Intravenous Regional Anaesthesia (TVRA) for Surgery of the Arm and Foot with 0.5, 0.75-, and 1.0% Prilocaine Summary Qualtity of anaesthesia and risk of intoxication are competing principles in IVRA. To evaluate the optimal prilocaine concentration with injection of 40 ml, 300 patients were randomly allocated to receive either a 0.5 (PM 0.5), 0.75 (PRI 0.5) or a 1.0 (PR1 1.0) per Cent solution. Using PFU 0.5, fifteen patients required supplementary fentanyl, with PRI 0.75 one, and with PRi 1.0 two (p I 0.05). General anaesthesia proved necessary in three patients of the PRI 0.5 and 0.75 groups, respectively, and in one patient of the PFU 1.0 group (NS). With PR1 1.0 seven patients had subjective signs of intoxication upon tourniquet release, with PRI 0.75 none, and with PR1 0.5 one (p I 0.05). Objective symptoms of local anaesthetic toxicity were not observed. The incidence of tourniquet-related pain was 25-30% in all three groups and not related to the prilocaine concentration. In conclusion, with 4 0 ml injection volume the 0.75% solution of prilocaine offers the optimal relation between incidence of anaesthesia and risk of intoxication. ZusammenfassungBei der IVRA treten mit Steigerung der Ge-

There is an increasing number of reports on anaphylactic reactions due to latex. We report on a 9-year-old boy who developed anaphylaxis shortly after induction of anaesthesia due to a combined latex and ethylene oxide allergy. Patients with multiple medical treatment and those with atopy seem to be at risk.

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Aims: To study the relationship between myocardial release of cTnI and myocardial cell death as assessed by the amount of apoptosis and necrosis after cardiac surgery. Methods: Eighteen young pigs were operated on with standardized cardiopulmonary bypass (CPB). Release of cTnI in the cardiac lymph (CL), coronary sinus (CS), and arterial blood (A) was related to postoperative myocardial cell death by both necrosis and apoptosis. Apoptotic cells were detected by a TUNEL detection kit. Necrotic cells were counted by light microscopy. Results: In all animals, cTnI was significantly released and reached peak values observed simultaneously in A (cTnI, 20.1±2.6 ng/ml) (mean ±SEM), CS (19.5±3.2 ng/ml) and CL (5202±2500 ng/ml). Percentage of total myocardial cell death was 3.1±0.5%, including 1.2±0.35% necrosis and 1.9±0.5% apoptosis. cTnI release during and after CPB did not correlate with the degree of myocardial apoptosis or necrosis. Conclusion: Cardiac operations with CPB are related to myocardial cell damage including myocardial cell death due to both necrosis and apoptosis. As the loss of cTnI is not related to the amount of cell death, our results suggest that increased cardiac myocyte membrane permeability more than cell death is responsible for intraoperative and postoperative cTnI release.

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