ObjectiveDesign A prospective study. Setting Nuffield Department of Obstetrics and Gynaecology, Oxford and The William HarveyInstitute, London.Sample Three groups of women: those with pre-eclampsia (n = 19), control pregnant women (n = 19) matched for gestation, age and parity and a group of non pregnant individuals of reproductive age (n = 7).Methods Citrated plasma was stored at -80°C with 20 pmol 0 hydroxytoluene to prevent autooxidation. Plasma samples were assayed for levels of 8 epi-prostaglandin F?,, lipid hydroperoxides, malondialdehyde and also the lipid soluble antioxidant vitamin E.Results There were no differences in 8 epi-prostaglandin F,, lipid peroxide or malondialdehyde levels between the groups of women with pre-eclampsia and those acting as pregnant controls. However, lipid hydroperoxides and malondialdehyde were significantly raised in both preeclampsia and normal pregnancy, compared with nonpregnant women. Vitamin E levels were similar in women with pre-eclampsia and those with a normal pregnancy, but in both groups levels were significantly higher than in nonpregnant women. ConclusionCirculating markers of oxidative stress are raised in normal pregnancy and preeclampsia.To determine whether circulating markers of oxidative stress are elevated in preeclampsia when appropriate precautions are taken to prevent in vitro oxidation

Combined suprascapular and axillary nerve block provides nonequivalent analgesia compared with ISB after arthroscopic shoulder surgery. While SSAX provides better quality pain relief at rest and fewer adverse effects at 24 hours, ISB provides better analgesia in the immediate postoperative period. For arthroscopic shoulder surgery, SSAX can be a clinically acceptable analgesic option with different analgesic profile compared with ISB.

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Insulin-dependent diabetes mellitus (IDDM) is associated with abnormal function of the vascular endothelium and it is proposed that this defect could underlie many of the associated vasculopathies [1]. Studies from our laboratory and others have reported impaired vasodilatory responses to the endothelium-dependent vasodilator acetylcholine (ACh) in isolated arteries from diabetic subjects [2] and in mesenteric [3], femoral [4] and aortic [5] arteries from the streptozotocin (STZ)-diabetic rat (an animal model of uncontrolled IDDM). Although a physiological endothelium-dependent dilatory role of ACh has sometimes been questioned, the reduced relaxation of arteries from diabetic animals to other endothelium-dependent dilators [1] and to increasing luminal flow [6] would suggest that the poor ACh responses reflect a generalised endothelial defect. The abnormal ACh response is likely to result from either decreased nitric oxide (NO) synthesis or increased NO degradation [3,4]. Several mechanisms have been hypothesised, among which is the suggestion that oxidative stress could play an important role [7,8]. Diabetologia (1998) Summary Impaired endothelium-dependent relaxation could underlie many of the vascular complications associated with insulin-dependent diabetes mellitus, and may be mediated by increased oxidative stress. The effect of antioxidants on vascular endothelial function and oxidative stress of streptozotocin-diabetic rats was assessed by dietary supplementation with vitamins E and C. Diabetic (i. v. streptozotocin, 45 mg/kg) male Sprague-Dawley rats were fed one of six supplemented diets containing 75.9, 250, or 500 mg vitamin E/kg chow, 250 mg vitamin C/kg H 2 0, 250 mg vitamin E/kg chow plus 250 mg vitamin C/kg H 2 O, or chow deficient in vitamin E, and then compared to standard-fed control rats. After 4 weeks, small mesenteric arteries were dissected and mounted on a small vessel myograph, concentration response curves were then constructed to noradrenaline, acetylcholine and sodium nitroprusside. Acetylcholinemediated relaxation was impaired in arteries from diabetic rats (pEC 50 6.701 ± SEM 0.120, n = 8) compared to controls (7.386 ± 0.078, n = 6; p < 0.05). The 500 mg/kg vitamin E diet further impaired maximum relaxation to acetylcholine (58.2 ± 10.5 vitamin E, n = 7 vs 84.4 ± 5.3 % standard, p < 0.05), and the combined vitamin E plus C diet impaired maximum relaxation to sodium nitroprusside (48.5 ± 4.1 in vitamin E + C, n = 8 vs 75.6 ± 3.9 % standard; p < 0.01). However, plasma 8-epi-prostaglandin (PG)F 2 a (measured as an estimate of oxidative stress) was dose-dependently decreased in rats on vitamin E supplemented diets. Dietary antioxidant supplementation did not reverse impaired endothelial function in this model of uncontrolled diabetes despite a concomitant decrease in oxidative stress. [Diabetologia (1998) 41: 148±156]

Purpose: To describe a case of ropivacaine toxicity following an ultrasound guided interscalene block and discuss the possible mechanisms involved. Clinical features:A 76-yr-old woman with multiple myeloma was scheduled for open reduction and internal fixation following a pathological fracture of her left upper humerus. She developed central nervous system toxicity with ropivacaine 15 min after a carefully placed ultrasound-guided interscalene catheter. The dose of ropivacaine was within recommended limits and there was no evidence that the catheter was intravascular. Surgery proceeded uneventfully under general anesthesia. The interscalene catheter was left in situ for postoperative evaluation and intravascular injection was ruled out with a colour Doppler study. The total ropivacaine plasma concentration was 3.68 µg·mL -1 . Neurological evaluation, contrast computerized tomography and electroencephalogram were normal. The patient was discharged home with no sequelae. Advanced age, malnutrition, epinephrine and possible elevation of α-1 -acid glycoprotein levels could have altered the pharmacokinetics of plasma ropivacaine and possibly contributed to delayed neurotoxicity. Conclusions:Local anesthetic toxicity is an uncommon but well documented complication of regional anesthesia. Careful monitoring and preparedness for managing complications during the conduct of regional anesthesia cannot be overemphasized. Experience from this case suggests that local anesthesia toxicity can happen within safe dose limits and without intravascular placement despite careful attention to needle and catheter placement, fractionated dosing and frequent aspirations.