Quantitative and selective assessment of sensory block during lumbar epidural anaesthesia with 1% or 2% lidocaine.
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We have examined sensory block during lumbar epidural anaesthesia using a cutaneous current perception threshold (CPT) sensory testing device in 20 patients who received 10 ml of either 1% or 2% lidocaine (lignocaine). CPT at 2000, 250 and 5 Hz stimulation at the trigeminal (V), ninth thoracic (T9) and second lumbar (L2) dermatomes, and dermatomal levels of block to light touch, temperature and pinprick discrimination were measured before and every 5 min until 60 min after epidural lidocaine. There were significant differences between 1% and 2% epidural lidocaine in all CPT at T9 and L2, in addition to maximal cephalad spread of the three sensory modalities. After 2% lidocaine, all CPT increased significantly at T9 and L2. In contrast, only at 250 and 5 Hz for L2 did epidural block with 1% lidocaine produce significant increases in CPT. Maximal level of loss of touch sensation after 1% lidocaine was significantly lower than that of cold and pinprick sensations. We conclude that the dose of lidocaine affected intensity of sensory block during lumbar epidural anaesthesia. In addition, differential neural block resulting from epidural anaesthesia appeared to be associated with a differential effect on nerve fibres of different sizes. (+info)
Comparison of the analgesic potency of xenon and nitrous oxide in humans evaluated by experimental pain.
(18/3693)
We have compared the analgesic potency of MAC-equivalent concentrations of xenon (10, 20, 30 and 40%) and nitrous oxide (15, 30, 45 and 60%) in humans using a multimodal experimental pain testing and assessment technique. We tested 12 healthy volunteers in a randomized, single-blind, crossover study. The following experimental pain tests were used: nociceptive reflex to repeated stimuli; pain tolerance to maximal effort tourniquet ischaemia; electrical stimulation; mechanical pressure; and cold. Reaction time was also measured. Xenon and nitrous oxide produced analgesia to ischaemic, electrical and mechanical stimulation, but not to cold pain. There was no difference in MAC-equivalent concentrations of xenon and nitrous oxide. Both increased reaction time in a similar manner. Xenon and nitrous oxide evoked nausea and vomiting in a large number of volunteers. (+info)
Dose-related beneficial long-term hemodynamic and clinical efficacy of irbesartan in heart failure.
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OBJECTIVES: The primary purpose of this study was to determine the acute and long-term hemodynamic and clinical effects of irbesartan in patients with heart failure. BACKGROUND: Inhibition of angiotensin II production by angiotensin-converting enzyme (ACE) inhibitors reduces morbidity and mortality in patients with heart failure. Irbesartan is an orally active antagonist of the angiotensin II AT1 receptor subtype with potential efficacy in heart failure. METHODS: Two hundred eighteen patients with symptomatic heart failure (New York Heart Association [NYHA] class II-IV) and left ventricular ejection fraction < or = 40% participated in the study. Serial hemodynamic measurements were made over 24 h following randomization to irbesartan 12.5 mg, 37.5 mg, 75 mg, 150 mg or placebo. After the first dose of study medication, patients receiving placebo were reallocated to one of the four irbesartan doses, treatment was continued for 12 weeks and hemodynamic measurements were repeated. RESULTS: Irbesartan induced significant dose-related decreases in pulmonary capillary wedge pressure (average change -5.9+/-0.9 mm Hg and -5.3+/-0.9 mm Hg for irbesartan 75 mg and 150 mg, respectively) after 12 weeks of therapy without causing reflex tachycardia and without increasing plasma norepinephrine. The neurohormonal effects of irbesartan were highly variable and none of the changes was statistically significant. There was a significant dose-related decrease in the percentage of patients discontinuing study medication because of worsening heart failure. Irbesartan was well tolerated without evidence of dose-related cough or azotemia. CONCLUSIONS: Irbesartan, at once-daily doses of 75 mg and 150 mg, induced sustained hemodynamic improvement and prevented worsening heart failure. (+info)
Effects of granulocyte colony-stimulating factor on night sleep in humans.
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Numerous animal studies suggest that cytokines such as interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) mediate increased sleep amount and intensity observed during infection and are, moreover, involved in physiological sleep regulation. In humans the role of cytokines in sleep-wake regulation is largely unknown. In a single-blind, placebo-controlled study, we investigated the effects of granulocyte colony-stimulating factor (G-CSF, 300 microgram sc) on the plasma levels of cytokines, soluble cytokine receptors, and hormones as well as on night sleep. G-CSF did not affect rectal temperature or the plasma levels of cortisol and growth hormone but did induce increases in the plasma levels of IL-1 receptor antagonist and both soluble TNF receptors within 2 h after injection. In parallel, the amount of slow-wave sleep and electroencephalographic delta power were reduced, indicating a lowered sleep intensity. We conclude that G-CSF suppresses sleep intensity via increased circulating amounts of endogenous antagonists of IL-1beta and TNF-alpha activity, suggesting that these cytokines are involved in human sleep regulation. (+info)
Dietary advice for acute diarrhoea in general practice: a pilot study.
