INTERNPurpose: To determine the magnitude of the potentiation of rocuronium by desflurane, isotlurane and sevotturane 1.5 MAC anaesthesia. Methods: In a prospective, randomised, study in 80 patients, the cumulative dose-effect curves for rocuronium were determined during anaesthesia with desflurane, sevoflurane and isoflurane (with N20 700/6, I 5 min steady state) or total intravenous anaesthesia (-i-lVA) using propofol/fentanyl. Neuromuscular block was assessed by acceleromyography CTOF-Guarcl| after t~in-of-four (-I-OF) stimulation of the ulnar nerve (2Hz every 12sec, 200 /.tsec duration), Rocuronium was administered in increments of 100/.tg'kg -~ until first twitch (TI) depression > 95%, Results: Rocuronium led to more pronounced T I depression with destturane or sevoflurane anaesthesia than with TIVA. The EDs0 and EDg.were lower during desflurane (95 _ 25 and 190 + 80 h,g'kg -t) and sevoflurane (120 _+ 30 and 210 _+ 40 pg-kg z~) than with TIVA (I 50 _+ 40 and 310 -+ 90 pg-kg -I) (P < .01), while the difference was not significant for isoflurane (I 30 + 40 and 250 + 90pg'kg-I), Following equi-effective dosing (T~ > 95%) the duration to 25% T recovery, recovery index (25/75), and TOF070 was: 13.2 ___ 1.8, 12.7 _+ 3.4, and 26.9 + 5.7 min during anaesthesia with desflurane; 5.5 +_ 5.0, I 1.4 _ 3.8, ai~d 31.0 _+ 6.0 min with sevoflurane; 13.9 + 4.7, 10.7 _ 3,3, and 26.3 +_ 8.9 min with isoflurane; and 13.9 -+ ,3.9, I 1,3 _+ 5.7, and 27.5 +-8.2 min with TIVA anaesthesia (P: NS). Conclusion: Interaction of rocuronium and volatile anaesthetics resulted in augmentation of the intensity of neuromuscular block but did not result in significant effects on duration of or recovery from the block. ', 13,9 +__ 4,7', I0,7 +--3,3 et 26,3 +_ 8,9 min avec l'isoflurane; enfin, 13,9 ---3,9; 11,3 __. 5,7 et 27,5 ---8,2 rain avec I'AEI (P: NS). Conclusion : l'interaction du rocuronium et des anesth~siques volatils a provoquE l'augmentation de l'intensitE . du bloc neuromusculaire mais n'a pas eu d'effet significatif sur la dur& du bloc ou sur la rEcupEration qui a suivi.

I The influence of ouabain (0.4 jM) on contractile force and cellular Na and K concentrations was investigated in isolated left atria of the guinea-pig at rest and at different beat frequencies. Simultaneously the binding of ouabain to the tissue was determined. 2 Strict dependence of rates of onset of positive iontropic action and of binding of ouabain on beat frequency are limited to conditions where no alterations of cellular Na and K concentrations occur. A correlation was observed between sodium flux per unit time and the development of positive inotropism and binding to the receptors of ouabain. 3 Ouabain exerts its positive inotropic effect without affecting the intracellular Na and K concentrations in spite of the fact that under these conditions even the majority of binding sites, i.e. Na-Kadenosine triphosphatases (Na-K-ATPases), are occupied by the drug. The positive inotropic effect. may be explained by a ouabain-induced conformational alteration of the Na-K-ATPase which leads to structural alterations of the plasmalemma connected with an increased availability of coupling calcium. 4 Increasing the frequency of stimulation over a critical value, which appears to be determined by an overloading of the Na pump, induces a decrease in contractile force, cellular accumulation of Na and loss of K, and eventually contracture.

The antibody response in hemodialysis patients was studied after one double dose of influenza vaccine versus one conventional dose plus a booster dose five weeks later. The influenza virus subtype specific IgA and IgG responses were recorded by means of an indirect immunofluorescence assay over a period of 20 weeks. Higher antibody titers, higher response rates and a higher rate of development of protective titers after the single double-dose vaccine indicated it was superior to the single dose/booster dose regimen. It is therefore suggested that hemodialysis patients are immunized with a higher dosage of influenza vaccine to achieve better protection rates.

The cardiac activity of toxin II, a basic polypeptide (m.w.: 4770) from the sea anemone Anemonia sulcata, was investigated in isolated electrically driven guinea-pig and rat auricles, Langendorff heart preparations of guinea-pigs and cat heart-lung preparations. Low concentrations of toxin II (2-100 nM) evoked a dose-dependent positive inotropic effect in the three different heart muscle preparations investigated. Higher concentrations of toxin II produced toxic symptoms like contracture and arrhythmia in auricles and atria (about 25 nM). In isolated cat hearts high toxin II concentrations (about 160 nM) caused unusual toxic symptoms such as long periods of ventricular fibrillation alternating with periods of normal cardiac activity. In rat and guinea-pig auricles as well as in Langendorff hearts of guinea-pigs the extent and rate of the positive inotropic effect induced by toxin II depended on the extracellular calcium concentration (0.45 to 2.7 mM). Toxin II did not alter the heart rate in spontaneously beating isolated cat hearts. In electrically driven guinea-pig auricles, the rate of the inotropic effect induced by toxin II was accelerated by increasing stimulation frequencies. Toxin II did not change the coronary flow in Langendorff heart preparations of guinea-pigs.

Topoisomerase IIalpha expression is tightly linked to cell cycling, and topoisomerase I is likely a reflection of gene transcription. Rapidly progressing glomerular disease therefore appears to be accompanied by active mesangial cell proliferation and increased metabolic activity in glomerular cells. The correlation with inflammatory infiltrates is likely to reflect a positive feedback mechanism involving cytokines, growth factors, and adhesion molecules. Assessment of topoisomerases may therefore be of diagnostic help and might allow prognostic predictions. Provided that our observations are supported by clinicopathological follow-up studies, one might envisage the use of topoisomerase inhibitors in the therapy of chronic proliferative renal disease refractory to current treatment protocols.