We have used the Leiden anaesthesia simulator, which makes use of a standard anaesthesia machine and monitors, and realistically simulates the anaesthesia work place. After obtaining informed consent, 28 anaesthetists and anaesthesia trainees in one hospital took part in the study. All participants were exposed to a pre-scripted simulated "control" scenario of anaphylactic shock (phase 1). The sessions were videotaped and the performances of individual participants were evaluated using a standardized scoring scheme. During phase 2, the participants were allocated randomly to undergo training in the management of either anaphylactic shock (group A, n = 13) or malignant hyperthermia (group B, n = 15) on the simulator. After 4 months, each participant underwent a blinded evaluation session with a pre-scripted "test" scenario of malignant hyperthermia (phase 3). These sessions were also videotaped and evaluated as for phase 1. The participants in group B responded more quickly, treated better and deviated less from the accepted procedure during phase 3 than those in group A. The total performance of participants in group B during phase 3 was significantly better than those in group A. We conclude that training on an anaesthesia simulator does improve the performance of anaesthetists in dealing with emergencies during anaesthesia.

Ventilation with nitric oxide (NO) is increasingly being used to treat pulmonary hypertension in the newborn. In the brain, NO has vasoactive properties and is involved in neurotransmission. However, the effect of inhaled NO on the cerebral blood flow (CBF) and on the cerebral activity is not known. Furthermore, there is little information on the influence of this free radical gas on the redox status in pulmonary vessels. We therefore investigated the effect of inhaled NO (2–60 ppm) on CBF, cerebral activity and redox status in blood effluent from the pulmonary circulation in 6 ventilated newborn lambs before and during group B streptococci (GBS)-induced pulmonary hypertension. Blood pressure in the pulmonary artery (P_ap) and aorta (P_ao), carotid artery blood flow (Q_car) to assess changes in CBF, and electrocortical activity were measured. Blood gases, indices of free radical status and methemoglobin were determined in blood samples obtained from the left ventricle. Inhalation of NO, before and during GBS-induced pulmonary hypertension, decreased P_ap and P_CO2 and increased P_O2. Multiple linear regression revealed that Q_car was positively related to P_CO2, but not to inhaled NO or P_O2 before or during GBS conditions. Electrocortical activity and indices of antioxidative capacity and lipid peroxidation did not change significantly. Methemoglobin was not detected. In conclusion, inhalation of NO (up to 60 ppm) lowered Pap without directly affecting CBF, electrocortical activity, and redox status in the pulmonary vessels. CBF, however, can indirectly be influenced by NO-mediated changes in P_CO2·