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BACKGROUND: Although there is no evidence that diet shortens acute diarrhoea, doctors tend to give dietary advice. AIM: To test the effects of eating and drinking normally on the duration of acute diarrhoea and on the feeling of well-being. METHOD: Randomized single-blinded, controlled trial in urban and semi-urbanized areas. Patients aged 3-70 years suffering with diarrhoea at least three times on the preceding day, lasting no more than five days, were eligible. Two regimes were randomly allocated to practices. In the intervention group, the advice was to eat everything one liked and to drink more. The control group was advised to follow a strict regime of fasting for 24 hours and was subsequently given specified limitations. RESULTS: No significant differences between the 44 patients in the intervention group and the 27 in the control group were found for the duration of watery diarrhoea (median 14 versus 13 hours), or the total number of evacuations (2 versus 2.5). Among the items concerning well-being, only nausea (51% versus 23%) showed a significant difference. CONCLUSION: In this pilot study, the null hypothesis that both treatments will show equal results cannot be confirmed or rejected because of the small number of participants. Despite our efforts, we included fewer patients than expected. This might be due to the data-forms, which were rather complicated and voluminous for both, including doctors and participants. (+info)
Intermittent compression for the treatment of the oedematous hand in hemiplegic stroke: a randomized controlled trial.
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OBJECTIVE: To evaluate the efficacy of intermittent pneumatic compression in treating oedema in the hemiplegic hand of stroke patients. DESIGN: Single-blind randomized control trial. SETTING: acute and rehabilitation elderly care wards in a teaching district. SUBJECTS: 37 Subjects with a first ever hemisphere stroke were randomized to treatment with standard physiotherapy either alone or combined with intermittent pneumatic compression. MAIN OUTCOME MEASURES: The effect of treatment on oedema was assessed using measures of the hand volume of the hemiplegic hand. The impact on function was assessed using the motricity index. RESULTS: The treated group showed no change in the mean stroke hand volume. In the control group the mean stroke hand volume decreased by 3.2 ml. There was no statistically significant difference between the groups. The median scores for the motricity index increased for both groups but there was no significant difference between the groups and any improvement in motor function was independent of any treatment effects. CONCLUSION: Intermittent pneumatic compression at the prescribed pressure and duration of this study is not an effective treatment for the oedematous stroke hand. (+info)
Effects of L-arginine on lower limb vasodilator reserve and exercise capacity in patients with chronic heart failure.
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OBJECTIVE: To determine whether the reactive hyperaemic response of the lower limb increases with improved exercise capacity after acute supplementation with L-arginine, the precursor of nitric oxide, in patients with chronic heart failure. METHODS: 19 patients with chronic heart failure were enrolled in the study. Rest calf blood flow and femoral occlusion induced calf blood flow changes were measured by venous occlusion plethysmography before and after intravenous infusion of 10% L-arginine solution (5 ml/kg for 30 minutes) or placebo. Postexercise calf blood flow was also measured after the experimental infusion. During both postinfusion periods, several exercise capacity indices were determined by a symptom limited cardiopulmonary exercise test using a bicycle ergometer. RESULTS: Baseline calf blood flow, systemic blood pressure, and heart rate showed no significant changes in either of the two experimental conditions. However, the occlusion induced blood flow response was significantly enhanced by L-arginine infusion (mean (SEM) peak flow, 19.6 (1.5) v 28.9 (3.1) ml/min/dl calf tissue; p < 0.01), but not by placebo (peak flow, 19.1 (1.4) v 20.9 (1.8) ml/min/dl calf tissue; NS). Calf blood flow response after exercise was also higher after L-arginine infusion than after placebo (peak flow, 4.8 (0.4) v 6.0 (0.8) ml/min/dl calf tissue; p < 0.05). L-arginine infusion had no significant effect compared with placebo on exercise capacity indices such as peak oxygen uptake (17.1 (1.0) v 15.8 (1.1) ml/min/kg; NS), anaerobic threshold (10.5 (0.6) v 10.4 (0.7) ml/min/kg; NS), and exercise time (296 (23) v 283 (22) s; NS). CONCLUSIONS: Acute supplementation with the nitric oxide precursor L-arginine increased lower limb reactive hyperaemia but did not lead to any significant improvement in exercise capacity in patients with chronic heart failure. (+info)
Adrenoceptors mediating the cardiovascular and metabolic effects of alpha-methylnoradrenaline in humans.
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alpha-Methylnoradrenaline is a widely used tool to study alpha2-adrenoceptor function, but its selectivity for this receptor has not been validated in humans in vivo. To characterize the adrenoceptors mediating cardiovascular and metabolic effects of alpha-methylnoradrenaline in humans, we have performed graded i.v. infusions of alpha-methylnoradrenaline in a randomized, placebo-controlled crossover study in six young, healthy males in the absence and presence of the beta-adrenoceptor antagonist propranolol, the alpha1-adrenoceptor antagonist doxazosin, and the alpha2-adrenoceptor antagonist yohimbine. alpha-Methylnoradrenaline dose-dependently increased heart rate, systolic blood pressure, cardiac output, blood glucose, serum insulin, free fatty acids, and gastrin, shortened the duration of heart rate-corrected electromechanical systole, and decreased diastolic blood pressure, total peripheral resistance, and plasma noradrenaline. Propranolol completely reversed the rise in heart rate and cardiac output, the fall in peripheral resistance, the shortening of electromechanical systole, and the rise in insulin; it blunted the increase in free fatty acids and gastrin. Yohimbine did not significantly influence most parameters but significantly potentiated the rise in insulin, blunted the increase in glucose, and prevented the fall in noradrenaline. Doxazosin was largely without effect on any of these parameters. We conclude that i.v. administered alpha-methylnoradrenaline primarily acts on beta-adrenoceptors in the human cardiovascular and metabolic system, but an alpha2-adrenergic component of the response is detectable for changes of plasma noradrenaline, blood glucose, and serum insulin. Whereas alpha-methylnoradrenaline is selective for alpha2- over alpha1-adrenoceptors, beta-adrenoceptor blockade is required to unmask alpha-adrenoceptor-mediated vasoconstriction. (+info)