA] and opsonized zymosan [OPZ]. Co-treatment with alpha-tocopherol resulted in no appreciable change in the CL response of whole blood when stimulated with PMA or OPZ but a further significant enhancement of CL response of isolated PMNs when these cells were stimulated by either PMA or OPZ. In osteoarthritic patients, diclofenac alone and when combined with alpha-tocopherol showed no significant change in CL response of whole blood. The CL response of PMNs from OA patients was decreased by diclofenac alone. However, this inhibitory effect was not observed when alpha-tocopherol was used together with diclofenac. The effect of diclofenac alone or in combination with alpha-tocopherol did not produce a consistent effect on the CL response of whole blood or isolated PMNs of healthy or osteoarthritic patients

Effect of entamoeba histolytica toxins on isolated human polymorphonuclear leukocytes' phagocytic function

This study was undertaken to investigate the effect of Entamoeba histolytica toxin [Ehp/t] obtained from HM1:IMSS strain on human polymorphonuclear leukocytes [PMN[s]] phagocytic function. A less virulent strain, i.e., NIH:200 was also used in this study for comparison. The results revealed that the toxin obtained from the strain HM1: IMSS inhibited the phagocytic activity of PMN[s] as measured by yeast uptake or chemiluminescence response while the toxin of strain NIH:200 did not show any significant effect. On the other hand, washing of PMN[s] that had been pre-exposed to the toxin of strain HM1:IMSS failed to reverse the effect of the toxin on PMN[s]. Heat inactivation of the toxin failed to alter its effect on PMN[s]. Addition of N-acetyl-D-galactosamine [GalNA[c]] to the PMN[s] did not alter the activity of Ehp/t toxin. These findings suggested that Ehp/t toxin might induce similar effect on PMN[s] of patients infected with ameba